Academic literature on the topic 'Memory Disorders – metabolism'
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Journal articles on the topic "Memory Disorders – metabolism"
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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.
Dissertations / Theses on the topic "Memory Disorders – metabolism"
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Bossy, Tanya. "Implication of a novel nerve growth factor (NGF) maturation and degradation cascade in the Fischer-344 rat model of age-associated memory deficits." Thesis, McGill University, 2009. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111573.
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Despite the overwhelming evidence for atrophy of the NGF-dependant Basal Forebrain Cholinergic neurons during aging, there is no persuasive evidence towards a decrease in NGF and/or NGF mRNA content in the brain of aged animals. Previous experiments from our laboratory have shown that NGF is released as a precursor protein and cleaved into the mature form in the extracellular space under the influence of a complex protease cascade. These recent findings have lead us to propose that any alterations in levels and/or activity of this maturation/degradation cascade might affect NGF's biological activity and perhaps lead to cognitive impairments in a subset of aged rats. To investigate this possibility, we measured protein and mRNA levels of the protease cascade players (NGF, pro-NGF, tPA, plasminogen, plasmin, MMP-9, neuroserpin). We found significantly decreased levels of both pro-NGF protein and NGF mRNA, but no difference in the remaining elements of the protease cascade, when comparing aged impaired (Al) to the aged unimpaired (AU) animals. Our second objective was to investigate whether animals trained in the Morris Water Maze would preserve their cognitive status in two additional behavioral paradigms, the Novel Object Location (NOL, spatial memory) and Novel Object Recognition (NOR, nonspatial memory) tasks. We found that both AU and AI animals in the MWM were impaired in the NOL when compared to the young controls, with the AI animals performing significantly worse than the AU in this particular task. In the NOR tasks, AI animals performed significantly worse compared to both young and AU animals. In conclusion, further experiments are required to better understand the implication of the complex protease cascade involved in NGF's maturation and degradation as well as its effect on memory of aged animals. In addition, because the segregation of animals (aged impaired/unimpaired) is a crucial step in aging research, we now have additional behavioral paradigms (NOL/NOR) that confirm the cognitive status of these animals.
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Santos, Taisa de Oliveira. "Injeção intracerebroventricular de estreptozotocina gera efeitos agudos e crônicos sobre a memória e sobre proteínas indicadoras de neurodereneração em ratos." Universidade de São Paulo, 2010. http://www.teses.usp.br/teses/disponiveis/47/47135/tde-16072010-091230/.
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A Doença de Alzheimer (DA) é a causa mais comum de demência e é caracterizada clinicamente por comprometimentos cognitivos. Histologicamente é caracterizada pela formação de placas senis e de emaranhados neurofibrilares intracelulares resultantes de alterações do metabolismo do peptídeo A e da hiperfosforilação da proteína tau, respectivamente. Essas alterações parecem, em parte, ser uma decorrência de uma deficiência na sinalização da insulina e conseqüente resistência do encéfalo a esse hormônio, sugerindo que a DA esporádica tenha uma relação com o Diabetes mellitus. A estreptozotocina tem sido utilizada como modelo de indução do Diabetes, e mais recentemente como modelo experimental da DA quando administrado intracerebroventricular. Nosso objetivo nesse estudo foi o de caracterizar o esse modelo experimental da DA induzido pela estreptozotocina, avaliando as conseqüências agudas e a longo prazo. Foram utilizados ratos Wistar machos de quatro meses de idade que receberam injeções intracerebroventriculares bilaterais de estreptozotocina ou de veículo. Os animais foram avaliados aguda e cronicamente por testes comportamentais de memória de referência e operacional utilizando o modelo do labirinto aquático de Morris que visavam avaliar o curso temporal dos prejuízos cognitivos após a injeção da droga. Em diferentes tempos após as injeções, os ratos foram sacrificados e regiões do encéfalo submetidas à técnica de immunoblotting para avaliação de proteínas indicadoras de neurodegeneração ou à técnica histoquimica pelo método de Fluoro-Jade C. A avaliação da memória operacional em períodos agudos mostrou que os prejuízos cognitivos parecem se instalar a partir de 3 horas da injeção de estreptozotocina. A avaliação crônica das memórias operacional e de referência mostrou que os ratos exibiram um prejuízo marcante no desempenho dessas tarefas ao longo dos testes, embora seja correto afirmar que esses animais ainda são capazes de adquirir informação relevante com relação à execução da tarefa, particularmente na versão de memória de referência. A análise de immunoblotting