Relevant bibliographies by topics / Atrophy signaling pathways

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  2. Dissertations / Theses
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  4. Conference papers

Academic literature on the topic 'Atrophy signaling pathways'

Author: Grafiati
Published: 18 April 2022
Last updated: 30 July 2025

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Journal articles on the topic "Atrophy signaling pathways"

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Hulmi, Juha J., Mika Silvennoinen, Maarit Lehti, Riikka Kivelä, and Heikki Kainulainen. "Altered REDD1, myostatin, and Akt/mTOR/FoxO/MAPK signaling in streptozotocin-induced diabetic muscle atrophy." American Journal of Physiology-Endocrinology and Metabolism 302, no. 3 (2012): E307—E315. http://dx.doi.org/10.1152/ajpendo.00398.2011.

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Type 1 diabetes, if poorly controlled, leads to skeletal muscle atrophy, decreasing the quality of life. We aimed to search highly responsive genes in diabetic muscle atrophy in a common diabetes model and to further characterize associated signaling pathways. Mice were killed 1, 3, or 5 wk after streptozotocin or control. Gene expression of calf muscles was analyzed using microarray and protein signaling with Western blotting. We identified translational repressor protein REDD1 (regulated in development and DNA damage responses) that increased seven- to eightfold and was associated with muscl
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Powers, Scott K., Andreas N. Kavazis, and Joseph M. McClung. "Oxidative stress and disuse muscle atrophy." Journal of Applied Physiology 102, no. 6 (2007): 2389–97. http://dx.doi.org/10.1152/japplphysiol.01202.2006.

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Skeletal muscle inactivity is associated with a loss of muscle protein and reduced force-generating capacity. This disuse-induced muscle atrophy results from both increased proteolysis and decreased protein synthesis. Investigations of the cell signaling pathways that regulate disuse muscle atrophy have increased our understanding of this complex process. Emerging evidence implicates oxidative stress as a key regulator of cell signaling pathways, leading to increased proteolysis and muscle atrophy during periods of prolonged disuse. This review will discuss the role of reactive oxygen species
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Clavel, Stephan, Sandrine Siffroi-Fernandez, Anne Sophie Coldefy, Kim Boulukos, Didier F. Pisani, and Benoît Dérijard. "Regulation of the Intracellular Localization of Foxo3a by Stress-Activated Protein Kinase Signaling Pathways in Skeletal Muscle Cells." Molecular and Cellular Biology 30, no. 2 (2009): 470–80. http://dx.doi.org/10.1128/mcb.00666-09.

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ABSTRACT Muscle atrophy is a debilitating process associated with many chronic wasting diseases, like cancer, diabetes, sepsis, and renal failure. Rapid loss of muscle mass occurs mainly through the activation of protein breakdown by the ubiquitin proteasome pathway. Foxo3a transcription factor is critical for muscle atrophy, since it activates the expression of ubiquitin ligase Atrogin-1. In several models of atrophy, inhibition of the phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathway induces nuclear import of Foxo3a through an Akt-dependent process. This study aimed to identify sign
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Glass, David J. "Skeletal muscle hypertrophy and atrophy signaling pathways." International Journal of Biochemistry & Cell Biology 37, no. 10 (2005): 1974–84. http://dx.doi.org/10.1016/j.biocel.2005.04.018.

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Bodine, Sue C. "Edward F. Adolph Distinguished Lecture. Skeletal muscle atrophy: Multiple pathways leading to a common outcome." Journal of Applied Physiology 129, no. 2 (2020): 272–82. http://dx.doi.org/10.1152/japplphysiol.00381.2020.

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Skeletal muscle atrophy continues to be a serious consequence of many diseases and conditions for which there is no treatment. Our understanding of the mechanisms regulating skeletal muscle mass has improved considerably over the past two decades. For many years it was known that skeletal muscle atrophy resulted from an imbalance between protein synthesis and protein breakdown, with the net balance shifting toward protein breakdown. However, the molecular and cellular mechanisms underlying the increased breakdown of myofibrils was unknown. Over the past two decades, numerous reports have ident
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Mañas-García, Laura, Charlotte Denhard, Javier Mateu, Xavier Duran, Joaquim Gea, and Esther Barreiro. "Beneficial Effects of Resveratrol in Mouse Gastrocnemius: A Hint to Muscle Phenotype and Proteolysis." Cells 10, no. 9 (2021): 2436. http://dx.doi.org/10.3390/cells10092436.

