期刊
BIOCHEMICAL SOCIETY TRANSACTIONS
卷 39, 期 -, 页码 933-938出版社
PORTLAND PRESS LTD
DOI: 10.1042/BST0390933
关键词
aging; Alzheimer's disease; axonal transport; Irontotemporal dementia; knockin mouse; microtubule-associated protein tau
资金
- Medical Research Council [G1000702]
- Alzheimer's Research UK [ART/PG2009/2]
- MRC [G1000702] Funding Source: UKRI
- Alzheimers Research UK [ART-PG2009-2] Funding Source: researchfish
- Biotechnology and Biological Sciences Research Council [BBS/E/B/0000C200] Funding Source: researchfish
- Medical Research Council [G1000702] Funding Source: researchfish
Considering the many differences between mice and humans, it is perhaps surprising how well mice model late-onset human neurodegenerative disease. Models of Alzheimer's disease, frontotemporal dementia, Parkinson's disease and Huntington's disease show some striking similarities to the corresponding human pathologies in terms of axonal transport disruption, protein aggregation, synapse loss and some behavioural phenotypes. However, there are also major differences. To extrapolate from mouse models to human disease, we need to understand how these differences relate to intrinsic limitations of the mouse system and to the effects of transgene overexpression. In the present paper, we use examples from an amyloid-overexpression model and a mutant-tau-knockin model to illustrate what we learn from each type of approach and what the limitations are. Finally, we discuss the further contributions that knockin and similar approaches can make to understanding pathogenesis and how best to model disorders of aging in a short-lived mammal.
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