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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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Deep phenotyping of Alzheimer’s disease leveraging electronic medical records identifies sex-specific clinical associations

TL;DR: In this paper , the authors utilize two independent electronic medical record (EMR) systems across 44,288 patients to perform deep clinical phenotyping and network analysis to gain insight into clinical characteristics and sex-specific clinical associations in Alzheimer's disease.
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The impact of comorbid depression-diabetes on proteomic outcomes among community-dwelling Mexican Americans with mild cognitive impairment

TL;DR: In Mexican Americans, medical comorbidities may impact the proteomics of MCI and AD, which lend support for a precision medicine approach to treating this disease.
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Amyloid-beta (Aβ1-42)-induced paralysis in Caenorhabditis elegans is reduced through NHR-49/PPARalpha.

TL;DR: Activation of NHR-49/PPARalpha inhibits the steroidal-signaling pathway which increases the nuclear translocation of DAF-16 and inhibits the Aβ-induced phenotype in an Alzheimer model of C. elegans.
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Human serum albumin in neurodegeneration

TL;DR: Serum albumin has been shown to be structurally modified in neurological conditions such as Alzheimer’s disease and is able to bind to the precursor agent of the AD, amyloid-beta, preventing its toxic effects in the periphery, and is being tested for treating this disease.
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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