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We hypothesized that the phenolic compound resveratrol mitigates muscle protein degradation and loss and improves muscle fiber cross-sectional area (CSA) in gastrocnemius of mice exposed to unloading (7dI). In gastrocnemius of mice (female C57BL/6J, 10 weeks) exposed to a seven-day period of hindlimb immobilization with/without resveratrol treatment, markers of muscle proteolysis (tyrosine release, systemic troponin-I), atrophy signaling pathways, and muscle phenotypic features and function were analyzed. In gastrocnemius of unloaded mice treated with resveratrol, body and muscle weight and fu
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Franch, Harold A., and S. Russ Price. "Molecular signaling pathways regulating muscle proteolysis during atrophy." Current Opinion in Clinical Nutrition and Metabolic Care 8, no. 3 (2005): 271–75. http://dx.doi.org/10.1097/01.mco.0000165005.01331.45.

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Yoshida, Tadashi, and Patrice Delafontaine. "Mechanisms of IGF-1-Mediated Regulation of Skeletal Muscle Hypertrophy and Atrophy." Cells 9, no. 9 (2020): 1970. http://dx.doi.org/10.3390/cells9091970.

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Insulin-like growth factor-1 (IGF-1) is a key growth factor that regulates both anabolic and catabolic pathways in skeletal muscle. IGF-1 increases skeletal muscle protein synthesis via PI3K/Akt/mTOR and PI3K/Akt/GSK3β pathways. PI3K/Akt can also inhibit FoxOs and suppress transcription of E3 ubiquitin ligases that regulate ubiquitin proteasome system (UPS)-mediated protein degradation. Autophagy is likely inhibited by IGF-1 via mTOR and FoxO signaling, although the contribution of autophagy regulation in IGF-1-mediated inhibition of skeletal muscle atrophy remains to be determined. Evidence h
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Cussonneau, Laura, Christian Boyer, Charlotte Brun та ін. "Concurrent BMP Signaling Maintenance and TGF-β Signaling Inhibition Is a Hallmark of Natural Resistance to Muscle Atrophy in the Hibernating Bear". Cells 10, № 8 (2021): 1873. http://dx.doi.org/10.3390/cells10081873.

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Muscle atrophy arises from a multiplicity of physio-pathological situations and has very detrimental consequences for the whole body. Although knowledge of muscle atrophy mechanisms keeps growing, there is still no proven treatment to date. This study aimed at identifying new drivers for muscle atrophy resistance. We selected an innovative approach that compares muscle transcriptome between an original model of natural resistance to muscle atrophy, the hibernating brown bear, and a classical model of induced atrophy, the unloaded mouse. Using RNA sequencing, we identified 4415 differentially e
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Sandri, Marco. "Signaling in Muscle Atrophy and Hypertrophy." Physiology 23, no. 3 (2008): 160–70. http://dx.doi.org/10.1152/physiol.00041.2007.

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Muscle performance is influenced by turnover of contractile proteins. Production of new myofibrils and degradation of existing proteins is a delicate balance, which, depending on the condition, can promote muscle growth or loss. Protein synthesis and protein degradation are coordinately regulated by pathways that are influenced by mechanical stress, physical activity, availability of nutrients, and growth factors. Understanding the signaling that regulates muscle mass may provide potential therapeutic targets for the prevention and treatment of muscle wasting in metabolic and neuromuscular dis
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Dissertations / Theses on the topic "Atrophy signaling pathways"

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Surrey, Verena [Verfasser], and Sibylle [Gutachter] Jablonka. "Identification of affected cellular targets, mechanisms and signaling pathways in a mouse model for spinal muscular atrophy with respiratory distress type 1 (SMARD1) / Verena Surrey ; Gutachter: Sibylle Jablonka." Würzburg : Universität Würzburg, 2020. http://d-nb.info/1203545371/34.