mostrou haver aumento da expressão do peptídeo beta amilóide significante em regiões como amigdala, córtex entorrinal, núcleos da base e do hipotálamo. Também foi observado um aumento significativo da fosforilação da proteína tau na amigdala, cerebelo, córtex, prosencéfalo basal e núcleos da base. Foi observada uma diminuição da enzima de síntese de acetilcolina, a colina acetil-transferase apenas na amigdala. Fibras em degeneração foram observadas no hipotálamo, na área septal e em neurônios piramidais na região CA1 após 1 dia da injeção de estreptozotocina. Já após 15 dias da injeção podemos observar marcação em neurônios do estriado e da região CA1 do hipocampo e em fibras próximas ao giro denteado. Em resumo a injeção intracerebroventricular de estreptozotocina parece produzir um bom modelo experimental da DA, pois reproduz as características cognitivas e histológicas encontradas nos pacientes com a doençaAlzheimer´s disease (AD) is the most common cause of dementia in aged humans. Recent reports have suggested a relationship between the onset of AD and an insulin-resistant brain condition. In this context, this study aimed at evaluating the effects of intracerebroventricular (ICV) injection of streptozotocin (STZ) in rats on behavior and neurodegeneration. Four month-old adult male Wistar rats were subjected to bilateral ICV injections of either STZ or vehicle and were tested for both reference and working memories in Morris water maze. After different survival times, rats were subjected to immunoblotting (to evaluate neurodegeneration markers) or to Fluoro-Jade C histochemistry. A marked disruption of performance in working memory was already observed after 3 hours of STZ injections. Immunoblotting analysis showed a significant increase of beta amyloid peptide expression in the amygdala, entorrinal cortex, basal ganglia, and hypothalamus. A significant increase of tau phosphorylation was also observed in the amygdala, cerebellum, cortex, basal forebrain and basal ganglia. Degenerating fibers were seen in the hypothalamus and septal area 1 day postinjection and in CA1 pyramidal neurons and close to the hippocampal dentate gyrus after 15 days. ICV injection of STZ seems therefore to produce an animal model of AD, as it reproduces the characteristic cognitive and histological changes of the disease
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Öfverman, Charlotte. "Progesterone metabolites learning, tolerance, antagonism & metabolism /." Umeå : Umeå university, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-27064.
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Bishop, Courtney Alexandra. "Development and application of image analysis techniques to study structural and metabolic neurodegeneration in the human hippocampus using MRI and PET." Thesis, University of Oxford, 2012. http://ora.ox.ac.uk/objects/uuid:2549bad2-432f-4d0e-8878-be9cce6ae0d2.
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Despite the association between hippocampal atrophy and a vast array of highly debilitating neurological diseases, such as Alzheimer’s disease and frontotemporal lobar degeneration, tools to accurately and robustly quantify the degeneration of this structure still largely elude us. In this thesis, we firstly evaluate previously-developed hippocampal segmentation methods (FMRIB’s Integrated Registration and Segmentation Tool (FIRST), Freesurfer (FS), and three versions of a Classifier Fusion (CF) technique) on two clinical MR datasets, to gain a better understanding of the modes of success and failure of these techniques, and to use this acquired knowledge for subsequent method improvement (e.g., FIRSTv3). Secondly, a fully automated, novel hippocampal segmentation method is developed, termed Fast Marching for Automated Segmentation of the Hippocampus (FMASH). This combined region-growing and atlas-based approach uses a 3D Sethian Fast Marching (FM) technique to propagate a hippocampal region from an automatically-defined seed point in the MR image. Region growth is dictated by both subject-specific intensity features and a probabilistic shape prior (or atlas). Following method development, FMASH is thoroughly validated on an independent clinical dataset from the Alzheimer’s Disease Neuroimaging Initiative (ADNI), with an investigation of the dependency of such atlas-based approaches on their prior information. In response to our findings, we subsequently present a novel label-warping approach to effectively account for the detrimental effects of using cross-dataset priors in atlas-based segmentation. Finally, a clinical application of MR hippocampal segmentation is presented, with a combined MR-PET analysis of wholefield and subfield hippocampal changes in Alzheimer’s disease and frontotemporal lobar degeneration. This thesis therefore contributes both novel computational tools and valuable knowledge for further neurological investigations in both the academic and the clinical field.
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Riha, Penny Denise 1975. "Metabolic impairment of the posterior cingulate cortex and reversal by methylene blue: a novel model and treatment of early stage Alzheimer's disease." Thesis, 2007. http://hdl.handle.net/2152/3663.
