Open AccessAging, Alzheimer’s Disease and Dysfunctional Glycolysis; Similar Effects of Too Much and Too Little
Author(s) -
Alan R. Hipkiss
Publication year - 2019
Publication title -
aging and disease
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.808
H-Index - 54
ISSN - 2152-5250
DOI - 10.14336/ad.2019.0611
Subject(s) - glycolysis , methylglyoxal , neurodegeneration , glycation , triosephosphate isomerase , disease , medicine , alzheimer's disease , biochemistry , enzyme , endocrinology , diabetes mellitus , chemistry
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.