期刊
MOLECULAR NEURODEGENERATION
卷 9, 期 -, 页码 -出版社
BMC
DOI: 10.1186/1750-1326-9-51
关键词
Amyloid; Tau; Alzheimer's disease; Animal models; Amyloid cascade hypothesis; Synaptic dysfunction; Inflammation; Prion
资金
- Belgian Fonds National pour la Recherche Scientifique -Fonds de la Recherche Scientifique (FNRS-FRS
- Qualified Researcher, Impulse Financing, Research Credits)
- Institute for the Promotion of Innovation by Science and Technology (IWT) (Belgium)
- European Commission (AgedBrainSYSBIO, FP7, ECGA) [305299]
- Interuniversity Attraction Poles Programme-Belgian State-Belgian Science Policy, The Belgian Fonds de la Recherche Scientifique Medicale
The amyloid cascade hypothesis has been the prevailing hypothesis in Alzheimer's Disease research, although the final and most wanted proof i.e. fully successful anti-amyloid clinical trials in patients, is still lacking. This may require a better in depth understanding of the cascade. Particularly, the exact toxic forms of A beta and Tau, the molecular link between them and their respective contributions to the disease process need to be identified in detail. Although the lack of final proof has raised substantial criticism on the hypothesis per se, accumulating experimental evidence in in vitro models, in vivo models and from biomarkers analysis in patients supports the amyloid cascade and particularly A beta-induced Tau-pathology, which is the focus of this review. We here discuss available models that recapitulate A beta-induced Tau-pathology and review some potential underlying mechanisms. The availability and diversity of these models that mimic the amyloid cascade partially or more complete, provide tools to study remaining questions, which are crucial for development of therapeutic strategies for Alzheimer's Disease.
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