期刊
PLOS ONE
卷 8, 期 5, 页码 -出版社
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0063589
关键词
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资金
- Fonds Wetenschappelijk Onderzoek-Vlaanderen (FWO-Vlaanderen)
- Instituut Wetenschap Techniek (IWT)
- EEC 6th & 7th Framework Program (MEMStick)
- EEC 6th & 7th Framework Program (neuroGSK3)
- EEC 6th & 7th Framework Program (EURON)
- EEC 6th & 7th Framework Program (NEURAD)
- de Rooms-fund
- KULeuven-Research Fund
- KULeuven-ResearchDevelopment
- Marie Curie fellowship [MEST CT 2005/020013 NEURAD]
Cell adhesion molecules are important structural substrates, required for synaptic plasticity and synaptogenesis. CAMs differ widely in their expression throughout different brain regions and their specific structural and functional roles in the brain remain to be elucidated. Here, we investigated selected cell adhesion molecules for alterations in expression levels and neuronal localization in validated mouse models for Alzheimer's disease that mimic the age-related progression of amyloid accumulation and tauopathy. Among the cell adhesion molecules analyzed, Nectin-3 expression was affected most and specifically in all mouse models with tauopathy. In particular was Nectin-3 depleted from the specific region of the hippocampus, known as the stratum lacunosum and moleculare, in mice that express wild-type or mutant human protein Tau, either chronically or sub-acutely. Tauopathy progresses from the entorhinal cortex to the hippocampus by unknown mechanisms that could involve transport by the myelinated axons of the temporoammonic and perforant pathways. The decreased expression of Nectin-3 in the stratum lacunosum moleculare is an early marker of impaired transport, and eventual synaptic problems, caused by beginning tauopathy.
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