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1
Surguladze, Simon, Paul Keedwell, and Mary Phillips. "Neural systems underlying affective disorders." Advances in Psychiatric Treatment 9, no. 6 (November 2003): 446–55. http://dx.doi.org/10.1192/apt.9.6.446.
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Three main approaches are used to explore the neural correlates of mood disorder: neuropsychological studies, neuroimaging studies and post-mortem investigations. Lesion studies implicate disturbances in the frontal lobe, basal ganglia, striatum and anterior temporal cortex. Early neurocognitive and neuropathological investigations led to a ‘hypofrontality’ hypothesis of unipolar and bipolar depression, but functional neuroimaging has revealed a more complex picture. Thus, increased metabolism may occur in the subgenual anterior cingulate gyrus in resting-state studies of depression and sad-mood induction. Antidepressants may reduce this activity. Amygdala hyperactivation also is associated with affective disorders. Task-related studies reveal abnormal biases in memory, the experience of pleasure and the perception of emotional facial expressions. There is still little clarity whether the abnormalities in brain activation represent state or trait characteristics of affective disorders.
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Rebelos, Eleni, Juha O. Rinne, Pirjo Nuutila, and Laura L. Ekblad. "Brain Glucose Metabolism in Health, Obesity, and Cognitive Decline—Does Insulin Have Anything to Do with It? A Narrative Review." Journal of Clinical Medicine 10, no. 7 (April 6, 2021): 1532. http://dx.doi.org/10.3390/jcm10071532.
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Imaging brain glucose metabolism with fluorine-labelled fluorodeoxyglucose ([18F]-FDG) positron emission tomography (PET) has long been utilized to aid the diagnosis of memory disorders, in particular in differentiating Alzheimer’s disease (AD) from other neurological conditions causing cognitive decline. The interest for studying brain glucose metabolism in the context of metabolic disorders has arisen more recently. Obesity and type 2 diabetes—two diseases characterized by systemic insulin resistance—are associated with an increased risk for AD. Along with the well-defined patterns of fasting [18F]-FDG-PET changes that occur in AD, recent evidence has shown alterations in fasting and insulin-stimulated brain glucose metabolism also in obesity and systemic insulin resistance. Thus, it is important to clarify whether changes in brain glucose metabolism are just an epiphenomenon of the pathophysiology of the metabolic and neurologic disorders, or a crucial determinant of their pathophysiologic cascade. In this review, we discuss the current knowledge regarding alterations in brain glucose metabolism, studied with [18F]-FDG-PET from metabolic disorders to AD, with a special focus on how manipulation of insulin levels affects brain glucose metabolism in health and in systemic insulin resistance. A better understanding of alterations in brain glucose metabolism in health, obesity, and neurodegeneration, and the relationships between insulin resistance and central nervous system glucose metabolism may be an important step for the battle against metabolic and cognitive disorders.
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Xu, Wenyi, Fengzhong Wang, Zhongsheng Yu, and Fengjiao Xin. "Epigenetics and Cellular Metabolism." Genetics & Epigenetics 8 (January 2016): GEG.S32160. http://dx.doi.org/10.4137/geg.s32160.
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Living eukaryotic systems evolve delicate cellular mechanisms for responding to various environmental signals. Among them, epigenetic machinery (DNA methylation, histone modifications, microRNAs, etc.) is the hub in transducing external stimuli into transcriptional response. Emerging evidence reveals the concept that epigenetic signatures are essential for the proper maintenance of cellular metabolism. On the other hand, the metabolite, a main environmental input, can also influence the processing of epigenetic memory. Here, we summarize the recent research progress in the epigenetic regulation of cellular metabolism and discuss how the dysfunction of epigenetic machineries influences the development of metabolic disorders such as diabetes and obesity; then, we focus on discussing the notion that manipulating metabolites, the fuel of cell metabolism, can function as a strategy for interfering epigenetic machinery and its related disease progression as well.
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Vinberg, Maj, Pernille Højman, Bente Klarlund Pedersen, Lars Vedel Kessing, and Kamilla W. Miskowiak. "Effects of erythropoietin on body composition and fat–glucose metabolism in patients with affective disorders." Acta Neuropsychiatrica 30, no. 6 (June 8, 2018): 342–49. http://dx.doi.org/10.1017/neu.2018.16.
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AbstractBackgroundErythropoietin (EPO) has been suggested to improve metabolism and also cognition, but human studies are scarce. This randomised controlled trial aimed to investigate whether EPO treatment influences body composition and fat and glycated haemoglobin (HbA1c) and fasting glucose, and whether these changes would be associated with previous observed cognitive benefits of EPO.MethodIn total, 84 non-obese patients with treatment-resistant unipolar depression or bipolar disorder in remission were randomised to 8 weekly EPO (40,000 IU) or saline (NaCl 0.9%) infusions in a double-blind, parallel-group design. Patients underwent dual X-ray absorptiometry scans at baseline and week 14 (6 weeks after treatment completion). Cognitive measures were assessed and fasting levels of cholesterol, lipoprotein fractions, triacylglycerides, glucose and HbA1c were obtained at baseline, week 9 and follow-up week 14.ResultsIn total, 79 patients had complete pre- and post-treatment data (EPO: N=40, saline: N=39). EPO had no cumulative effect on body composition and markers of fat metabolism. The EPO-treated group exhibited significantly lower HbA1c levels after 8 weeks treatment [F(1, 80)=8.51, p=0.005], however, 6 weeks after treatment termination a significantly higher fasting glucose levels [F(1, 79)=5.85, p=0.02] and HbA1c levels [F(1, 79)=5.85, p=0.02] were seen. The latter increase in HbA1c was further significantly correlated with a better cognitive outcome on verbal memory (r=0.25, p=0.03).ConclusionRepeated EPO infusions had no cumulative effect on body composition in this cohort of patients with affective disorders, however, EPO modulated HbA1c and fasting glucose and this was associated with patients’ improvement of verbal memory.
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van der Kooij, Michael A., Tanja Jene, Giulia Treccani, Isabelle Miederer, Annika Hasch, Nadine Voelxen, Stefan Walenta, and Marianne B. Müller. "Chronic social stress-induced hyperglycemia in mice couples individual stress susceptibility to impaired spatial memory." Proceedings of the National Academy of Sciences 115, no. 43 (October 9, 2018): E10187—E10196. http://dx.doi.org/10.1073/pnas.1804412115.
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Stringent glucose demands render the brain susceptible to disturbances in the supply of this main source of energy, and chronic stress may constitute such a disruption. However, whether stress-associated cognitive impairments may arise from disturbed glucose regulation remains unclear. Here we show that chronic social defeat (CSD) stress in adult male mice induces hyperglycemia and directly affects spatial memory performance. Stressed mice developed hyperglycemia and impaired glucose metabolism peripherally as well as in the brain (demonstrated by PET and induced metabolic bioluminescence imaging), which was accompanied by hippocampus-related spatial memory impairments. Importantly, the cognitive and metabolic phenotype pertained to a subset of stressed mice and could be linked to early hyperglycemia 2 days post-CSD. Based on this criterion, ∼40% of the stressed mice had a high-glucose (glucose >150 mg/dL), stress-susceptible phenotype. The relevance of this biomarker emerges from the effects of the glucose-lowering sodium glucose cotransporter 2 inhibitor empagliflozin, because upon dietary treatment, mice identified as having high glucose demonstrated restored spatial memory and normalized glucose metabolism. Conversely, reducing glucose levels by empagliflozin in mice that did not display stress-induced hyperglycemia (resilient mice) impaired their default-intact spatial memory performance. We conclude that hyperglycemia developing early after chronic stress threatens long-term glucose homeostasis and causes spatial memory dysfunction. Our findings may explain the comorbidity between stress-related and metabolic disorders, such as depression and diabetes, and suggest that cognitive impairments in both types of disorders could originate from excessive cerebral glucose accumulation.
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Hiroi, Noboru, and Takahira Yamauchi. "Modeling and Predicting Developmental Trajectories of Neuropsychiatric Dimensions Associated With Copy Number Variations." International Journal of Neuropsychopharmacology 22, no. 8 (May 28, 2019): 488–500. http://dx.doi.org/10.1093/ijnp/pyz026.
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AbstractCopy number variants, such as duplications and hemizygous deletions at chromosomal loci of up to a few million base pairs, are highly associated with psychiatric disorders. Hemizygous deletions at human chromosome 22q11.2 were found to be associated with elevated instances of schizophrenia and autism spectrum disorder in 1992 and 2002, respectively. Following these discoveries, many mouse models have been developed and tested to analyze the effects of gene dose alterations in small chromosomal segments and single genes of 22q11.2. Despite several limitations to modeling mental illness in mice, mouse models have identified several genes on 22q11.2—Tbx1, Dgcr8, Comt, Sept5, and Prodh—that contribute to dimensions of autism spectrum disorder and schizophrenia, including working memory, social communication and interaction, and sensorimotor gating. Mouse studies have identified that heterozygous deletion of Tbx1 results in defective social communication during the neonatal period and social interaction deficits during adolescence/adulthood. Overexpression of Tbx1 or Comt in adult neural progenitor cells in the hippocampus delays the developmental maturation of working memory capacity. Collectively, mouse models of variants of these 4 genes have revealed several potential neuronal mechanisms underlying various aspects of psychiatric disorders, including adult neurogenesis, microRNA processing, catecholamine metabolism, and synaptic transmission. The validity of the mouse data would be ultimately tested when therapies or drugs based on such potential mechanisms are applied to humans.
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Namazbaeva, Zulkiya, Sharbanu Battakova, Lyazat Ibrayeva, and Zhanbol Sabirov. "Change in metabolic and cognitive state among people of the Aral zone of ecological disaster." Israel Journal of Ecology and Evolution 64, no. 1-4 (November 10, 2018): 44–55. http://dx.doi.org/10.1163/22244662-20181035.
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Risk factors in Aral Sea region include toxic metals that competitively interact with essential elements influencing their metabolism, affecting metabolic and cognitive functions. According to epidemiological data, cerebrovascular disease and thyroid function abnormality are the leading disorders. Cognitive and metabolic disorders are considered as risk factors in cerebrovascular diseases. Thus, the objective of current work was to determine the metabolic and cognitive state of people in Aralsk, associated with an imbalance of essential trace elements and find correlation between toxic metals load and psychoemotional status. 275 people between the ages of 21 and 45 years were involved. In evaluating cognitive state, a decrease in short-term memory for numbers and an increase in depression among subjects was found. An inverse correlation between the copper level in blood and short-term memory for numbers, between depression and iodine level in blood, between the zinc level in blood and the “attentional capacity” was also found. The results showed a significant metabolic stress among subjects during adaptation to a high chemical load. Data represent a cross-sectional age-dependent review of metabolic and cognitive processes and microelement metabolism among population, living in the Aral Sea region for a long time.
