Aging, Alzheimer's Disease and Dysfunctional Glycolysis; Similar Effects of Too Much and Too Little

被引：35

作者：

Hipkiss, Alan R. ^{[1
]}

机构：

[1] Aston Univ, ARCHA, Sch Life & Hlth Sci, Birmingham B4 7ET, W Midlands, England

来源：

AGING AND DISEASE | 2019年 / 10卷 / 06期

关键词：

glycolysis; triosephosphate isomerase; methylglyoxal; glycation; erythrocytes; alpha-synuclein; TRIOSEPHOSPHATE ISOMERASE; DEAMIDATION; DEATH;

D O I：

10.14336/AD.2019.0611

中图分类号：

R592 [老年病学]; C [社会科学总论];

学科分类号：

03 ; 0303 ; 100203 ;

摘要：

Aging and much related dysfunction can be delayed by decreased glycolysis, however dysfunctional glycolysis appears to play a causative role in Alzheimer's disease (AD). It is proposed here that this apparent contradiction can be reconciled by suggesting that both over-use and inhibition of the glycolytic enzyme triosephosphate isomerase can limit NADH generation and increase protein glycation. It is also suggested that excessive glycolysis in erythrocytes may provide a source of systemic methylglyoxal and glycated alpha-synuclein, both of which accelerate aging onset and neurodegeneration.

引用

页码：1328 / 1331

页数：4

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