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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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Journal ArticleDOI

Association between Parkinson’s Disease and Diabetes Mellitus: From Epidemiology, Pathophysiology and Prevention to Treatment

TL;DR: In this article , the epidemiological and pathophysiological association between DM and PD and summarize the antidiabetic drugs used in animal models and clinical trials of PD, which may provide reference for the clinical translation of antidisabetic drugs in PD treatment.
Book ChapterDOI

Bioactive Metabolites Isolated from Microorganisms for Healthcare: Types and Delivery Routes

TL;DR: There are reports suggesting that microbial metabolites are more reliable in terms of efficacy and potential when compared to its chemical counterparts for curing human diseases.
Journal ArticleDOI

Evaluation of Cognitive Impairment in Type 2 Diabetic Patients with Chronic Periodontitis: A Cross-sectional Study.

TL;DR: Cognitive impairment was found to coexist with HbA1c levels ≥7% and moderate-to-severe periodontitis in the elderly diabetics and adds opportunities to form disease modifiable areas in the Elderly diabetic population at a risk for the development of dementia.
Journal ArticleDOI

Disruption of Glucose Metabolism in Aged Octodon degus: A Sporadic Model of Alzheimer's Disease.

TL;DR: In this paper, the authors measured several markers of glucose metabolism, namely, glucose uptake, ATP production, and glycolysis and pentose phosphate pathway (PPP) flux, in hippocampal slices from degus of different ages.
Journal ArticleDOI

Advances in PPARs Molecular Dynamics and Glitazones as a Repurposing Therapeutic Strategy through Mitochondrial Redox Dynamics against Neurodegeneration

TL;DR: In this article , a review of the role of peroxisome proliferator-activated receptors (PPARs) and their receptor isoforms in neural systems, and neurodegeneration in human beings is presented.
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.
Journal ArticleDOI

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.
Journal ArticleDOI

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.
Journal ArticleDOI

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.
Journal ArticleDOI

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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