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Kupper, Thomas S. "Tissue Resident Memory Cells." Blood 132, Supplement 1 (November 29, 2018): SCI—5—SCI—5. http://dx.doi.org/10.1182/blood-2018-99-109534.
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Abstract Tissue resident memory T cells (TRM) are a relatively newly discovered subset of memory T cells. Rather than inhabiting secondary lymphoid tissue, they are lodged in peripheral tissues. While TRM can appear in any tissue, they are most abundant in tissues that abut the environment--skin, lung, gut, oral and vaginal mucosa. They accumulate as a result of T cell mediated inflammatory processes which occur in response to infection or encounter with a non-pathogenic antigen. Strategically, they can respond almost immediately to a subsequent encounter with the antigen for which they are specific, and thus play a critical role in host defense. CD8 TRM specific for pathogenic viruses have been described, as well as CD4 TRM for pathogenic fungi and other microorganisms. While TRM play a role in host defense, inappropriate activation of TRM in response to autoantigen or otherwise innocuous antigen is thought to play a key role in several T cell mediated inflammatory diseases, including psoriasis, spondyloarthritides, multiple sclerosis, type I diabetes, and asthma. Dislodging pathogenic TRM from tissue has proven difficult or impossible, and thus many of these disorders are relapsing even if successfully treated. Their dependence on cytokines such as IL-15, fatty acid metabolism, and expression of CD69 may represent targets of therapeutic opportunity. Disclosures No relevant conflicts of interest to declare.
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Peyton, Lee, Alfredo Oliveros, Maximilian Tufvesson-Alm, Lilly Schwieler, Phillip Starski, Göran Engberg, Sopie Erhardt, and Doo-Sup Choi. "Lipopolysaccharide Increases Cortical Kynurenic Acid and Deficits in Reference Memory in Mice." International Journal of Tryptophan Research 12 (January 2019): 117864691989116. http://dx.doi.org/10.1177/1178646919891169.
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Kynurenic acid (KYNA), a glial-derived metabolite of tryptophan metabolism, is an antagonist of the alpha 7 nicotinic acetylcholine receptor and the glycine-binding site of N-methyl-d-aspartate (NMDA) receptors. Kynurenic acid levels are increased in both the brain and cerebrospinal fluid of several psychiatric disorders including bipolar disorder, schizophrenia, and Alzheimer disease. In addition, pro-inflammatory cytokines have been found to be elevated in the blood of schizophrenic patients suggesting inflammation may play a role in psychiatric illness. As both pro-inflammatory cytokines and KYNA can be elevated in the brain by peripheral lipopolysaccharide (LPS) injection, we therefore sought to characterize the role of neuroinflammation on learning and memory using a well-described dual-LPS injection model. Mice were injected with an initial injection (0.25 mg/kg LPS, 0.50 mg/kg, or saline) of LPS and then administrated a second injection 16 hours later. Our results indicate both 0.25 and 0.50 mg/kg dual-LPS treatment increased l-kynurenine and KYNA levels in the medial pre-frontal cortex (mPFC). Mice exhibited impaired acquisition of CS+ (conditioned stimulus) Pavlovian conditioning. Notably, mice showed impairment in reference memory while working memory was normal in an 8-arm maze. Taken together, our findings suggest that neuroinflammation induced by peripheral LPS administration contributes to cognitive dysfunction.
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Vo, An, Bruce T. Volpe, Chris C. Tang, Wynne K. Schiffer, Czeslawa Kowal, Patricio T. Huerta, Aziz M. Ulug, Stephen L. Dewey, David Eidelberg, and Betty Diamond. "Regional Brain Metabolism in a Murine Systemic Lupus Erythematosus Model." Journal of Cerebral Blood Flow & Metabolism 34, no. 8 (May 14, 2014): 1315–20. http://dx.doi.org/10.1038/jcbfm.2014.85.
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Systemic lupus erythematosus (SLE) is characterized by multiorgan inflammation, neuropsychiatric disorders (NPSLE), and anti-nuclear antibodies. We previously identified a subset of anti-DNA antibodies (DNRAb) cross-reactive with the N-methyl-D-aspartate receptor, present in 30% to 40% of patients, able to enhance excitatory post-synaptic potentials and trigger neuronal apoptosis. DNRAb + mice exhibit memory impairment or altered fear response, depending on whether the antibody penetrates the hippocampus or amygdala. Here, we used 18F-fluorodeoxyglucose (FDG) microPET to plot changes in brain metabolism after regional blood-brain barrier (BBB) breach. In DNRAb + mice, metabolism declined at the site of BBB breach in the first 2 weeks and increased over the next 2 weeks. In contrast, DNRAb — mice exhibited metabolic increases in these regions over the 4 weeks after the insult. Memory impairment was present in DNRAb + animals with hippocampal BBB breach and altered fear conditioning in DNRAb + mice with amygdala BBB breach. In DNRAb + mice, we observed an inverse relationship between neuron number and regional metabolism, while a positive correlation was observed in DNRAb — mice. These findings suggest that local metabolic alterations in this model take place through different mechanisms with distinct time courses, with important implications for the interpretation of imaging data in SLE subjects.
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Zhou, Liyuan, Lin Kang, Xinhua Xiao, Lijing Jia, Qian Zhang, and Mingqun Deng. "“Gut Microbiota-Circadian Clock Axis” in Deciphering the Mechanism Linking Early-Life Nutritional Environment and Abnormal Glucose Metabolism." International Journal of Endocrinology 2019 (August 27, 2019): 1–9. http://dx.doi.org/10.1155/2019/5893028.
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The prevalence of diabetes mellitus (DM) has been increasing dramatically worldwide, but the pathogenesis is still unknown. A growing amount of evidence suggests that an abnormal developmental environment in early life increases the risk of developing metabolic diseases in adult life, which is referred to as the “metabolic memory” and the Developmental Origins of Health and Disease (DOHaD) hypothesis. The mechanism of “metabolic memory” has become a hot topic in the field of DM worldwide and could be a key to understanding the pathogenesis of DM. In recent years, several large cohort studies have shown that shift workers have a higher risk of developing type 2 diabetes mellitus (T2DM) and worse control of blood glucose levels. Furthermore, a maternal high-fat diet could lead to metabolic disorders and abnormal expression of clock genes and clock-controlled genes in offspring. Thus, disorders of circadian rhythm might play a pivotal role in glucose metabolic disturbances, especially in terms of early adverse nutritional environments and the development of metabolic diseases in later life. In addition, as a peripheral clock, the gut microbiota has its own circadian rhythm that fluctuates with periodic feeding and has been widely recognized for its significant role in metabolism. In light of the important roles of the gut microbiota and circadian clock in metabolic health and their interconnected regulatory relationship, we propose that the “gut microbiota-circadian clock axis” might be a novel and crucial mechanism to decipher “metabolic memory.” The “gut microbiota-circadian clock axis” is expected to facilitate the future development of a novel target for the prevention and intervention of diabetes during the early stage of life.
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Justo, Rayssa, Marcelo Cesar, Edimilson Migowski, and Rafael Cisne. "Relation between vitamins of the b complex, GABA and glutamate, and their role in neurocognitive disorders -Brief review." International Journal of Basic and Applied Sciences 5, no. 4 (November 29, 2016): 229. http://dx.doi.org/10.14419/ijbas.v5i4.6707.
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Vitamins, especially the water-soluble complex of vitamins B, are highlighted in the daily clinical practice. Numerous studies emphasize the need for supplementation, mainly in groups with deficiency of these vitamins, such as the elderly, pregnant women, children and patients with diseases associates with cognitive disorder. Thiamine (B1), a vitamin of the diet, is an important cofactor for the three key enzymes involved in the citric acid cycle and the pentose phosphate cycle. Pyridoxine (B6) and cobalamin (B12) act in the CNS as a cofactor in the metabolism reactions of homocysteine. Deficiency of some neurotransmitter precursors can also cause symptoms of attention deficit hyperactivity disorder in children, especially amino acid and vitamin B deficiency. Inhibitory and excitatory neurotransmitters regulate diverse behavioral processes, including sleep, learning, memory and sensation of pain. They are also implicated in many pathological processes, such as epilepsy and neurotoxicity. Studies suggest that the excitatory amino acids may play a role in learning and memory. The binding of glutamate to its receptor triggers molecular and cellular events associated with numerous physiological and pathophysiological pathways, including the development of an increased sensation of pain (hyperalgesia), brain neurotoxicity or synaptic alterations involved in certain types of memory formation. Between the two major classes of neuroactive amino acids, γ-aminobutyric acid (GABA) is the major inhibitory amino acid. It is known that GABA plays a fundamental role in encoding information and behavioral control, in the regulation of motor function and in motor learning. The inter-relationships between diet, the brain and behavior are complex. However, micronutrients are known to have a direct influence on cognitive function through their involvement in the energy metabolism of neurons and glia cells, the synthesis of neurotransmitters, receptor binding and the maintenance of membrane ion pumps.
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Rentschler, Katherine M., Annalisa M. Baratta, Audrey L. Ditty, Nathan T. J. Wagner, Courtney J. Wright, Snezana Milosavljevic, Jessica A. Mong, and Ana Pocivavsek. "Prenatal Kynurenine Elevation Elicits Sex-Dependent Changes in Sleep and Arousal During Adulthood: Implications for Psychotic Disorders." Schizophrenia Bulletin 47, no. 5 (April 5, 2021): 1320–30. http://dx.doi.org/10.1093/schbul/sbab029.
