Cognitive and emotional alterations in App knock-in mouse models of Aβ amyloidosis.

ABSTRACT:

Background

Alzheimer's disease (AD), the most common cause of dementia, is characterized by the progressive deposition of amyloid-β (Aβ) peptides and neurofibrillary tangles. Mouse models of Aβ amyloidosis generated by knock-in (KI) of a humanized Aβ sequence provide distinct advantages over traditional transgenic models that rely on overexpression of amyloid precursor protein (APP). In App-KI mice, three familial AD-associated mutations were introduced into the endogenous mouse App locus to recapitulate Aβ pathology observed in AD: the Swedish (NL) mutation, which elevates total Aβ production; the Beyreuther/Iberian (F) mutation, which increases the Aβ42/Aβ40 ratio; and the Arctic (G) mutation, which promotes Aβ aggregation. App^NL-G-F mice harbor all three mutations and

SUBMITTER: Sakakibara Y 

PROVIDER: S-EPMC6064053 | biostudies-literature | 2018 Jul

REPOSITORIES: biostudies-literature