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Alzheimer's disease (AD) is associated with decreased brain energy metabolism. Hypometabolism in the posterior cingulate cortex (PCC) occurs before the onset of memory deficits in subjects at genetic risk for AD who are not yet cognitively impaired. There is a specific inhibition in cytochrome oxidase (C.O.) in the PCC, an area involved in spatial navigation. Creating an animal model that exhibits the early pathophysiology of AD is important for developing and testing drugs that could reverse memory problems associated with such deficits. Methylene blue (MB) is a compound that improves C.O. activity and memory retention in rats. This dissertation had three specific aims: 1) to examine if isolated PCC hypometabolism causes spatial memory deficits in rats; 2) to find a dose of MB that improves memory without nonspecific behavioral effects; and 3) to prevent memory deficits from PCC hypometabolism with low dose MB. PCC hypometabolism was produced by focal administration of sodium azide, an inhibitor of C.O. activity. PCC hypometabolism resulted in impaired spatial memory in a hole board food-search task, increased oxidative damage, and neurotoxicity in the PCC. In addition, PCC hypometabolism resulted in reduced inter-regional correlations in brain activity. Our second set of studies examined the dose-response effects of MB. Our findings demonstrated that a low dose of MB: 1) enhanced memory in open field habituation and object recognition tasks; 2) did not affect general locomotor activity, exploration, motivation, or anxiety; and 3) increased brain oxygen consumption 24 hr after in vivo administration. Finally, our last study found that low dose MB prevented the deficits caused by PCC hypometabolism. MB did not prevent PCC inhibition or cell loss caused by sodium azide. Inter-regional correlations of brain metabolic activity suggested that rats treated with MB were using a different, but equally efficient, strategy for memory retrieval. This animal model of C.O. hypometabolism in the PCC can provide information to understand the mechanisms that regulate early pathological degeneration and reveal new therapeutic strategies aimed at reducing or preventing cognitive decline. Studies of low dose MB in humans are needed to examine its effects in AD patients.
Books on the topic "Memory Disorders – metabolism"
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McCully, Kilmer Serjus. Pioneer of the Homocysteine Theory: Exploring Homocysteine and the Causes of Arteriosclerosis, Cancer and Aging -- a Memoir of Discovery, Exile and Redemption. Nova Science Publishers, Incorporated, 2016.
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Harney, Jacob P., Kathryn Gudsnuk, Ami Patel, Anantha R. Vellipuram, Sathyajit Bandaru, and David Butler. Endocrine and Reproductive Effects of Ketogenic Diets. Edited by Detlev Boison. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780190497996.003.0025.
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This chapter reviews endocrine, behavioral, and reproductive outcomes of the ketogenic diet (KD) in rodent mouse and rat models. KD treatment can result in conditions seen in metabolic syndrome, including dyslipidemia and inflammation. Females raised on low protein KDs will experience delayed puberty onset. Results presented suggest an increase in ketones and a decrease in spatial memory as percent protein drops. Postpubertal female pups fed KD experienced similar cognitive decline to KD-fed dams, despite consuming only normal rodent chow since weaning. This finding is consistent with the development of anatomical differences in the brains of pups from KD-fed versus rodent chow–fed controls. A thorough evaluation of the effects of different lipid and protein profiles (amount and type) will be necessary if KDs are going to be safe and effective long-term therapies for both sexes and in neurological disorders besides pediatric intractable epilepsy.
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(Editor), T. Kumazawa, L. Kruger (Editor), and K. Mizumura (Editor), eds. The Polymodal Receptor - A Gateway to Pathological Pain (Progress in Brain Research). Elsevier Science, 1996.
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Takao, Kumazawa, Kruger Lawrence, and Mizumura Kazue, eds. The polymodal receptor: A gateway to pathological pain. Amsterdam: Elsevier, 1996.
Find full textBook chapters on the topic "Memory Disorders – metabolism"
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Javitt, Daniel C. "Glutamate in the pathophysiology of schizophrenia." In Psychotic Disorders, edited by Michael A. P. Bloomfield and Oliver D. Howes, 287–96. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780190653279.003.0032.