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Abstract Dysregulation of the kynurenine pathway (KP) of tryptophan catabolism has been implicated in psychotic disorders, including schizophrenia and bipolar disorder. Kynurenic acid (KYNA) is a KP metabolite synthesized by kynurenine aminotransferases (KATs) from its biological precursor kynurenine and acts as an endogenous antagonist of N-methyl-D-aspartate and α7-nicotinic acetylcholine receptors. Elevated KYNA levels found in postmortem brain tissue and cerebrospinal fluid of patients are hypothesized to play a key role in the etiology of cognitive symptoms observed in psychotic disorders. Sleep plays an important role in memory consolidation, and sleep disturbances are common among patients. Yet, little is known about the effect of altered KP metabolism on sleep–wake behavior. We presently utilized a well-established experimental paradigm of embryonic kynurenine (EKyn) exposure wherein pregnant dams are fed a diet laced with kynurenine the last week of gestation and hypothesized disrupted sleep–wake behavior in adult offspring. We examined sleep behavior in adult male and female offspring using electroencephalogram and electromyogram telemetry and determined sex differences in sleep and arousal in EKyn offspring. EKyn males displayed reduced rapid eye movement sleep, while female EKyn offspring were hyperaroused compared to controls. We determined that EKyn males maintain elevated brain KYNA levels, while KYNA levels were unchanged in EKyn females, yet the activity levels of KAT I and KAT II were reduced. Our findings indicate that elevated prenatal kynurenine exposure elicits sex-specific changes in sleep–wake behavior, arousal, and KP metabolism.
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Lin, Ai-Ling, Daniel A. Pulliam, Sathyaseelan S. Deepa, Jonathan J. Halloran, Stacy A. Hussong, Raquel R. Burbank, Andrew Bresnen, et al. "Decreased in vitro Mitochondrial Function is Associated with Enhanced Brain Metabolism, Blood Flow, and Memory in Surfl-Deficient Mice." Journal of Cerebral Blood Flow & Metabolism 33, no. 10 (July 10, 2013): 1605–11. http://dx.doi.org/10.1038/jcbfm.2013.116.
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Recent studies have challenged the prevailing view that reduced mitochondrial function and increased oxidative stress are correlated with reduced longevity. Mice carrying a homozygous knockout (KO) of the Surf1 gene showed a significant decrease in mitochondrial electron transport chain Complex IV activity, yet displayed increased lifespan and reduced brain damage after excitotoxic insults. In the present study, we examined brain metabolism, brain hemodynamics, and memory of Surf1 KO mice using in vitro measures of mitochondrial function, in vivo neuroimaging, and behavioral testing. We show that decreased respiration and increased generation of hydrogen peroxide in isolated Surf1 KO brain mitochondria are associated with increased brain glucose metabolism, cerebral blood flow, and lactate levels, and with enhanced memory in Surf1 KO mice. These metabolic and functional changes in Surf1 KO brains were accompanied by higher levels of hypoxia-inducible factor 1 alpha, and by increases in the activated form of cyclic AMP response element-binding factor, which is integral to memory formation. These findings suggest that Surf1 deficiency-induced metabolic alterations may have positive effects on brain function. Exploring the relationship between mitochondrial activity, oxidative stress, and brain function will enhance our understanding of cognitive aging and of age-related neurologic disorders.
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Ling, Shuang, and Jin-Wen Xu. "Biological Activities of 2,3,5,4′-Tetrahydroxystilbene-2-O-β-D-Glucoside in Antiaging and Antiaging-Related Disease Treatments." Oxidative Medicine and Cellular Longevity 2016 (2016): 1–14. http://dx.doi.org/10.1155/2016/4973239.
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2,3,5,4′-Tetrahydroxystilbene-2-O-β-D-glucoside (THSG) is active component of the Chinese medicinal plantPolygonum multiflorumThunb. (THSG). Pharmacological studies have demonstrated that THSG exhibits numerous biological functions in treating atherosclerosis, lipid metabolism, vascular and cardiac remodeling, vascular fibrosis, cardiac-cerebral ischemia, learning and memory disorders, neuroinflammation, Alzheimer and Parkinson diseases, diabetic complications, hair growth problems, and numerous other conditions. This review focuses on the biological effects of THSG in antiaging and antiaging-related disease treatments and discusses its molecular mechanisms.
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Rokot, Natasya Trivena, Timothy Sean Kairupan, Kai-Chun Cheng, Joshua Runtuwene, Nova Hellen Kapantow, Marie Amitani, Akinori Morinaga, Haruka Amitani, Akihiro Asakawa, and Akio Inui. "A Role of Ginseng and Its Constituents in the Treatment of Central Nervous System Disorders." Evidence-Based Complementary and Alternative Medicine 2016 (2016): 1–7. http://dx.doi.org/10.1155/2016/2614742.
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Ginseng, a perennial plant belonging to thePanaxgenus of the Araliaceae family, has been used in China, Korea, and Japan as a traditional herbal medicine for thousands of years. Ginseng is recorded to have exhibited a wide variety of beneficial pharmacological effects and has become a popular and worldwide known health supplement and drug. The protective effects of ginseng on central nervous system are discussed in this review. Ginseng species and ginsenosides and their intestinal metabolism and bioavailability are concisely introduced. The molecular mechanisms of the effects of ginseng on central nervous system, mainly focused on the neuroprotection properties of ginseng, memory, and learning enhanced properties, and the effects on neurodegenerative disorders are presented. Thus, ginseng and its constituents are of potential merits in the treatment of cerebral disorders.
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Joshi, H., and K. Megeri. "Cognition improving effects of clerodendron phlomidis linn. bark extract in mice." European Psychiatry 26, S2 (March 2011): 1250. http://dx.doi.org/10.1016/s0924-9338(11)72955-8.
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Normal ageing is known to deteriorate memory in human beings. Oxygen free radicals, the harmful byproducts of oxidative metabolism are known to cause organic damage to the living system, which may be responsible for the development of Alzheimer's disease in elderly. Clerodendron phlomidis Linn. (Verbenaceae) is known as Agnimantha in sanskrit. Bark of the plant is used in treating various nervous disorders. In the present study C. phlomidis was investigated for its potential as a nootropic agent in mice. The aqueous extract of the C. phlomidis (100 and 200 mg/kg, p.o.) was administered for 6 successive days to both young and aged mice. Exteroceptive behavioral models such as elevated plus maze and passive avoidance paradigm were employed to evaluate short term and long term memory respectively. Scopolamine, diazepam were used to induce amnesia in mice. To delineate the mechanism by which C. phlomidis exerts nootropic action, its effect on brain acetyl cholinesterase levels were determined. Piracetam was used as a standard nootropic agent. Pretreatment with C. phlomidis (100 and 200 mg/kg, p.o.) for 6 successive days significantly improved learning and memory in mice. It reversed the amnesia induced by scopolamine, diazepam and natural ageing. It also decreased the acetyl cholinesterase levels in the whole brain. The bark of C. phlomidis can be useful in treatment of cognitive disorders such as amnesia and Alzheimer's disease.
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Svensson, J., M. Diez, J. Engel, C. Wass, Å Tivesten, J.-O. Jansson, O. Isaksson, T. Archer, T. Hökfelt, and C. Ohlsson. "Endocrine, liver-derived IGF-I is of importance for spatial learning and memory in old mice." Journal of Endocrinology 189, no. 3 (June 2006): 617–27. http://dx.doi.org/10.1677/joe.1.06631.
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IGF-I is a neuroprotective hormone, and neurodegenerative disorders, including Alzheimer’s disease, have been associated with decreased serum IGF-I concentration. In this study, IGF-I production was inactivated in the liver of adult mice (LI-IGF-I−/−), resulting in an approximately 80–85% reduction of circulating IGF-I concentrations. In young (6-month-old) mice there was no difference between the LI-IGF-I−/− and the control mice in spatial learning and memory as measured using the Morris water maze test. In old (aged 15 and 18 months) LI-IGF-I−/− mice, however, the acquisition of the spatial task was slower than in the controls. Furthermore, impaired spatial working as well as reference memory was observed in the old LI-IGF−/− mice. Histochemical analyses revealed an increase in dynorphin and enkephalin immunoreactivities but decreased mRNA levels in the hippocampus of old LI-IGF-I−/− mice. These mice also displayed astrocytosis and increased metabotropic glutamate receptor 7a-immunoreactivity. These neurochemical disturbances suggest synaptic dysfunction and early neurodegeneration in old LI-IGF-I−/− mice. The decline in serum IGF-I with increasing age may therefore be important for the age-related decline in memory function.
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Dienel, Gerald A. "Brain Glucose Metabolism: Integration of Energetics with Function." Physiological Reviews 99, no. 1 (January 1, 2019): 949–1045. http://dx.doi.org/10.1152/physrev.00062.2017.
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Glucose is the long-established, obligatory fuel for brain that fulfills many critical functions, including ATP production, oxidative stress management, and synthesis of neurotransmitters, neuromodulators, and structural components. Neuronal glucose oxidation exceeds that in astrocytes, but both rates increase in direct proportion to excitatory neurotransmission; signaling and metabolism are closely coupled at the local level. Exact details of neuron–astrocyte glutamate–glutamine cycling remain to be established, and the specific roles of glucose and lactate in the cellular energetics of these processes are debated. Glycolysis is preferentially upregulated during brain activation even though oxygen availability is sufficient (aerobic glycolysis). Three major pathways, glycolysis, pentose phosphate shunt, and glycogen turnover, contribute to utilization of glucose in excess of oxygen, and adrenergic regulation of aerobic glycolysis draws attention to astrocytic metabolism, particularly glycogen turnover, which has a high impact on the oxygen–carbohydrate mismatch. Aerobic glycolysis is proposed to be predominant in young children and specific brain regions, but re-evaluation of data is necessary. Shuttling of glucose- and glycogen-derived lactate from astrocytes to neurons during activation, neurotransmission, and memory consolidation are controversial topics for which alternative mechanisms are proposed. Nutritional therapy and vagus nerve stimulation are translational bridges from metabolism to clinical treatment of diverse brain disorders.
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Pirela, Daniela Victoria, Victor Cevallos, and Jorge G. Ruiz. "Mild Cognitive Impairment Screening in Older Adults With Type 2 DM." Journal of the Endocrine Society 5, Supplement_1 (May 1, 2021): A416—A417. http://dx.doi.org/10.1210/jendso/bvab048.850.