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Penedo, Vázquez Antonio 1994. "Estrategias terapéuticas en un modelo experimental de caquexia cancerosa : efectos de los polifenoles curcumina y resveratol." Doctoral thesis, TDX (Tesis Doctorals en Xarxa), 2021. http://hdl.handle.net/10803/672881.

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La caquexia es un síndrome metabólico complejo asociado con enfermedades crónicas como el cáncer, se caracteriza por una atrofia progresiva del músculo esquelético que conduce a una disminución del peso corporal, inicia procesos metabólicos de deterioro y aumenta en gran medida la mortalidad. La curcumina y el resveratrol, dos compuestos naturales, han mostrado efectos favorables contra la disfunción muscular y el desgaste. Se empleó un modelo de ratones con caquexia cancerosa que fueron tratados con curcumina y resveratrol respectivamente. Ambos tratamientos indujeron efectos beneficiosos (p
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Wyke, Stacey M. "Cellular signalling pathways involved in muscle atrophy in cancer cachexia." Thesis, Aston University, 2004. http://publications.aston.ac.uk/11059/.

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Skeletal muscle proteolysis in cancer cachexia is mediated by a sulphated glycoprotein with a relative molecular mass of 24kDa, termed Proteolysis-Inducing Factor (PIF). PIF induced a significant increase in protein degradation, peaking at 4.2nM PIF (p<0.001), 'chymotrypsin-like' activity of the proteasome (p<0.001) and increased expression of components of the ATP-ubiquitin dependent proteolytic pathway. This was attenuated in vitro by pre-incubation with the PKC inhibitor calphostin C (100μM) and NF-κB the inhibitors SN50 (18μM), curcumin (50μM) and resveratrol (30μM), 2 hours prior to the a
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Cunha, Telma Fátima da. "Contribuição do estresse oxidativo para a ativação das vias NF-kB, FOXO e MAPK para atrofia muscular associada à insuficiência cardíaca: efeito do treinamento físico aeróbico." Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/39/39132/tde-08042015-080511/.

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A musculatura esquelética tem um papel fundamental para a manutenção da homeostase do organismo. A perda de massa muscular está relacionada a prejuízos na qualidade de vida de indivíduos saudáveis, além de piorar o prognóstico de pacientes com doenças sistêmicas, como o câncer, o diabetes e a insuficiência cardíaca. Em quadros mais graves de insuficiência cardíaca, a perda excessiva de massa muscular associada a um reduzido consumo de oxigênio de pico, são considerados como preditores independentes de mortalidade. O aumento do estresse oxidativo tem sido apontado como um dos principais desenca
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Bassil, Fares. "Multiple system atrophy : a translational approach Characterization of the insulin/IGF-1 signaling pathway." Thesis, Bordeaux, 2015. http://www.theses.fr/2015BORD0131/document.

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Ce travail porte sur des approches translationnelles dans les synucléinopathies notamment l’atrophie multisystématisée (AMS). Au-delà de leur rôle dans la régulation du glucose, l’insulin et l’insulin like growth factor-1 (IGF-1) ont des propriétés neurotrophiques. Des études ont montrées que la signalisation de l’insuline/IGF-1 est altérée dans la maladie d'Alzheimer et des données suggèrent l’altération de l’insuline/IGF-1 dans la maladie de Parkinson (MP) et l’AMS. Nous avons mis en évidence une résistance à l’insuline dans les neurones des patients MP et AMS ainsi que dans les oligodendroc
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Sishi, Balindiwe J. N. "An investigation into the P13-K/AKT signalling pathway in TNF-a-induced muscle proeolysis in L6 myotubes." Thesis, Stellenbosch : Stellenbosch University, 2008. http://hdl.handle.net/10019.1/3039.

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Thesis (MSc (Physiological Sciences))--Stellenbosch University, 2008.<br>Introduction: Skeletal muscle atrophy is a mitigating complication that is characterized by a reduction in muscle fibre cross-sectional area as well as protein content, reduced force, elevated fatigability and insulin resistance. It seems to be a highly ordered and regulated process and signs of this condition are often seen in inflammatory conditions such as cancer, AIDS, diabetes and chronic heart failure (CHF). It has long been understood that an imbalance between protein degradation (increase) and protein synthes
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Lejmi, Mrad Rim. "Genetic and Pharmacologic Inhibition of Cellular Inhibitor of Apoptosis 1 (cIAP1) Protein Expression Protects Against Denervation-Induced Skeletal Muscle Atrophy In Vivo." Thesis, Université d'Ottawa / University of Ottawa, 2016. http://hdl.handle.net/10393/34260.

