Models of β-amyloid induced Tau-pathology: the long and “folded” road to understand the mechanism

Molecular Neurodegeneration

Ilse Dewachter¹  Dick Terwel²  Bruno Vasconcelos¹  Ilie-Cosmin Stancu¹ 

[1] Catholic University of Louvain, Institute of Neuroscience, Alzheimer Dementia, Av. E. Mounier 53, Av. Hippocrate 54, B-1200 Brussels, Belgium;reMYND nv, Gaston Geenslaan 1, B-3001 Leuven, Belgium

关键词: Prion;    Inflammation;    Synaptic dysfunction;    Amyloid cascade hypothesis;    Animal models;    Alzheimer’s disease;    Tau;    Amyloid;   

Others  :  1138627
DOI  :  10.1186/1750-1326-9-51

 received in 2014-05-12, accepted in 2014-10-14,  发布年份 2014

【 摘 要 】

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 Aβ 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 Aβ-induced Tau-pathology, which is the focus of this review. We here discuss available models that recapitulate Aβ-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.

【 授权许可】

   
2014 Stancu et al.; licensee BioMed Central Ltd.

【 图 表 】

Figure 1.

Figure 2.

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