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Abstract Introduction: Older adults (O-A), more than 65 years old, are a heterogeneous group of patients in terms of functionality, social support and health status that implies a wide range of co-morbidities including mild cognitive impairment (MCI) and unidentified dementia. De-intensification of treatment is recommended for O-A with T2DM, tight glycemic control and high risk of hypoglycemia. Assessment of all geriatric domains (medical, functional, social and psychological including screening for MCI) is encouraged to support a complete clinical picture that leads to appropriate targets and adequate therapeutic approach. The literature suggests that de-intensification of treatment in this population is uncommon, which calls for the development of new strategies to prevent potential harm, however we also question if previously established tools are being used. Methods: We performed a retrospective chart review of a community-dwelling Veterans with at least two office visits in the Geriatric Clinic between January 1st 2018 to December 31st 2019. 210 patients with 65 years of age or older with T2DM and A1C < 7.5 were found. 64 (30%) of the patients where on hypoglycemic medication including sulfonylureas or insulin. From this subgroup, only 9 (14%) patients where recommended to de-intensify therapy. 189 (90%) of all the patients were screened for memory disorders. Interestingly 20 patients (31%) of those using sulfonylureas or insulin as part of their diabetes treatment were not screened, which was a higher percentage compared to 48 (25%) patients not on hypoglycemic medications also not screened for memory disorders. Conclusion: similar to previous studies de-intensification is uncommon not only among endocrinologist but in other sub-specialties involved in the care of the Geriatric population. This data emphasizes the importance of using previously developed treatment tools specially in those with at higher risk of overtreatment side effects such as older adults with tight glycemic control and hypoglycemic medication
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Ismail, Muhammad-Al-Mustafa, Laura Mateos, Silvia Maioli, Paula Merino-Serrais, Zeina Ali, Maria Lodeiro, Eric Westman, et al. "27-Hydroxycholesterol impairs neuronal glucose uptake through an IRAP/GLUT4 system dysregulation." Journal of Experimental Medicine 214, no. 3 (February 17, 2017): 699–717. http://dx.doi.org/10.1084/jem.20160534.
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Hypercholesterolemia is associated with cognitively deteriorated states. Here, we show that excess 27-hydroxycholesterol (27-OH), a cholesterol metabolite passing from the circulation into the brain, reduced in vivo brain glucose uptake, GLUT4 expression, and spatial memory. Furthermore, patients exhibiting higher 27-OH levels had reduced 18F-fluorodeoxyglucose uptake. This interplay between 27-OH and glucose uptake revealed the engagement of the insulin-regulated aminopeptidase (IRAP). 27-OH increased the levels and activity of IRAP, countered the IRAP antagonist angiotensin IV (AngIV)–mediated glucose uptake, and enhanced the levels of the AngIV-degrading enzyme aminopeptidase N (AP-N). These effects were mediated by liver X receptors. Our results reveal a molecular link between cholesterol, brain glucose, and the brain renin-angiotensin system, all of which are affected in some neurodegenerative diseases. Thus, reducing 27-OH levels or inhibiting AP-N maybe a useful strategy in the prevention of the altered glucose metabolism and memory decline in these disorders.
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Klein, Matthew E., Hannah Monday, and Bryen A. Jordan. "Proteostasis and RNA Binding Proteins in Synaptic Plasticity and in the Pathogenesis of Neuropsychiatric Disorders." Neural Plasticity 2016 (2016): 1–11. http://dx.doi.org/10.1155/2016/3857934.
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Decades of research have demonstrated that rapid alterations in protein abundance are required for synaptic plasticity, a cellular correlate for learning and memory. Control of protein abundance, known as proteostasis, is achieved across a complex neuronal morphology that includes a tortuous axon as well as an extensive dendritic arbor supporting thousands of individual synaptic compartments. To regulate the spatiotemporal synthesis of proteins, neurons must efficiently coordinate the transport and metabolism of mRNAs. Among multiple levels of regulation, transacting RNA binding proteins (RBPs) control proteostasis by binding to mRNAs and mediating their transport and translation in response to synaptic activity. In addition to synthesis, protein degradation must be carefully balanced for optimal proteostasis, as deviations resulting in excess or insufficient abundance of key synaptic factors produce pathologies. As such, mutations in components of the proteasomal or translational machinery, including RBPs, have been linked to the pathogenesis of neurological disorders such as Fragile X Syndrome (FXS), Fragile X Tremor Ataxia Syndrome (FXTAS), and Autism Spectrum Disorders (ASD). In this review, we summarize recent scientific findings, highlight ongoing questions, and link basic molecular mechanisms to the pathogenesis of common neuropsychiatric disorders.
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Salmina, A. B., N. A. Yauzina, N. V. Kuvacheva, M. M. Petrova, T. Ye Taranushenko, N. A. Malinovskaya, O. L. Lopatina, et al. "INSULIN AND INSULIN RESISTANCE: NEW MOLECULE MARKERS AND TARGET MOLECULE FOR THE DIAGNOSIS AND THERAPY OF DISEASES OF THE CENTRAL NERVOUS SYSTEM." Bulletin of Siberian Medicine 12, no. 5 (October 28, 2013): 104–18. http://dx.doi.org/10.20538/1682-0363-2013-5-104-118.
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The review summarizes current data on the role of insulin in the regulation of t glucose metabolism in the central nervous system at physiologic and pathologic conditions. For many years, the brain has been considered as an insulin-independent organ which utilizes glucose without insulin activity. However, it is become clear now that insulin not only regulates glucose transport and metabolism, but also has modulatory efftects in impact on excitability, proliferation and differentiation of brain progenitor cells, synaptic plasticity and memory formation, secretion of neurotransmitters, apoptosis. We have critically reviewed literature information and our own data on the role of insulin and insulin resistance in neuron-glia metabolic coupling, regulation of NAD+ metabolism and action of NAdependent enzymes, neurogenesis, brain development in (patho)physiological conditions. The paper clarifies interrelations between alterations in glucose homeostasis, development of insulin resistance and development of neurodegeneration (Alzheimer's disease and Parkinson's disease), autism, stroke, and depression. We discuss the application of novel molecular markers of insulin resistance (adipokines, α-hydroxybutyrate, BDNF, insulin-regulated aminopeptidase, provasopressin) and molecular targets for diagnostics and treatment of brain disorders associated with insulin resistance.
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Spaas, Jan, Lieve van Veggel, Melissa Schepers, Assia Tiane, Jack van Horssen, David M. Wilson, Pablo R. Moya, et al. "Oxidative stress and impaired oligodendrocyte precursor cell differentiation in neurological disorders." Cellular and Molecular Life Sciences 78, no. 10 (March 10, 2021): 4615–37. http://dx.doi.org/10.1007/s00018-021-03802-0.
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AbstractOligodendrocyte precursor cells (OPCs) account for 5% of the resident parenchymal central nervous system glial cells. OPCs are not only a back-up for the loss of oligodendrocytes that occurs due to brain injury or inflammation-induced demyelination (remyelination) but are also pivotal in plastic processes such as learning and memory (adaptive myelination). OPC differentiation into mature myelinating oligodendrocytes is controlled by a complex transcriptional network and depends on high metabolic and mitochondrial demand. Mounting evidence shows that OPC dysfunction, culminating in the lack of OPC differentiation, mediates the progression of neurodegenerative disorders such as multiple sclerosis, Alzheimer’s disease and Parkinson’s disease. Importantly, neurodegeneration is characterised by oxidative and carbonyl stress, which may primarily affect OPC plasticity due to the high metabolic demand and a limited antioxidant capacity associated with this cell type. The underlying mechanisms of how oxidative/carbonyl stress disrupt OPC differentiation remain enigmatic and a focus of current research efforts. This review proposes a role for oxidative/carbonyl stress in interfering with the transcriptional and metabolic changes required for OPC differentiation. In particular, oligodendrocyte (epi)genetics, cellular defence and repair responses, mitochondrial signalling and respiration, and lipid metabolism represent key mechanisms how oxidative/carbonyl stress may hamper OPC differentiation in neurodegenerative disorders. Understanding how oxidative/carbonyl stress impacts OPC function may pave the way for future OPC-targeted treatment strategies in neurodegenerative disorders.
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Agrawal, Rahul, Emily Noble, Laurent Vergnes, Zhe Ying, Karen Reue, and Fernando Gomez-Pinilla. "Dietary fructose aggravates the pathobiology of traumatic brain injury by influencing energy homeostasis and plasticity." Journal of Cerebral Blood Flow & Metabolism 36, no. 5 (October 1, 2015): 941–53. http://dx.doi.org/10.1177/0271678x15606719.
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Fructose consumption has been on the rise for the last two decades and is starting to be recognized as being responsible for metabolic diseases. Metabolic disorders pose a particular threat for brain conditions characterized by energy dysfunction, such as traumatic brain injury. Traumatic brain injury patients experience sudden abnormalities in the control of brain metabolism and cognitive function, which may worsen the prospect of brain plasticity and function. The mechanisms involved are poorly understood. Here we report that fructose consumption disrupts hippocampal energy homeostasis as evidenced by a decline in functional mitochondria bioenergetics (oxygen consumption rate and cytochrome C oxidase activity) and an aggravation of the effects of traumatic brain injury on molecular systems engaged in cell energy homeostasis (sirtuin 1, peroxisome proliferator-activated receptor gamma coactivator-1alpha) and synaptic plasticity (brain-derived neurotrophic factor, tropomyosin receptor kinase B, cyclic adenosine monophosphate response element binding, synaptophysin signaling). Fructose also worsened the effects of traumatic brain injury on spatial memory, which disruption was associated with a decrease in hippocampal insulin receptor signaling. Additionally, fructose consumption and traumatic brain injury promoted plasma membrane lipid peroxidation, measured by elevated protein and phenotypic expression of 4-hydroxynonenal. These data imply that high fructose consumption exacerbates the pathology of brain trauma by further disrupting energy metabolism and brain plasticity, highlighting the impact of diet on the resilience to neurological disorders.
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Duarte, Ana I., Paula I. Moreira, and Catarina R. Oliveira. "Insulin in Central Nervous System: More than Just a Peripheral Hormone." Journal of Aging Research 2012 (2012): 1–21. http://dx.doi.org/10.1155/2012/384017.
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Insulin signaling in central nervous system (CNS) has emerged as a novel field of research since decreased brain insulin levels and/or signaling were associated to impaired learning, memory, and age-related neurodegenerative diseases. Thus, besides its well-known role in longevity, insulin may constitute a promising therapy against diabetes- and age-related neurodegenerative disorders. More interestingly, insulin has been also faced as the potential missing link between diabetes and aging in CNS, with Alzheimer's disease (AD) considered as the “brain-type diabetes.” In fact, brain insulin has been shown to regulate both peripheral and central glucose metabolism, neurotransmission, learning, and memory and to be neuroprotective. And a future challenge will be to unravel the complex interactions between aging and diabetes, which, we believe, will allow the development of efficient preventive and therapeutic strategies to overcome age-related diseases and to prolong human “healthy” longevity. Herewith, we aim to integrate the metabolic, neuromodulatory, and neuroprotective roles of insulin in two age-related pathologies: diabetes and AD, both in terms of intracellular signaling and potential therapeutic approach.
