Premium
Animal models of amyloid‐β‐related pathologies in Alzheimer’s disease
Author(s) -
Philipson Ola,
Lord Anna,
Gumucio Astrid,
O’Callaghan Paul,
Lannfelt Lars,
Nilsson Lars N.G.
Publication year - 2010
Publication title -
the febs journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.981
H-Index - 204
eISSN - 1742-4658
pISSN - 1742-464X
DOI - 10.1111/j.1742-4658.2010.07564.x
Subject(s) - transgene , disease , genetically modified mouse , neuroscience , biology , animal model , alzheimer's disease , gene knockout , missense mutation , genetics , computational biology , gene , medicine , mutation , pathology , endocrinology
In the early 1990s, breakthrough discoveries on the genetics of Alzheimer’s disease led to the identification of missense mutations in the amyloid‐β precursor protein gene. Research findings quickly followed, giving insights into molecular pathogenesis and possibilities for the development of new types of animal models. The complete toolbox of transgenic techniques, including pronuclear oocyte injection and homologous recombination, has been applied in the Alzheimer’s disease field, to produce overexpressors, knockouts, knockins and regulatable transgenics. Transgenic models have dramatically advanced our understanding of pathogenic mechanisms and allowed therapeutic approaches to be tested. Following a brief introduction to Alzheimer’s disease, various nontransgenic and transgenic animal models are described in terms of their values and limitations with respect to pathogenic, therapeutic and functional understandings of the human disease.