期刊
JOURNAL OF NEURAL TRANSMISSION
卷 122, 期 4, 页码 531-539出版社
SPRINGER WIEN
DOI: 10.1007/s00702-014-1342-8
关键词
Energy metabolism; Hibernation; Neurodegeneration; NMDA signaling; Synaptic gain; Torpor
Sporadic Alzheimer's disease (AD) is a chronic progressive neurodegenerative disorder of unknown cause characterized by fibrillar accumulation of the A-peptide and aggregates of the microtubule-associated protein tau in a hyperphosphorylated form. Already at preclinical stages, AD is characterized by hypometabolic states which are a good predictor of cognitive decline. Here, we summarize recent evidence derived from the study of hibernating animals that brain hypometabolism can trigger PHF-like hyperphosphorylation of tau. We put forward the concept that particular types of neurons respond to a hypometabolic state with an elevated phosphorylation of tau protein which represents a physiological mechanism involved in regulating synaptic gain. If, in contrast to hibernation, the hypometabolic state is not terminated after a definite time but rather persists and progresses, the elevated phosphorylation of tau protein endures and the protective reaction associated with it might turn into a pathological cascade leading to neurodegeneration.
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