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Biswas, Tanima, and Shankar Kumar Dey. "Association of Thyroid Dysfunction and Mood Disorders and Role of Imaging: a Review." Bangladesh Journal of Nuclear Medicine 17, no. 2 (June 14, 2016): 146–52. http://dx.doi.org/10.3329/bjnm.v17i2.28202.
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Thyroid hormones play a critical role in the adult brain impacting mood and cognition. Some psychiatric symptoms are produced by thyroid illnesses and there is a frequent association of thyroid dysfunction with mood disorders. It is now clear that without optimal thyroid function, mood disturbance, cognitive impairment and other phychiatric symptoms can emerge. The usefulness of adding thyroid hormones to antidepressive treatment in euthyroid patients to obtain a potentiation effect has been proved repeatedly. The most common strategy is potentiation with T3 , but high doses of T4 have been also used in patients with resistant depression. Brain imaging techniques evaluating cerebral metabolism, perfusion, and anatomy enabled encouraging insights into the thyroid-brain relationship. The most consistent finding in patients with hypothyroidism is global diffuse hypoperfusion more pronounced in posterior brain region or in parietal lobe. Functional MRI in patients with thyroid diseases of different length and severity could help to identify functional aberrations such as memory impairments or altered emotional processing, which has long been suggested from animal studies. Structural changes related to myelin, which have been observed in various animal models, can now be studied with quantitative T2 or quantitative magnetization transfer (MT) imaging. Diffusion tensor imaging (DTI) can reveal information on white matter integrity.Bangladesh J. Nuclear Med. 17(2): 146-152, July 2014
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Yuruyen, Mehmet, Gozde Gultekin, Gizem Cetiner Batun, Hakan Yavuzer, Fundan Engin Akcan, Alper Doventas, and Murat Emul. "Does plasma phoenixin level associate with cognition? Comparison between subjective memory complaint, mild cognitive impairment, and mild Alzheimer's disease." International Psychogeriatrics 29, no. 9 (May 29, 2017): 1543–50. http://dx.doi.org/10.1017/s1041610217000825.
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ABSTRACTBackground:Alteration in energy expenditure or metabolism is the most accused risk issue for the onset and for the course of neurodegenerative cognitive disorders. Neuropeptides are suggested to be related with learning and memory. Phoenixin (PNX) is the most recently reported neuropeptide and we aimed to compare the plasma level in people with subjective memory complaints, patients with mild cognitive impairment, and mild Alzheimer's disease (AD).Methods:Ninety two participants enrolled in the study. After screening tests, all participants were assessed with a neuropsychological battery for further cognitive evaluations. We used ELISA kit to assay the level of Human PNX.Results:Patients with AD were significantly older than people in subjective memory complaint group (p = 0.02). There was no significant difference between groups according to gender (p = 0.435). Mean plasma PNX level was not significantly different between groups (p = 0.279). Mean plasma PNX level in MCI group was positively correlated with BMI (r = 0.402 and p = 0.028), serum HDL level (r = 0.454 and p = 0.012), blood systolic pressure (r = 0.428 and p = 0.018) and negatively correlated with logical memory (r=−0.335 and p=0.031). The mean plasma PNX level was positively correlated with immediate recall in subjective memory complaint group (r = 0.417 and p = 0.034).Conclusion:This study is the first studying the association of plasma PNX level and cognitive complaints or decline. The knowledge about the role, interaction, and physiological functions of PNX is lacking. Lower plasma PNX level might be important in prodromal stages as MCI and the predictive role of PNX should be investigated in further studies.
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Cebrián, Paula D., and Omar Cauli. "Analysis of Functional and Cognitive Impairment in Institutionalized Individuals with Movement Disorders." Endocrine, Metabolic & Immune Disorders - Drug Targets 19, no. 7 (October 11, 2019): 1022–31. http://dx.doi.org/10.2174/1871530319666190311104247.
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Background: Many neurological disorders lead to institutionalization and can be accompanied in their advanced stages by functional impairment, and progressive loss of mobility, and cognitive alterations. Objective: We analyzed the relationship between functional impairment and cognitive performance and its related subdomains in individuals with Parkinson’s disease, Alzheimer’s disease accompanied by motor dysfunction, and with other neurological disorders characterized by both motor and cognitive problems. Methods: All participants lived in nursing homes (Valencia, Spain) and underwent cognitive evaluation with the Mini-Mental State Examination; functional assessment of independence in activities of daily living using the Barthel score and Katz index; and assessment of mobility with the elderly mobility scale. Results: The mean age of the subjects was 82.8 ± 0.6 years, 47% of the sample included individuals with Parkinson’s disease, and 48 % of the sample presented severe cognitive impairment. Direct significant relationships were found between the level of cognitive impairment and functional capacity (p < 0.01) and mobility (p < 0.05). Among the different domains, memory impairment was not associated with altered activities of daily living or mobility. The functional impairment and the risk of severe cognitive impairment were significantly (p<0.05) higher in female compared to male patients. Among comorbidities, overweight/obesity and diabetes were significantly (p < 0.05) associated with poor cognitive performance in those individuals with mild/moderate cognitive impairment. Conclusion: In institutionalized individuals with movement disorders there is an association between functional and cognitive impairment. Reduction of over-weight and proper control of diabetes may represent novel targets for improving cognitive function at such early stages.
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Noble, Emily E., Charles J. Billington, Catherine M. Kotz, and ChuanFeng Wang. "The lighter side of BDNF." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 300, no. 5 (May 2011): R1053—R1069. http://dx.doi.org/10.1152/ajpregu.00776.2010.
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Brain-derived neurotrophic factor (BDNF) mediates energy metabolism and feeding behavior. As a neurotrophin, BDNF promotes neuronal differentiation, survival during early development, adult neurogenesis, and neural plasticity; thus, there is the potential that BDNF could modify circuits important to eating behavior and energy expenditure. The possibility that “faulty” circuits could be remodeled by BDNF is an exciting concept for new therapies for obesity and eating disorders. In the hypothalamus, BDNF and its receptor, tropomyosin-related kinase B (TrkB), are extensively expressed in areas associated with feeding and metabolism. Hypothalamic BDNF and TrkB appear to inhibit food intake and increase energy expenditure, leading to negative energy balance. In the hippocampus, the involvement of BDNF in neural plasticity and neurogenesis is important to learning and memory, but less is known about how BDNF participates in energy homeostasis. We review current research about BDNF in specific brain locations related to energy balance, environmental, and behavioral influences on BDNF expression and the possibility that BDNF may influence energy homeostasis via its role in neurogenesis and neural plasticity.
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Bulgakova, S., P. Romanchuk, and A. Volobuev. "Clinical and Biophysical Principles of Vascular Dementia and Alzheimer’s Disease Treatment." Bulletin of Science and Practice 5, no. 5 (May 15, 2019): 57–72. http://dx.doi.org/10.33619/2414-2948/42/08.
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Biophysics of blood circulation in Alzheimer’s disease is characterized by disorders of laminar blood flow and cerebral hypoperfusion. As a result, failure intracellular metabolism, there is a cascade of changes in neurons associated with the processes of excitotoxicity and oxidant stress, which in turn stimulates amyloidogenesis. Experimental and 25-year observations have shown that the long-existing state of hypoperfusion leads to hippocampal disorders. This process is accompanied by memory impairment, structural changes in the capillaries in the hippocampus, impaired glucose and protein metabolism, β–amyloid deposition, activation of glial tissue, death of hippocampal neurons. Neuroreflex disruption in the ‘cerebral heart’ and a violation of cerebrovascular homeostasis contributes to the development of vascular dementia through the following mechanisms, including cerebral microangiopathy, endothelial dysfunction, oxidative stress, neuronal damage, the increase in β–amyloid neurotoxicity, apoptosis, etc. The duration of therapy with antiglutamatergic and multimodal drugs in Alzheimer’s disease requires constant multidisciplinary monitoring of targets and medical and social control in the system of long-term care. Lifelong acquisition of knowledge, information positive Nano communication enable the preservation of mental health and active longevity. Innovative methods of P4-medicine of neuroplasticity management allow to carry out timely prevention of the factors reducing neuroplasticity, to keep factors of positive influence on visceral and cognitive brain, and the main thing — in due time to apply in practical health care the combined methods of preservation and development of the human cognitive brain.
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Bahaeddin, Zahra, Asal Yans, Fariba Khodagholi, and Shamim Sahranavard. "Dietary supplementation with Allium hirtifolium and/or Astragalus hamosus improved memory and reduced neuro-inflammation in the rat model of Alzheimer’s disease." Applied Physiology, Nutrition, and Metabolism 43, no. 6 (June 2018): 558–64. http://dx.doi.org/10.1139/apnm-2017-0585.
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Allium hirtifolium Boiss and Astragalus hamosus L. are mentioned in Iranian traditional medicine documentation as therapy for a kind of dementia with the features and symptoms similar to those of Alzheimer’s disease (AD). In the present study, the effects of these herbs on neuro-inflammation and memory have been evaluated as new therapies in amyloid beta (Aβ)-induced memory impairment model. Separate groups of rats were fed with A. hirtifolium or A. hamosus extract (both 100 mg/(kg·day)−1) started 1 week before stereotaxic surgery to 24 h before behavioral testing (totally, for 16 successive days). The effects of oral administration of mentioned extracts on the memory and neuro-inflammation were assessed in the Aβ-injected rats. The results of this study showed that oral administration of both A. hirtifolium and A. hamosus improved the memory, examined by using Y-maze test and shuttle box apparatus. Also, Western blotting analysis of cyclooxygenase-2, interleukin-1β, and tumor necrosis factor-α showed that these herbs have ameliorating effects against the neuro-inflammation caused by Aβ. These findings suggest that the use of A. hirtifolium and A. hamosus as herbal therapy may be suitable for decreasing AD-related symptoms and treatment of other neurodegenerative disorders.
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van Iersel, Laura, Zhenghong Li, Deo Kumar Srivastava, Tara M. Brinkman, Kari L. Bjornard, Carmen L. Wilson, Daniel M. Green, et al. "Hypothalamic-Pituitary Disorders in Childhood Cancer Survivors: Prevalence, Risk Factors and Long-Term Health Outcomes." Journal of Clinical Endocrinology & Metabolism 104, no. 12 (August 2, 2019): 6101–15. http://dx.doi.org/10.1210/jc.2019-00834.
