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.
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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.
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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.
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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.
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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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Journal ArticleDOI
Evaluating the Association between Diabetes, Cognitive Decline and Dementia.
Omorogieva Ojo,Joanne Brooke +1 more
TL;DR: There is evidence of the association between diabetes, cognitive decline and dementia including the shared pathogenesis between diabetes and Alzheimer’s disease, and the self management of diabetes is affected by dementia and cognitive decline.
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Abnormal interaction of oligomeric amyloid-β with phosphorylated tau: implications to synaptic dysfunction and neuronal damage.
TL;DR: It is concluded that Aβ interacts with phosphorylated tau and may damage neuronal structure and function, particularly synapses, leading to cognitive decline in AD patients, and suggest that binding sites between Aβ and phosphorylation tau need to be identified and molecules developed to inhibit this interaction.
Journal ArticleDOI
High carbohydrate diets and Alzheimer's disease.
TL;DR: In this article, the epsilon-4 variant (E4) of the apolipoprotein E gene was found to be a risk factor for late onset Alzheimer's disease.
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Neuronal stress signaling and eIF2α phosphorylation as molecular links between Alzheimer's disease and diabetes.
TL;DR: The concept that targeting defective brain insulin signaling and neuronal stress mechanisms with anti-diabetes agents may be an attractive approach to fight memory decline in AD is discussed.
Journal ArticleDOI
Advanced glycation endproduct precursor alters intracellular amyloid- β/AβPP carboxy-terminal fragment aggregation and cytotoxicity
TL;DR: It is shown that A beta/CTF aggregation and cytotoxicity may be profoundly altered by aldehydes associated with diabetes and that in the case of MG, this process is suppressed by alpha-tocopherol.
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