Wednesday, January 10, 2018 at 12:00pm to 1:00pm
Zilkha Neurogenetic Institute (ZNI), Herklotz Seminar Room, 112
1501 San Pablo, Los Angeles, CA 90033
An expanding body of evidence argues that the Aβ and tau proteins share important characteristics of prion propagation to cause pathogenesis in Alzheimer’s disease (AD). Aβ and tau form a number of amyloids (β-sheet rich structures) with distinct conformations (“strains”), some of which give rise to different diseases and associated pathologies. Using principal component analysis of multiple structure-sensitive fluorescent amyloid-binding dyes and confocal-based spectral imaging in brain slices, we identified conformational strains of Aβ in heritable and sporadic forms of AD patient samples. We demonstrate that distinct strains of Aβ can be discerned in different disease types, or in different brain compartments within a given patient. Our findings may potentially explain the spectrum of clinical and pathologic features observed in AD.