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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.
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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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Receptor-mediated toxicity of human amylin fragment aggregated by short- and long-term incubations with copper ions.

TL;DR: Results indicate that copper(II) influences the aggregation process and hA17–29 toxicities are especially attributable to oligomeric aggregates.
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Brain Under Stress and Alzheimer's Disease.

TL;DR: Interventions that reduce stress-induced detrimental effects as etiological factors of AD are attractive because they can be reduced by several approaches including behavioral and pharmacological interventions.
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Streptozotocin-induced hippocampal astrogliosis and insulin signaling malfunction as experimental scales for subclinical sporadic Alzheimer model.

TL;DR: STZ1 and 0.5mg/kg-treated animals are suggested as a suitable experimental model of MCI, and sub-clinical stage, in order to mimic the characteristic feature of sAD in rats.
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The Action of Polyphenols in Diabetes Mellitus and Alzheimer's Disease: A Common Agent for Overlapping Pathologies.

TL;DR: The aim of this review is to understand the extent to which DM and AD are related pathologies, the degree of similarity and the relationship between them, to detail the molecular mechanisms by which polyphenols may exert a protective effect, such as antioxidant and anti-inflammatory effects, and highlight possible advantages of their use as common preventive and therapeutic alternatives.
References
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Journal ArticleDOI

Akt Promotes Cell Survival by Phosphorylating and Inhibiting a Forkhead Transcription Factor

TL;DR: It is demonstrated that Akt also regulates the activity of FKHRL1, a member of the Forkhead family of transcription factors, which triggers apoptosis most likely by inducing the expression of genes that are critical for cell death, such as the Fas ligand gene.
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Akt Phosphorylation of BAD Couples Survival Signals to the Cell-Intrinsic Death Machinery

TL;DR: It is shown that growth factor activation of the PI3'K/Akt signaling pathway culminates in the phosphorylation of the BCL-2 family member BAD, thereby suppressing apoptosis and promoting cell survival.
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Diffusible, nonfibrillar ligands derived from Aβ1–42 are potent central nervous system neurotoxins

TL;DR: It is hypothesized that impaired synaptic plasticity and associated memory dysfunction during early stage Alzheimer's disease and severe cellular degeneration and dementia during end stage could be caused by the biphasic impact of Abeta-derived diffusible ligands acting upon particular neural signal transduction pathways.
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Interleukin-3-Induced Phosphorylation of BAD Through the Protein Kinase Akt

TL;DR: The proapoptotic function of BAD is regulated by the PI 3-kinase-Akt pathway, and active, but not inactive, forms of Akt were found to phosphorylate BAD in vivo and in vitro at the same residues that are phosphorylated in response to IL-3.
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Synthesis and Function of 3-Phosphorylated Inositol Lipids

TL;DR: This review is focused on the 3-phosphoinositide lipids, the synthesis of which is acutely triggered by extracellular stimuli, the enzymes responsible for their synthesis and metabolism, and their cell biological roles.
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