Is Alzheimer's disease a Type 3 Diabetes? A critical appraisal.
TLDR
Significant shared mechanisms between AD and diabetes are discussed and therapeutic avenues for diabetes and AD are provided and the effects of insulin in the pathology of AD through cellular and molecular mechanisms are provided.About:
This article is published in Biochimica et Biophysica Acta.The article was published on 2017-05-01 and is currently open access. It has received 376 citations till now. The article focuses on the topics: Insulin resistance & Insulin.read more
Citations
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Oxidative Stress, Synaptic Dysfunction, and Alzheimer’s Disease
Eric Tönnies,Eugenia Trushina +1 more
TL;DR: The role of oxidative stress in synaptic dysfunction in AD, innovative therapeutic strategies evolved based on a better understanding of the complexity of molecular mechanisms of AD, and the dual role ROS play in health and disease are discussed.
Journal ArticleDOI
Melatonin and inflammation—Story of a double‐edged blade
TL;DR: A particular role in melatonin's actions seems to be associated with the upregulation of sirtuin‐1 (SIRT1), which shares various effects known from melatonin and additionally interferes with the signaling by the mechanistic target of rapamycin and Notch, and reduces the expression of the proinflammatory lncRNA‐CCL2.
Journal ArticleDOI
Obesity pandemic: causes, consequences, and solutions—but do we have the will?
TL;DR: The many causes of obesity are described, including key roles that a dysbiotic intestinal microbiome plays in metabolic derangements accompanying obesity, increased calorie absorption, and increased appetite and fat storage.
Journal ArticleDOI
Nutrient regulation of signaling and transcription.
TL;DR: This review will present an overview of the current understanding of O-GlcNAc's regulation, functions, and roles in chronic diseases of aging.
Journal ArticleDOI
Comprehensive review of mechanisms of pathogenesis involved in Alzheimer's disease and potential therapeutic strategies.
Piyoosh Sharma,Pavan Srivastava,Ankit Seth,Prabhash Nath Tripathi,Anupam G. Banerjee,Sushant K. Shrivastava +5 more
TL;DR: The present review provides an insight to the different molecular mechanisms involved in the development and progression of the AD and potential therapeutic strategies, enlightening perceptions into structural information of conventional and novel targets along with the successful applications of computational approaches for the design of target-specific inhibitors.
References
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Paths of Convergence: Sirtuins in Aging and Neurodegeneration
Li Gan,Lennart Mucke +1 more
TL;DR: How progress in understanding the neurobiology of sirtuins is shedding light on the pathogenesis of aging-related neurodegenerative diseases is discussed and the potential and challenges of targeting sirtuin pathways therapeutically are examined.
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Insulin regulates soluble amyloid precursor protein release via phosphatidyl inositol 3 kinase-dependent pathway
Daniela C. Solano,Marita Sironi,Claudia Bonfini,S. Bruno Solerte,Stefano Govoni,Marco Racchi +5 more
TL;DR: A novel intracellular pathway that increases the rate of secretion of soluble APP through the activity of phosphati‐dyl‐inositol 3 kinase (PI3‐K) is demonstrated, which is speculated to act at the level of vesicular trafficking.
Book ChapterDOI
Causes and Consequences of Disturbances of Cerebral Glucose Metabolism in Sporadic Alzheimer Disease: Therapeutic Implications
TL;DR: Findings from both basic and clinical studies showed that Ginkgo biloba extract (EGb 761) may be appropiate to approach the improvement of the neuronal energy state in SAD.
Journal ArticleDOI
Specificity in ligand binding and intracellular signalling by insulin and insulin-like growth factor receptors.
K. Siddle,Birgitte Ursø,C. A. Niesler,Diane L. Cope,L. Molina,Kathy H. Surinya,Maria A. Soos +6 more
TL;DR: To compare signalling capacities, chimaeras containing intracellular domains of insulin or IGF receptors fused to the extracellular portion of TrkC were constructed and revealed subtle differences in signalling and end-point responses, which may depend on cell background.
Journal ArticleDOI
Insulin and insulin-like growth factor II permit nerve growth factor binding and the neurite formation response in cultured human neuroblastoma cells.
TL;DR: In serum-free medium, SH-SY5Y human neuroblastoma cells specifically and reversibly lost the capacity to bind 125I-labeled nerve growth factor to the high-affinity sites (slow sites) and to respond by neurite outgrowth, unless physiological concentrations of insulin or insulin-like growth factor II were present.
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