Back to Search Start Over

Do tau-synaptic long-term depression interactions in the hippocampus play a pivotal role in the progression of Alzheimer's disease?

Authors :
Hu Z
Ondrejcak T
Yu P
Zhang Y
Yang Y
Klyubin I
Kennelly SP
Rowan MJ
Hu NW
Source :
Neural regeneration research [Neural Regen Res] 2023 Jun; Vol. 18 (6), pp. 1213-1219.
Publication Year :
2023

Abstract

Cognitive decline in Alzheimer's disease correlates with the extent of tau pathology, in particular tau hyperphosphorylation that initially appears in the transentorhinal and related regions of the brain including the hippocampus. Recent evidence indicates that tau hyperphosphorylation caused by either amyloid-β or long-term depression, a form of synaptic weakening involved in learning and memory, share similar mechanisms. Studies from our group and others demonstrate that long-term depression-inducing low-frequency stimulation triggers tau phosphorylation at different residues in the hippocampus under different experimental conditions including aging. Conversely, certain forms of long-term depression at hippocampal glutamatergic synapses require endogenous tau, in particular, phosphorylation at residue Ser396. Elucidating the exact mechanisms of interaction between tau and long-term depression may help our understanding of the physiological and pathological functions of tau/tau (hyper)phosphorylation. We first summarize experimental evidence regarding tau-long-term depression interactions, followed by a discussion of possible mechanisms by which this interplay may influence the pathogenesis of Alzheimer's disease. Finally, we conclude with some thoughts and perspectives on future research about these interactions.<br />Competing Interests: None

Details

Language :
English
ISSN :
1673-5374
Volume :
18
Issue :
6
Database :
MEDLINE
Journal :
Neural regeneration research
Publication Type :
Academic Journal
Accession number :
36453396
Full Text :
https://doi.org/10.4103/1673-5374.360166