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Skeletal muscle atrophy is a debilitating condition caused by pathological conditions including cancer cachexia, disuse and denervation. Disuse atrophy is characterized by reduction in fiber size, fiber-type change and induction of markers of atrophy such as MuRF1 and Fn14. Recent studies have focused on understanding the fundamental role of signalling pathways and the proteolytic system in response to muscle atrophy. Unfortunately the exact mechanisms behind atrophy remain poorly understood. I recently demonstrated that cIAP1 and/or cIAP2 proteins are critical regulators of NF-kB activation,
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Arumugam, Saravanan. "A Study on the Role of NF-kB Signaling Pathway Members in Regulating Survival Motor Neuron Protein level and in the Pathogenesis of Spinal Muscular Atrophy." Doctoral thesis, Universitat de Lleida, 2017. http://hdl.handle.net/10803/400607.

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L’atròfia muscular espinal (AME) és una malaltia neuromuscular causada per mutació o deleció en el gen SMN1, que codifica per la proteïna ubiqua SMN (de l’anglès survival motor neuron). L’AME es caracteritza per atròfia muscular i degeneració de les motoneurones (MN) de la medul·la espinal. Els esdeveniments moleculars que causen la vulnerabilitat específica de les MN amb nivells baixos de proteïna SMN encara no es coneixen. La via de l’NF-κB (nuclear factor-κB) ha destacat recentment ja que sembla jugar un paper cabdal en la supervivència de les MN i en les malalties neurodegeneratives. Els f
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Wang, Guo-Chang, and 王國昌. "The Signaling Pathways of Skeletal Myoblast C2C12 Cell Atrophy Induced by In Vitro Inflammatory Model." Thesis, 2015. http://ndltd.ncl.edu.tw/handle/34783388117325099147.

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碩士<br>輔仁大學<br>基礎醫學研究所碩士班<br>103<br>In human body, skeletal muscle accounts for 40% to 50% of the total body mass and is the major structure to responsible for movement and physiological homeostasis. Unfortunately, it is also the main target to be attacked from cachexia. Cachexia usually occurs with chronic diseases, such as CKD, CHF, COPD, aging, AIDS and diabetes mellitus, which causes the loss of skeletal muscle mass and muscle atrophy. Chronic diseases-induced muscle atrophy involves skeletal muscle weakness, inflammation, wasting, and leads to an estimated of 20% to 30% deaths of cancer pa
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Csukly, Kristina. "Skeletal muscle disuse atrophy : implications on intracellular signaling pathways and mitochondrial permeability transition pore function." Thèse, 2006. http://hdl.handle.net/1866/15465.

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Book chapters on the topic "Atrophy signaling pathways"

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Hoogaars, Willem M. H., and Richard T. Jaspers. "Past, Present, and Future Perspective of Targeting Myostatin and Related Signaling Pathways to Counteract Muscle Atrophy." In Advances in Experimental Medicine and Biology. Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-13-1435-3_8.

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Chen, Linlin, Hong Zhang, Mengyi Chi, Quanjun Yang, and Cheng Guo. "Drugs for the Treatment of Muscle Atrophy." In Background and Management of Muscular Atrophy. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.93503.

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Muscle mass is maintained through an interplay between anabolic and catabolic pathways. The ubiquitin-proteasome system plays an important role in the proteolysis progress during skeletal muscle atrophy which can be blocked by some proteasome inhibitors. But few studies have demonstrated the ability of these inhibitors to preserve muscle mass and architecture under catabolic condition in vivo. The insulin-like growth factor-1/phosphatidylinositide 3-kinases/protein kinase B/mammalian target of rapamycin (IGF-1/PI3K/Akt/mTOR) pathway was associated with anabolic pathways. The activation of IGF-
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Kwatra, Mohit, Sahabuddin Ahmed, Samir Ranjan Panda, Vegi Ganga Modi Naidu, and Nitika Gupta. "Molecular Mechanisms, Therapeutic Targets and Pharmacological Interventions: An Update." In Background and Management of Muscular Atrophy. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.95996.

