M. Azhar Chishti

TL;DR: Aβ immunization reduces both deposition of cerebral fibrillar Aβ and cognitive dysfunction in the TgCRND8 murine model of Alzheimer's disease without, however, altering total levels of Aβ in the brain, which implies that either a ∼50% reduction in dense-cored Aβ plaques is sufficient to affect cognition, or that vaccination may modulate the activity/abundance of a small subpopulation of especially toxic Aβ species.

TL;DR: High level production of the pathogenic Aβ42 form of Aβ peptide was associated with an early impairment in TgCRND8 mice in acquisition and learning reversal in the reference memory version of the Morris water maze, present by 3 months of age.

TL;DR: The data suggest that the beneficial effect of the txJ mutation on CNS Aβ burden may proceed by a previously undescribed mechanism, likely involving increased clearance of peripheral pools of Aβ peptide.

TL;DR: The data suggest that covalent variants of PrPC arising in this manner may, in concert with Cu(II), generate PrPSc-like species capable of initiating sporadic prion disease.

TL;DR: It is suggested that TgTauR406W mice would be a useful model in the study of frontotemporal dementia and other tauopathies such as Alzheimer's disease (AD).