Amyloid-β in Alzheimer's disease - front and centre after all?

Currently, there is an increasing trend towards the use of more representative ‘knock-in’ mouse models, in which the endogenous mouse app gene is replaced by a humanized version bearing one or more familial AD mutations, expressed under control of the endogenous app promoter to ensure these animals are free of transgene overexpression [ 136 ].

also in 63,971 other papers

We propose that this observation is potentially highly significant as it suggests that Aβ, despite the substantial concerns over the level of its involvement in AD, may very well still play a critical, central role in pathogenesis.

also in 132,142 other papers