期刊
JOURNAL OF ALZHEIMERS DISEASE
卷 5, 期 4, 页码 301-308出版社
IOS PRESS
DOI: 10.3233/JAD-2003-5405
关键词
Alzheimer's disease; glycogen synthase kinase 3; lithium; neurodegeneration; protein aggregation; tauopathy
资金
- Sanofi-Synthelabo
- Fundacion Lilly
- Comunidad de Madrid
- Spanish CICYT
- Fundacion Ramon Areces
Tau protein hyperphosphorylation and aggregation into neurofibrillary tangles are characteristic features of several neurodegenerative disorders referred to as tauopathies. Among them, frontotemporal dementia and Parkinsonism linked to chromosome 17 may be caused by dominant missense mutations in the tau gene. Transgenic mice expressing mutant tau serve as valid model systems to study the ethiopathogenesis of these diseases and assay possible therapeutic interventions. Here we report that chronic lithium treatment of a transgenic mouse strain expressing human tau with three missense mutations results in decreased glycogen synthase kinase-3-dependent-tau phosphorylation and a reduction of filamentous aggregates. These data indicate that lithium, presumably acting through the inhibition of glycogen synthase kinase 3, may be useful to curb neurodegeneration in tauopathies.
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