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High-fat, high-sugar, and high-cholesterol consumption does not impact tau pathogenesis in a mouse model of Alzheimer's disease-like tau pathology.

Abstract：

:Aggregates of hyperphosphorylated tau protein are a pathological hallmark of Alzheimer's disease (AD). The origin of AD is multifactorial, and many metabolic disorders originating from overconsumption of fat, cholesterol, and sugar are associated with higher risk of AD later in life. However, the effects of fat, cholesterol, and sugar overconsumption on tau pathology in AD remain controversial. Using the hTau mice, a model of AD-like tau pathology, we assessed the effects of high-fat, high-cholesterol, and/or high-sugar diets on tau pathogenesis. Surprisingly, we found no effects of these compounds, even combined, on tau phosphorylation, O-GlcNAcylation, splicing, cleavage, and aggregation, suggesting that their overconsumption does not seem to worsen tau pathology in these mice.

journal_name

Neurobiol Aging

journal_title

Neurobiology of aging

authors

Gratuze M,Julien J,Morin F,Calon F,Hébert SS,Marette A,Planel E

doi

10.1016/j.neurobiolaging.2016.07.016

subject

Has Abstract

pub_date

2016-11-01 00:00:00

pages

71-73

eissn

0197-4580

issn

1558-1497

pii

S0197-4580(16)30153-1

journal_volume

47

pub_type

杂志文章

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