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Abstract Context Data on hypothalamic-pituitary (HP) disorders in systematically evaluated childhood cancer survivors are limited. Objective To describe prevalence, risk factors, and associated adverse health outcomes of deficiencies in GH deficiency (GHD), TSH deficiency (TSHD), LH/FSH deficiency (LH/FSHD), and ACTH deficiency (ACTHD), and central precocious puberty (CPP). Design Retrospective with cross-sectional health outcomes analysis. Setting Established cohort; tertiary care center. Patients Participants (N = 3141; median age, 31.7 years) were followed for a median 24.1 years. Main Outcome Measure Multivariable logistic regression was used to calculate ORs and 95% CIs for associations among HP disorders, tumor- and treatment-related risk factors, and health outcomes. Results The estimated prevalence was 40.2% for GHD, 11.1% for TSHD, 10.6% for LH/FSHD, 3.2% for ACTHD, and 0.9% for CPP among participants treated with HP radiotherapy (n = 1089), and 6.2% for GHD, and <1% for other HP disorders without HP radiotherapy. Clinical factors independently associated with HP disorders included HP radiotherapy (at any dose for GHD, TSHD, LH/FSHD, >30 Gy for ACTHD), alkylating agents (GHD, LH/FSHD), intrathecal chemotherapy (GHD), hydrocephalus with shunt placement (GHD, LH/FSHD), seizures (TSHD, ACTHD), and stroke (GHD, TSHD, LH/FSHD, ACTHD). Adverse health outcomes independently associated with HP disorders included short stature (GHD, TSHD), severe bone mineral density deficit (GHD, LH/FSHD), obesity (LH/FSHD), frailty (GHD), impaired physical health-related quality of life (TSHD), sexual dysfunction (LH/FSHD), impaired memory, and processing speed (GHD, TSHD). Conclusion HP radiotherapy, central nervous system injury, and, to a lesser extent, chemotherapy are associated with HP disorders, which are associated with adverse health outcomes.
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Lee, Gil-Yong, Chan Lee, Gyu Hwan Park, and Jung-Hee Jang. "Amelioration of Scopolamine-Induced Learning and Memory Impairment byα-Pinene in C57BL/6 Mice." Evidence-Based Complementary and Alternative Medicine 2017 (2017): 1–9. http://dx.doi.org/10.1155/2017/4926815.
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Increasing evidence suggests that neurodegenerative disorders such as Alzheimer’s disease (AD) are mediated via disruption of cholinergic neurons and enhanced oxidative stress. Therefore, attention has been focused on searching for antioxidant phytochemicals for the prevention and/or treatment of AD through their ability to fortify cholinergic function and antioxidant defense capacity. In this study, we have investigated the neuroprotective effect ofα-pinene (APN) against learning and memory impairment induced by scopolamine (SCO, 1 mg/kg, i.p.), a muscarinic receptor antagonist in C57BL/6 mice. Administration of APN (10 mg/kg, i.p.) significantly improved SCO-induced cognitive dysfunction as assessed by Y-maze and passive avoidance tests. In Morris water-maze test, APN effectively shortened the mean escape latency to find the hidden platform during training days. To further elucidate the molecular mechanisms underlying the neuroprotective effect of APN, the expression of proteins involved in the acetylcholine metabolism and antioxidant system was examined. Particularly, APN treatment increased mRNA expression of choline acetyltransferase in the cortex and protein levels of antioxidant enzymes such as heme oxygenase-1 and manganese superoxide dismutase in the hippocampus via activation of NF-E2-related factor 2. These findings suggest the possible neuroprotective potentials of APN for the management of dementia with learning and memory loss.
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Hill, Alice, Colin Johnston, and Joanna L. Spencer-Segal. "Corticosterone Enhances Formation of Neutral but Not Fear Memory During Infectious Illness." Journal of the Endocrine Society 5, Supplement_1 (May 1, 2021): A534—A535. http://dx.doi.org/10.1210/jendso/bvab048.1089.
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Abstract Survivors of critical illness often report traumatic memories of their illness period, and these memories are thought to contribute to development of neuropsychiatric disorders, such as PTSD. Many patients are treated with high doses of glucocorticoids for their vasoactive and anti-inflammatory properties, and glucocorticoids have also been shown to prevent the development of PTSD after trauma. Due to their activity in the hippocampus and amygdala, the putative protective effect of glucocorticoids may occur via memory formation during illness. To examine the effect of glucocorticoids on memory formation during acute infectious illness, male and female C57BL/6 mice (N=80, 40 male/40 female) underwent cecal ligation and puncture and were treated with either corticosterone (16 mg/kg) or vehicle in the early afternoon daily for five days beginning on the day of surgery. All mice were habituated to a neutral object in their home cage for five days and underwent one 30-minute footshock/no shock training session during the illness period. After physiologic recovery (2 weeks), the mice underwent behavioral testing including open field exploration, object recognition testing in which they were presented with both the familiar (habituated) object and a novel object, and testing in the shock context. The results showed that drug treatment had no effect on behavior in the open field, including time spent in the center (VEH: 20.19±10.81 vs CORT: 22.32±12.87 sec; P=0.476). Drug treatment increased overall object exploration (12.28±10.79 vs 19.17±15.88 sec; P=0.049). Corticosterone-treated mice showed a preference for the familiar object (60.9±23.0% of total exploration time with familiar object; P=0.015), while vehicle-treated mice did not (54.1±23.3%; P=0.378). The increase in overall object exploration seen in corticosterone-treated mice could be accounted for by an increase in exploration of the familiar object. History of footshock increased freezing in the training context (3.96±2.54% vs 36.08±15.42%; P<0.0001) and corticosterone treatment had no effect (18.06±17.65% vs 22.16±21.19%; P=0.557). In conclusion, administration of corticosterone during infectious illness facilitated memory of a neutral object from the illness period, and recovered mice exhibited a preference for this object over a novel one. Corticosterone treatment had no impact on fear memory formed during illness. This is consistent with human literature suggesting that hydrocortisone decreases PTSD symptoms without impacting traumatic memories. These findings suggest that glucocorticoids selectively enhance the formation, consolidation, and/or recall of neutral but not fear memories during illness, which may rely on hippocampal circuitry. We further suggest that accurate memories of the illness period may influence patients’ perception of this experience and alter their risk for psychiatric sequelae.
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Santaguida, Maria Giulia, Ilenia Gatto, Giorgio Mangino, Camilla Virili, Ilaria Stramazzo, Poupak Fallahi, Alessandro Antonelli, Patrizia Gargiulo, Giovanna Romeo, and Marco Centanni. "Breg Cells in Celiac Disease Isolated or Associated to Hashimoto’s Thyroiditis." International Journal of Endocrinology 2018 (October 8, 2018): 1–6. http://dx.doi.org/10.1155/2018/5290865.
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Hashimoto’s thyroiditis (HT) may occur associated with celiac disease (CD). Regulatory B cells (Breg) subsets have been shown to play a significant role in autoimmune processes. Therefore, we have characterized their distribution in the peripheral blood obtained from 10 patients with isolated HT, 10 patients with HT + CD, 9 patients with isolated CD, and 9 healthy donors (HD). Th17 cells were significantly increased in patients with HT and in patients bearing both HT and CD, while patients with isolated CD exhibited a lower percentage of Th17, as compared with healthy donors. CD24hiCD38hiBreg cells were significantly higher in patients with HT + CD and in patients with isolated CD as compared to both HD patients and patients with isolated HT (p=0.0010). On the contrary, Breg memory phenotypes (CD24hiCD38−and CD24hiCD27+) significantly decreased in patients with HT + CD as compared with the isolated disorders. Following CpG oligodeoxynucleotide stimulation, IL-10+CD24hiCD38hiBreg cells were similar in all groups of patients, despite these cells would have been higher in CD patients. In conclusion, celiac disease, isolated and even more when associated with HT, determines a peculiar behavior of Breg cells which are increased in number but possibly functionally defective. Furthermore, the association CD + HT was characterized by a reduction of Breg memory subsets as compared with the isolated disorders. The behavior of Th17 subset in patients with celiac disease associated with HT might have been sensitive to the effect of long-lasting GFD, and it is essentially determined by the presence of thyroid autoimmunity.
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Tumminia, Andrea, Federica Vinciguerra, Miriam Parisi, and Lucia Frittitta. "Type 2 Diabetes Mellitus and Alzheimer’s Disease: Role of Insulin Signalling and Therapeutic Implications." International Journal of Molecular Sciences 19, no. 11 (October 24, 2018): 3306. http://dx.doi.org/10.3390/ijms19113306.
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In the last two decades, numerous in vitro studies demonstrated that insulin receptors and theirs downstream pathways are widely distributed throughout the brain. This evidence has proven that; at variance with previous believes; insulin/insulin-like-growth-factor (IGF) signalling plays a crucial role in the regulation of different central nervous system (CNS) tasks. The most important of these functions include: synaptic formation; neuronal plasticity; learning; memory; neuronal stem cell activation; neurite growth and repair. Therefore; dysfunction at different levels of insulin signalling and metabolism can contribute to the development of a number of brain disorders. Growing evidences demonstrate a close relationship between Type 2 Diabetes Mellitus (T2DM) and neurodegenerative disorders such as Alzheimer’s disease. They, in fact, share many pathophysiological characteristics comprising impaired insulin sensitivity, amyloid β accumulation, tau hyper-phosphorylation, brain vasculopathy, inflammation and oxidative stress. In this article, we will review the clinical and experimental evidences linking insulin resistance, T2DM and neurodegeneration, with the objective to specifically focus on insulin signalling-related mechanisms. We will also evaluate the pharmacological strategies targeting T2DM as potential therapeutic tools in patients with cognitive impairment.
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Rocha, Kellen Mariane Athaide, Aline da Silva Goulart, Márcio Tavares Costa, Andréia Caroline Fernandes Salgueiro, and Vanderlei Folmer. "The role of type 2 Diabetes mellitus as a risk factor for Alzheimer's and Parkinson's diseases." Research, Society and Development 10, no. 1 (January 9, 2021): e23410111673. http://dx.doi.org/10.33448/rsd-v10i1.11673.
