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Open AccessJournal ArticleDOI

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.

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Citations
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Oxidative Stress, Synaptic Dysfunction, and Alzheimer’s Disease

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.

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

Preclinical evidence of Alzheimer's disease in persons homozygous for the epsilon 4 allele for apolipoprotein E.

TL;DR: In late middle age, cognitively normal subjects who are homozygous for the epsilon 4 allele for apolipoprotein E have reduced glucose metabolism in the same regions of the brain as in patients with probable Alzheimer's disease.

Impaired insulin and insulin-like growth factor expression and signaling mechanisms in Alzheimer disease-is this type 3 diabetes?

E Steen
TL;DR: In this article, the authors demonstrate extensive abnormalities in insulin and insulin-like growth factor type I and II (IGF-I and IGF-II) signaling mechanisms in brains with sporadic Alzheimer's disease and show that while each of the corresponding growth factors is normally made in central nervous system (CNS) neurons, the expression levels are markedly reduced in AD.
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Transcription-dependent and -independent control of neuronal survival by the PI3K-Akt signaling pathway

TL;DR: The PI3K-Akt signaling pathway plays a critical role in mediating survival signals in a wide range of neuronal cell types and may also use metabolic pathways to regulate cell survival.
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Alzheimer's disease-affected brain: Presence of oligomeric Aβ ligands (ADDLs) suggests a molecular basis for reversible memory loss

TL;DR: This article verifies the predicted accumulation of soluble oligomers in AD frontal cortex and confirms the prediction that soluble oligomeric Aβ ligands are intrinsic to AD pathology, and validate their use in new approaches to therapeutic AD drugs and vaccines.
Journal ArticleDOI

Protein kinase B/Akt-mediated phosphorylation promotes nuclear exclusion of the winged helix transcription factor FKHR1.

TL;DR: It is shown that the activation of phosphatidylinositol 3 (PI3) kinase by extracellular growth factors induces phosphorylation, nuclear export, and transcriptional inactivation of FKHR1, a member of the FK HR subclass of the forkhead family of transcription factors.
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