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Muscles are the enriched reservoir of proteins in the body. During any workout or exercise, the demand in the form of energy is essentially required by the muscle. Energy expenditure of skeletal muscle is more dependent on the type of demand. There is particular homeostasis within the body that avoid surplus energy expenditure and this prevents any muscle loss. Muscle atrophy is termed as the loss of skeletal muscle mass due to immobility, malnutrition, medications, aging, cancer cachexia, variety of injuries or diseases that impact the musculoskeletal or nervous system. Hence, atrophy within
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Shen, Zhen, Sunfeng Pan, Fengjie Wu, Kaitao Luo, and Yanbo Shi. "Revisiting Skeletal Muscle Atrophy: Links between Copper Overload, Cuproptosis, and Muscle Atropy." In Cell Death Regulation in Pathology [Working Title]. IntechOpen, 2025. https://doi.org/10.5772/intechopen.1009603.

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Skeletal muscle senescence is a significant biological process in the aging of the body, marked by a reduction in muscle mass and function. In recent years, there has been growing interest in understanding the role of copper in skeletal muscle aging. During aging and various pathological conditions, skeletal muscle often exhibits an accumulation of excess copper. This abnormal buildup can trigger specific molecular mechanisms that lead to programmed cell death pathways such as apoptosis, pyroptosis, ferroptosis, and cuproptosis, as well as promote the aggregation of α-synuclein. These effects
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Sun, Miao-Kun, and Daniel L. Alkon. "Treating Alzheimer’s Disease: Focusing on Neurodegenerative Consequences." In Advances in Alzheimer’s Disease. IOS Press, 2024. https://doi.org/10.3233/aiad240020.

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Neurodegenerative disorders involve progressive dysfunction and loss of synapses and neurons and brain atrophy, slowly declining memories and cognitive skills, throughout a long process. Alzheimer’s disease (AD), the leading neurodegenerative disorder, suffers from a lack of effective therapeutic drugs. Decades of efforts targeting its pathologic hallmarks, amyloid plaques and neurofibrillary tangles, in clinical trials have produced therapeutics with marginal benefits that lack meaningful clinical improvements in cognition. Delivering meaningful clinical therapeutics to treat or prevent neuro
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Jeyaram Bharathi, J., and Justin Antony. "TrkA Signalling and Parkinson’s Dementia." In Dementia in Parkinson's Disease [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.99106.

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Cognitive impairment and dementia are the most frequently occurring nonmotor symptoms in Parkinson’s disease (PD), yet these symptoms are mostly overlooked and are not diagnosed and treated exceptionally like the cardinal motor symptoms in clinical practice. It is only in the late twentieth century that dementia has been recognized as a major clinical manifestation in PD. The possible mechanisms that cause dementia are complex with different patterns of cognitive behavior that disrupt the patient’s quality of life. It is preeminently considered that the cholinergic denervation in the basal for
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de la Monte, Suzanne M. "Conquering Insulin Network Dysfunctions in Alzheimer’s Disease: Where Are We Today?" In Advances in Alzheimer’s Disease. IOS Press, 2024. https://doi.org/10.3233/aiad240025.

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Functional impairments in the brain’s insulin and insulin-like growth factor (IGF) signal transduction networks are recognized mediators of dysregulated energy metabolism, a major driver of the Alzheimer’s disease (AD) neurodegeneration cascade. AD-associated insulin-deficient and insulin-resistant states mimic those of diabetes mellitus and affect all cell types in the brain. Besides accounting for abundant amyloid-β and hyperphosphorylated tau lesions in AD, insulin/IGF pathway dysfunctions cause cortical atrophy, loss of synaptic plasticity, white matter myelin/oligodendrocyte degeneration,
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Conference papers on the topic "Atrophy signaling pathways"

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Lopez, Diana M., Roberto Carrio-Jardines, Marta Torroella-Kouri, and Vijaya Iragavarapu-Charyulu. "Abstract 792: Tumor-induced thymic atrophy: Alteration in interferons and Jak/Stats signaling pathways." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-792.

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