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Currently, one of the most significant health problems is the increased incidence of obesity and type 2 Diabetes mellitus (DM2). The most recent epidemiological and clinical research studies have indicated that low physical activity, as well as many genetic and environmental factors are the main causes of these metabolic disorders. It is widely recognized that insulin resistance plays a key role in the development of DM2, disrupting not only the functioning of peripheral tissues, but also the brain. Insulin plays a critical role in the central nervous system participating in neuronal survival, neuroplasticity, memory and cognitive functions. In addition, peripheral insulin resistance results in loss of brain function, which indicates a strong relationship between metabolic disorders, cognitive impairment and the emergence of neurodegenerative diseases. There are links between these different pathologies, such as increased oxidative stress, neuroinflammation, changes in glucose metabolism as well as insulin resistance. Advances in the knowledge of these links may contribute to the development of treatments for the prevention of these pathological events. Based on the above, this study aimed to review the mechanisms associated with DM2 in the development of neurodegenerative diseases, such as Alzheimer’s and Parkinson’s diseases.
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Rocha, Kellen Mariane Athaide, Aline da Silva Goulart, Márcio Tavares Costa, Andréia Caroline Fernandes Salgueiro, and Vanderlei Folmer. "The role of type 2 Diabetes mellitus as a risk factor for Alzheimer's and Parkinson's diseases." Research, Society and Development 10, no. 1 (January 9, 2021): e23410111673. http://dx.doi.org/10.33448/rsd-v10i1.11673.
Full textAbstract:
Currently, one of the most significant health problems is the increased incidence of obesity and type 2 Diabetes mellitus (DM2). The most recent epidemiological and clinical research studies have indicated that low physical activity, as well as many genetic and environmental factors are the main causes of these metabolic disorders. It is widely recognized that insulin resistance plays a key role in the development of DM2, disrupting not only the functioning of peripheral tissues, but also the brain. Insulin plays a critical role in the central nervous system participating in neuronal survival, neuroplasticity, memory and cognitive functions. In addition, peripheral insulin resistance results in loss of brain function, which indicates a strong relationship between metabolic disorders, cognitive impairment and the emergence of neurodegenerative diseases. There are links between these different pathologies, such as increased oxidative stress, neuroinflammation, changes in glucose metabolism as well as insulin resistance. Advances in the knowledge of these links may contribute to the development of treatments for the prevention of these pathological events. Based on the above, this study aimed to review the mechanisms associated with DM2 in the development of neurodegenerative diseases, such as Alzheimer’s and Parkinson’s diseases.
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Sidneva, Yuliya G., Ludmila I. Astafyeva, Boris A. Kadashev, Pavel L. Kalinin, Maxim A. Kutin, and Larisa K. Dzeranova. "The state of erection in a patient with craniopharyngioma, panhypopituitarism and diencephalic obesity." Obesity and metabolism 16, no. 2 (September 16, 2019): 83–88. http://dx.doi.org/10.14341/omet10062.
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The article presents a clinical case from the practice of a patient with craniopharyngioma. The man of reproductive age with diencephalic obesity (BMI 35 kg/m2), recurrent craniopharyngioma, a long history of endocrine disorders (panhypopituitarism, including secondary hypogonadism, with the corresponding sexual function disorders and the lack of sexual activity), with visual disorders and psychiatric symptoms in the early postoperative period after shunting surgery and reducing the volume of the craniopharyngioma cyst, erection conditions arose against the background of episodes of disorders of consciousness within the framework of sleep dissociation.
After the operation (installation of the Ommaya system), the patient had a state of spontaneous erection lasting up to 30 minutes against the background of dream-oneiric states of impaired consciousness with erotic experiences. These states were observed for 3 nights, the patient remembered the experiences and events that occurred to him in a dream, and could tell about them to others on the next morning. The identity of the patient remained intact, he was active in the department, ordered in behavior; memory for current events and new information was intact. These disorders in the patient did not require specialized treatment, regressed independently on the 6th day of the postoperative period.
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Hung, Ming Wai, Zai Jun Zhang, Shang Li, Benson Lei, Shuai Yuan, Guo Zhen Cui, Pui Man Hoi, Kelvin Chan, and Simon Ming Yuen Lee. "From Omics to Drug Metabolism and High Content Screen of Natural Product in Zebrafish: A New Model for Discovery of Neuroactive Compound." Evidence-Based Complementary and Alternative Medicine 2012 (2012): 1–20. http://dx.doi.org/10.1155/2012/605303.
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The zebrafish (Danio rerio) has recently become a common model in the fields of genetics, environmental science, toxicology, and especially drug screening. Zebrafish has emerged as a biomedically relevant model forin vivohigh content drug screening and the simultaneous determination of multiple efficacy parameters, including behaviour, selectivity, and toxicity in the content of the whole organism. A zebrafish behavioural assay has been demonstrated as a novel, rapid, and high-throughput approach to the discovery of neuroactive, psychoactive, and memory-modulating compounds. Recent studies found a functional similarity of drug metabolism systems in zebrafish and mammals, providing a clue with why some compounds are active in zebrafishin vivobut notin vitro, as well as providing grounds for the rationales supporting the use of a zebrafish screen to identify prodrugs. Here, we discuss the advantages of the zebrafish model for evaluating drug metabolism and the mode of pharmacological action with the emerging omics approaches. Why this model is suitable for identifying lead compounds from natural products for therapy of disorders with multifactorial etiopathogenesis and imbalance of angiogenesis, such as Parkinson's disease, epilepsy, cardiotoxicity, cerebral hemorrhage, dyslipidemia, and hyperlipidemia, is addressed.
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Bockaert, Joël, and Philippe Marin. "mTOR in Brain Physiology and Pathologies." Physiological Reviews 95, no. 4 (October 2015): 1157–87. http://dx.doi.org/10.1152/physrev.00038.2014.
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TOR (target of rapamycin) and its mammalian ortholog mTOR have been discovered in an effort to understand the mechanisms of action of the immunosuppressant drug rapamycin extracted from a bacterium of the Easter Island (Rapa Nui) soil. mTOR is a serine/threonine kinase found in two functionally distinct complexes, mTORC1 and mTORC2, which are differentially regulated by a great number of nutrients such as glucose and amino acids, energy (oxygen and ATP/AMP content), growth factors, hormones, and neurotransmitters. mTOR controls many basic cellular functions such as protein synthesis, energy metabolism, cell size, lipid metabolism, autophagy, mitochondria, and lysosome biogenesis. In addition, mTOR-controlled signaling pathways regulate many integrated physiological functions of the nervous system including neuronal development, synaptic plasticity, memory storage, and cognition. Thus it is not surprising that deregulation of mTOR signaling is associated with many neurological and psychiatric disorders. Preclinical and preliminary clinical studies indicate that inhibition of mTORC1 can be beneficial for some pathological conditions such as epilepsy, cognitive impairment, and brain tumors, whereas stimulation of mTORC1 (direct or indirect) can be beneficial for other pathologies such as depression or axonal growth and regeneration.
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Moro, Joanna, Daniel Tomé, Philippe Schmidely, Tristan-Chalvon Demersay, and Dalila Azzout-Marniche. "Histidine: A Systematic Review on Metabolism and Physiological Effects in Human and Different Animal Species." Nutrients 12, no. 5 (May 14, 2020): 1414. http://dx.doi.org/10.3390/nu12051414.
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Histidine is an essential amino acid (EAA) in mammals, fish, and poultry. We aim to give an overview of the metabolism and physiological effects of histidine in humans and different animal species through a systematic review following the guidelines of PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses). In humans, dietary histidine may be associated with factors that improve metabolic syndrome and has an effect on ion absorption. In rats, histidine supplementation increases food intake. It also provides neuroprotection at an early stage and could protect against epileptic seizures. In chickens, histidine is particularly important as a limiting factor for carnosine synthesis, which has strong anti-oxidant effects. In fish, dietary histidine may be one of the most important factors in preventing cataracts. In ruminants, histidine is a limiting factor for milk protein synthesis and could be the first limiting AA for growth. In excess, histidine supplementation can be responsible for eating and memory disorders in humans and can induce growth retardation and metabolic dysfunction in most species. To conclude, the requirements for histidine, like for other EAA, have been derived from growth and AA composition in tissues and also have specific metabolic roles depending on species and dietary levels.
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Czapski, Grzegorz A., Lidia Babiec, Henryk Jęśko, Magdalena Gąssowska-Dobrowolska, Magdalena Cieślik, Marta Matuszewska, Małgorzata Frontczak-Baniewicz, Karolina Zajdel, and Agata Adamczyk. "Synaptic Alterations in a Transgenic Model of Tuberous Sclerosis Complex: Relevance to Autism Spectrum Disorders." International Journal of Molecular Sciences 22, no. 18 (September 17, 2021): 10058. http://dx.doi.org/10.3390/ijms221810058.
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Tuberous sclerosis complex (TSC) is a rare, multi-system genetic disease with serious neurological and mental symptoms, including autism. Mutations in the TSC1/TSC2 genes lead to the overactivation of mTOR signalling, which is also linked to nonsyndromic autism. Our aim was to analyse synaptic pathology in a transgenic model of TSC: two-month-old male B6;129S4-Tsc2tm1Djk/J mice with Tsc2 haploinsufficiency. Significant brain-region-dependent alterations in the expression of several synaptic proteins were identified. The most prominent changes were observed in the immunoreactivity of presynaptic VAMP1/2 (ca. 50% increase) and phospho-synapsin-1 (Ser62/67) (ca. 80% increase). Transmission electron microscopy demonstrated serious ultrastructural abnormalities in synapses such as a blurred structure of synaptic density and a significantly increased number of synaptic vesicles. The impairment of synaptic mitochondrial ultrastructure was represented by excessive elongation, swelling, and blurred crista contours. Polyribosomes in the cytoplasm and swollen Golgi apparatus suggest possible impairment of protein metabolism. Moreover, the delamination of myelin and the presence of vacuolar structures in the cell nucleus were observed. We also report that Tsc2+/− mice displayed increased brain weights and sizes. The behavioural analysis demonstrated the impairment of memory function, as established in the novel object recognition test. To summarise, our data indicate serious synaptic impairment in the brains of male Tsc2+/− mice.
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Liashevych, A. M., І. S. Lupaina, and M. Yu Makarchuk. "The Influence of Corvitin on the Cholates Content in the Male Rats’ Liver under the Conditions of Chronic Social Stress." Ukraïnsʹkij žurnal medicini, bìologìï ta sportu 6, no. 4 (September 20, 2021): 186–92. http://dx.doi.org/10.26693/jmbs06.04.186.