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Glutamate theories of schizophrenia were first proposed over 30 years ago and since that time have become increasingly accepted. Theories are supported by the ability of N-methyl-D-aspartate receptor (NMDAR) antagonists such as phencyclidine (PCP) or ketamine to induce symptoms that closely resemble those of schizophrenia. Moreover, NMDAR antagonists uniquely reproduce the level of negative symptoms and cognitive deficits observed in schizophrenia, suggesting that such models may be particularly appropriate to poor outcome forms of the disorder. As opposed to dopamine, which is most prominent within frontostriatal brain regions, glutamate neurons are present throughout cortex and subcortical structures. Thus, NMDAR theories predict widespread disturbances across cortical and thalamic pathways, including sensory brain regions. In auditory cortex, NMDAR play a critical role in the generation of mismatch negativity (MMN), which may therefore serve as a translational marker of NMDAR dysfunction across species. In the visual system, NMDAR play a critical role in function of the magnocellular visual system. Deficits in both auditory and visual processing contribute to social and communication deficits, which, in turn, lead to poor functional outcome. By contrast, NMDAR dysfunction within the frontohippocampal system may contribute to well described deficits in working memory, executive processing and long-term memory formation. Deficits in NMDAR function may be driven by disturbances in presynaptic glutamate release, impaired metabolism of NMDAR modulators such as glycine or D-serine, or intrinsic abnormalities in NMDAR themselves.
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Kopelman, Michael D. "Amnesic syndromes." In New Oxford Textbook of Psychiatry, 403–11. Oxford University Press, 2012. http://dx.doi.org/10.1093/med/9780199696758.003.0052.
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Systematic clinical descriptions of amnesic disorders and their underlying pathology have become more detailed and rigorous over the years. In particular, recent advances in neuro-imaging (structural, metabolic, and activation) have provided the opportunity to relate particular cognitive abnormalities to specific changes in brain function. The use of pharmacological agents, in parallel with such imaging techniques, may promote the development of pharmacological agents more potent than the meagre array that we have at present for the treatment of severe memory disorder.
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Kapur, Narinder. "Infectious, metabolic and related diseases." In Memory Disorders in Clinical Practice, 143–57. Elsevier, 1988. http://dx.doi.org/10.1016/b978-0-407-00712-3.50013-1.
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Kapur, Narinder. "Infectious, metabolic and related diseases." In Memory Disorders in Clinical Practice, 143–57. Psychology Press, 2017. http://dx.doi.org/10.4324/9781315799162-7.
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"In Memory." In Metabolic Disorders and Shen in Integrative Cardiovascular Chinese Medicine, v. Elsevier, 2021. http://dx.doi.org/10.1016/b978-0-12-818922-1.03001-4.
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Scolding, Neil, and C. D. Marsden. "Acquired metabolic disorders and the nervous system." In Oxford Textbook of Medicine, 5150–57. Oxford University Press, 2010. http://dx.doi.org/10.1093/med/9780199204854.003.2419.
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Case History—A 65 yr old man presenting with poor memory a few months after a surgical admission. Case History—An 80 yr old man presenting with falls, reduced mobility, muscular weakness and peripheral neuropathy. Case History—A 34 yr old woman presenting with twitching of the face and jerking of the legs and arms...
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P. James, Steven, and Dena Bondugji. "Gamma-Aminobutyric Acid (GABA) and the Endocannabinoids: Understanding the Risks and Opportunities." In Gamma-Aminobutyric Acid - Neuropsychiatric and Therapeutic Implications [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.99242.
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The Gamma-aminobutyric acid (GABA) system is the main inhibitory neurotransmitter system in the central nervous system (CNS) of vertebrates and is involved in critical cellular communication and brain function. The endocannabioid system (ECS) was only recenty discovered and quickly recognized to be abundantly expressed in GABA-rich areas of the brain. The strong relationship between the GABA system and ECS is supported both by studies of the neuraoanatomy of mammalian nervous systems and the chemical messaging between neurons. The ECS is currently known to consist of two endocannabinoids, Anandamide (AEA) and 2-Arachidonyl Glycerol (2-AG), that function as chemical messengers between neurons, at least two cannabinoid receptors (CB1 and CB2), and complex synthetic and degradative metabolic systems. The ECS differs from the GABA system and other neurotransmitter systems in multiple ways including retrograde communication from the activated post-synaptic neuron to the presynaptic cell. Together, this molecular conversation between the ECS and GABA systems regulate the homeostasis and the chemical messaging essential for higher cortical functions such as learning and memory and may play a role in several human pathologies. Phytocannabinoids are synthesized in the plant Cannabis sativa (C. sativa). Within the family of phytocannabinoids at least 100 different cannabinoid molecules or derivatives have been identified and share the properties of binding to the endogenous cannabinoid receptors CB1 and CB2. The well-known psychoactive phytocannabinoid Δ9-tetrahydrocannabinol (THC) and the non-psychoactive cannabidiol (CBD) are just two of the many substances synthesized within C. sativa that act on the body. Although the phytocannabinoids THC and CBD bind to these endogenous receptors in the mammalian CNS, these plant derived molecules have little in common with the endocannabinoids in structure, distribution and metabolism. This overlap in receptor binding is likely coincidental since phytocannabinoids evolved within the plant kingdom and the ECS including the endocannabinoids developed within animals. The GABA and ECS networks communicate through carefully orchestrated activities at localized synaptic level. When phytocannabinoids become available, the receptor affinities for CB1 and CB2 may compete with the naturally occurring endocannabinoid ligands and influence the GABA-ECS communication. In some instances this addition of phytocannabinoids may provide some therapeutic benefit while in other circumstances the presence of these plant derived ligands for the CB1 and CB2 receptors binding site may lead to disruption of important functions within the CNS. The regulatory approval of several THC products for nausea and vomiting and anorexia and CBD for rare pediatric seizure disorders are examples of some of the benefits of phytocannabinoids. Concerns regarding cannabis exposure in utero and in the child and adolescence are shrill warnings of the hazards associated with disrupting the normal maturation of the developing CNS.
