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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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Insulin Resistance as a Common Link Between Current Alzheimer's Disease Hypotheses

TL;DR: In this paper, the authors present the striking points of the long scientific path followed since the description of the first AD case and the main AD hypotheses discussed over the last decades and also propose insulin resistance as a common link between many other hypotheses.
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Are Tanycytes the Missing Link Between Type 2 Diabetes and Alzheimer's Disease?

TL;DR: A comprehensive understanding of the physiological mechanisms underlying tanycytes neuroplasticity, glucosensing, and cross talk with endothelial cells will enable us to achieve metabolic homeostasis in type 2 diabetes patients and possibly delay the progression of Alzheimer’s disease and hopefully improve cognitive function.
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Genome-wide profiling and predicted significance of post-mortem brain microRNA in Alzheimer’s disease

TL;DR: A dysregulation on a subset of these miRNAs appear to affect a range of genes (notably PTEN) and pathways so to provide grounds for neuronal death by apoptotic signaling, autophagy and/or oxidative damage.
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Sialic acid associated with oxidative stress and total antioxidant capacity (TAC) expression level as a predictive indicator in moderate to severe Alzheimer's disease.

TL;DR: During AD pathology, sialic acid, protein carbonyl, and lipid peroxidation were found as the more sensitive marker that may be used as a diagnostic and prognostic biomarker.
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Hypothesis and Theory: Circulating Alzheimer's-Related Biomarkers in Type 2 Diabetes. Insight From the Goto-Kakizaki Rat.

TL;DR: It is proposed that the spontaneous model of T2D in GK rat could be a suitable model to investigate molecular mechanisms linking T1D to AD, and the first evidence that certain circulating AD biomarkers are found in diabetic GK rats is provided.
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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