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The creation of universally effective and safe correctors of biliary secretion disorders is becoming more timely. There is an urgent need for scientists to find drugs that would correct blood cholesterol levels and metabolism in liver effectively and without limiting side effects. The purpose of the study was to investigate the possibility of using corvitin to correct stress-induced biliary disorders of the liver of male rats. Materials and methods. The article looks at recent research dealing with changes in the bile acid composition of outbred male rats’ bile under chronic social stress (social defeat in daily male confrontations, 14 days) when using Corvitin (1 mg/kg, intragastrically, 7 days). Chronic social stress was created by daily agonistic interactions between animals. The state of memory and the level of research activity in the object recognition test (cognitive test) were also studied. The main fractions of conjugated bile acids (taurocholic, taurohenodeoxycholic and taurodeoxycholic, glycocholic, glycochenodeoxycholic and glycodeoxycholic and free ones – cholic, chenodeoxycholic and deoxycholic) were determined by the method of thin layer chromatography of bile. Results and discussion. Chronic social stress leads to a slight increase in the overall activity of the experimental animals, but significantly impairs the processes of recognition and memory. Social stress significantly inhibits the processes that ensure the synthesis, biotransformation and transport of bile acids in the bile. Also, chronic social stress causes changes in bile production, which reduce the solubilization properties of bile and increase the risk of lithogenesis. Conclusion. The use of Corvitin simultaneously with the simulation of experimental social stress normalized the biliary secretory function of the liver, which indicates a high potential for the use of Corvitin as a corrective factor in chronic social stress. Corvitin used by us in the conditions of experimental social stress to some extent corrected the content of bile acids in the liver of male rats, which indicates the ability of this drug to interfere with the metabolism of cholate in liver cells, in the mechanisms of bile acid transport. Correction of stress-induced pathologies of liver bile-secretory function by Corvitin requires further thorough experimental studies
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Toffa, DH, C. Kpadonou, D. Gams Massi, M. Ouedraogo, AD Sow, M. Ndiaye, and A. Samb. "P.041 Magnesium and calcium reduce severity of spatial memory impairments in kainate mouse model of mesial temporal lobe epilepsy." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 46, s1 (June 2019): S24—S25. http://dx.doi.org/10.1017/cjn.2019.141.
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Background: Calcium (Ca) and magnesium (Mg) are crucial in metabolism, excitability and neuroglial plasticity. Our aim was to evaluate whether Mg (20 mg/kg) or Ca (100 mg/kg) could improve the memory prognosis in the kainic model of mesial temporal epilepsy. Methods: Seizures were induced by systemic injection of kainate (8mg/kg) and mice were then treated by ions every 48 hours. A placebo (physiological solution) replaced kainate or ions in specific groups. Six cohorts were studied for seven weeks: control group (G0: no kainate and no ion, only placebo); untreated reference group (GR: kainate and then placebo); G1 groups were treated from the third day (G1m, G1c: kainate and then Mg/Ca); G2 groups were treated from the third week (G2m, G2c: kainate and then Mg/Ca). Radial maze and a classic maze were used for cognition evaluation. Results: The memory (short/long term) was differently affected by kainate or improved by Mg/Ca. The treated groups performed better than GR mice, but Mg was more effective. In addition, Mg demonstrated an increasing therapeutic effect over time while Ca showed an acute and apparently decreasing action in the G1c group. Conclusions: Mg should be considered for a clinical evaluation of its effect on epileptic disorders.
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Chugani, Harry T. "Imaging Brain Metabolism in the Newborn." Journal of Child Neurology 33, no. 13 (August 16, 2018): 851–60. http://dx.doi.org/10.1177/0883073818792308.
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In this review, we discuss molecular brain imaging studies using positron emission tomography (PET) with 2-deoxy-2(18F)fluoro-d-glucose (FDG) in human newborns and infants, and illustrate how this technology can be applied to probe the neuropathophysiology of neonatal neurologic disorders. PET studies have been difficult to perform in sick babies because of patient transportation issues and suboptimal spatial resolution. With approval from the FDA and the institutional review board, we modified and installed the Focus 220 animal microPET scanner (Concorde Microsystems, Knoxville, TN) directly in our neonatal intensive care unit in Children’s Hospital of Michigan and verified the high spatial resolution (<2 mm full-width-at-half-maximum) of this microPET. The neonatal pattern of glucose metabolism is very consistent, with the highest degree of activity in primary sensory and motor cortex, medial temporal region, thalamus, brain stem, and cerebellar vermis. Prior studies have shown that increases of glucose utilization are seen by 2 to 3 months in the parietal, temporal, cingulate, and primary visual cortex; basal ganglia; and cerebellar hemispheres. Between 6 and 8 months, lateral and inferior frontal cortex becomes more functionally active and, eventually, between 8 and 12 months, the dorsal and medial frontal regions also show a maturational increase. These findings are consistent with the physical, behavioral, and cognitive maturation of the infant. At birth, metabolic rates of glucose utilization in cortex are about 30% lower than in adults but rapidly rise such that, by 3 years, the cerebral cortical rates exceed adult rates by more than 2-fold. At around puberty, the rates for cerebral cortex begin to decline and gradually reach adult values by 16-18 years. These nonlinear changes of glucose utilization indirectly reflect programed periods of synaptic proliferation and pruning in the brain. Positron emission tomographic (PET) imaging of GABAA receptors (using 11C-flumazenil) in newborns also show a pattern very different from adults, with high binding in amygdala-hippocampus, sensory-motor cortex, thalamus, brain stem, and basal ganglia, in that order. We speculate that the early development of amygdala/hippocampus prepares the baby for bonding, attachment, and memory, and the deprivation of such experiences during a sensitive period results in malfunction of these networks and psychopathology, as has been shown in studies on severely socioemotionally deprived children. Recently developed hybrid PET/magnetic resonance (MR) scanners allow the simultaneous acquisition of PET and MR data sets with advanced applications. These devices are particularly advantageous for scanning babies and infants because of the high spatial resolution, automated coregistration of anatomical and functional images and, in the case of need for sedation, maximal data acquired in 1 session.
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Sedaghat, Katayoun. "A review on insulin presence and function in brain." International Journal of Scientific Reports 6, no. 3 (February 25, 2020): 118. http://dx.doi.org/10.18203/issn.2454-2156.intjscirep20200649.
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<p class="abstract">Hormones have major role in maintaining the homeostasis of the body and mental functions. One of the crucial hormones that act to regulate the metabolism and growth is insulin. Insulin activity in the periphery has been the subject of study since long time ago, though, beginning to understand the central activity of insulin is rather recent and because of complexity of actions and interference with neurodegenerative diseases such as Alzheimer’s and Parkinson’s and mood disorders, like anxiety and depression, it is considered very crucial hormone in the maintenance of the mental health. This mini-review will discuss briefly the recent main aspects of insulin transfer to the brain, receptor and mediators, signaling pathways with particular attention to neural system and its role in cognitive and emotional processing in brain. Insulin is an endocrine hormone with receptor distribution in different parts of brain and has role in various neural functions such as; growth factor, modulating learning or memory, mood, neural growth and survival, also controlling neurotransmitters functions in different brain regions. Insulin regulates metabolic homeostasis in brain through complex routes, which inevitably makes it involved with some neurodegenerative or affective disorders, that raises its importance for more serious studies.</p>
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Sun, Yanan, Cao Ma, Hui Sun, Huan Wang, Wei Peng, Zibo Zhou, Hongwei Wang, Chenchen Pi, Yingai Shi, and Xu He. "Metabolism: A Novel Shared Link between Diabetes Mellitus and Alzheimer’s Disease." Journal of Diabetes Research 2020 (January 30, 2020): 1–12. http://dx.doi.org/10.1155/2020/4981814.
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As a chronic metabolic disease, diabetes mellitus (DM) is broadly characterized by elevated levels of blood glucose. Novel epidemiological studies demonstrate that some diabetic patients have an increased risk of developing dementia compared with healthy individuals. Alzheimer’s disease (AD) is the most frequent cause of dementia and leads to major progressive deficits in memory and cognitive function. Multiple studies have identified an increased risk for AD in some diabetic populations, but it is still unclear which diabetic patients will develop dementia and which biological characteristics can predict cognitive decline. Although few mechanistic metabolic studies have shown clear pathophysiological links between DM and AD, there are several plausible ways this may occur. Since AD has many characteristics in common with impaired insulin signaling pathways, AD can be regarded as a metabolic disease. We conclude from the published literature that the body’s diabetic status under certain circumstances such as metabolic abnormalities can increase the incidence of AD by affecting glucose transport to the brain and reducing glucose metabolism. Furthermore, due to its plentiful lipid content and high energy requirement, the brain’s metabolism places great demands on mitochondria. Thus, the brain may be more susceptible to oxidative damage than the rest of the body. Emerging evidence suggests that both oxidative stress and mitochondrial dysfunction are related to amyloid-β (Aβ) pathology. Protein changes in the unfolded protein response or endoplasmic reticulum stress can regulate Aβ production and are closely associated with tau protein pathology. Altogether, metabolic disorders including glucose/lipid metabolism, oxidative stress, mitochondrial dysfunction, and protein changes caused by DM are associated with an impaired insulin signal pathway. These metabolic factors could increase the prevalence of AD in diabetic patients via the promotion of Aβ pathology.
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Sáez-Orellana, Francisco, Jean-Noël Octave, and Nathalie Pierrot. "Alzheimer’s Disease, a Lipid Story: Involvement of Peroxisome Proliferator-Activated Receptor α." Cells 9, no. 5 (May 14, 2020): 1215. http://dx.doi.org/10.3390/cells9051215.
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Alzheimer’s disease (AD) is the leading cause of dementia in the elderly. Mutations in genes encoding proteins involved in amyloid-β peptide (Aβ) production are responsible for inherited AD cases. The amyloid cascade hypothesis was proposed to explain the pathogeny. Despite the fact that Aβ is considered as the main culprit of the pathology, most clinical trials focusing on Aβ failed and suggested that earlier interventions are needed to influence the course of AD. Therefore, identifying risk factors that predispose to AD is crucial. Among them, the epsilon 4 allele of the apolipoprotein E gene that encodes the major brain lipid carrier and metabolic disorders such as obesity and type 2 diabetes were identified as AD risk factors, suggesting that abnormal lipid metabolism could influence the progression of the disease. Among lipids, fatty acids (FAs) play a fundamental role in proper brain function, including memory. Peroxisome proliferator-activated receptor α (PPARα) is a master metabolic regulator that regulates the catabolism of FA. Several studies report an essential role of PPARα in neuronal function governing synaptic plasticity and cognition. In this review, we explore the implication of lipid metabolism in AD, with a special focus on PPARα and its potential role in AD therapy.