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Manzoor, Farkhanda, and Mahnoor Pervez. "Pesticide Impact on Honeybees Declines and Emerging Food Security Crisis." In Global Decline of Insects [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.98871.
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Bee crisis is threatening worldwide food security. Pesticides are extensively used in the agricultural zone. Unfortunately, these pesticides cause severe toxicity toward pollinators than the target pests such as honeybees. This review summarizes the different studies related to pesticide hazards of bees. This paper reported risks of pesticides neurological and physiological poisoning toward honeybees. Pesticides act as poison and ruin vital functions involved in leaning and cognition, behavior and, the body physiological mechanisms. Many laboratory and field research data evaluated the lethal and sub-lethal poisoning on bee foraging dance, learning, and memory abilities of honeybees. Insecticide residues are detected in bee bodies and LD50 and LC50 values evaluated. It is also studied that in honeybees systemic insecticide residues and, its metabolite adulterated in their body during foraging activities. Similarly, pesticide-contaminated food stored in a hive consumed continuously by honeybees may cause sub-lethal toxicity effects. Which causes anomalous bee social behavior and ultimately leads to colony collapse disorder. If population of pollinator decline it will disturb the food chain and leads to food crisis. This review emphasized causes of bee decline with the emergence of pesticides in agricultural domains.
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Poole-Di Salvo, Elizabeth. "Intrauterine and Postnatal Exposure to Tobacco and Secondhand Smoke and Child Cognitive and Behavioral Development." In Cognitive and Behavioral Abnormalities of Pediatric Diseases. Oxford University Press, 2010. http://dx.doi.org/10.1093/oso/9780195342680.003.0070.
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Children’s involuntary exposure to tobacco smoke is a common and substantial health problem that has been receiving increasing attention from the pediatric, public health and research communities. According to the 2006 Surgeon General’s Report, there is no safe level of tobacco smoke exposure, yet at least 30% of children in the United States live in households with at least one adult smoker, and nearly 60% have evidence of recent exposure (Machlin, Hill, and Liang 2006). Tobacco smoke exposure has been causally linked to numerous adverse health outcomes and is currently a leading preventable cause of both low birth weight and sudden infant death syndrome, and a major contributor to lower respiratory infections, otitis media, and increased asthma severity (American Academy of Pediatrics, Committee on Environmental Health 1997; Cook and Strachan 1999; DiFranza et al. 2004). Recently, associations between tobacco smoke exposure and other childhood health problems, such as increased rates of dental caries (Aligne et al. 2003; Iida et al. 2007), food insecurity (Cutler et al. in press), and the metabolic syndrome (Weitzman et al. 2005) have been identified. As discussed in this chapter, a growing human and animal literature, which expands upon a more than 25-year-old body of work, also indicates that involuntary exposure to tobacco smoke during the pre- and/or postnatal periods is associated with adverse cognitive and behavioral outcomes in children. Tobacco smoke exposure has been associated with decrements in IQ, problems with learning and memory, difficulty with auditory processing, neonatal hyperactivity, attention-deficit hyperactivity disorder (ADHD), internalizing and externalizing behavioral problems, and conduct disorder. Animal models have provided evidence that tobacco is toxic to the developing brain, and there are plausible biologic pathways that appear to mediate these effects. Exciting new studies have begun to identify specific genes that play a role in the relationship between tobacco smoke exposure and adverse cognitive and behavioral outcomes in children. The term “secondhand smoke” (SHS), also referred to as “environmental tobacco smoke” (ETS), refers to the smoke that is exhaled from a smoker’s lungs, as well as the smoke from the smoldering end of a cigarette.