Deletion of Abi3/Gngt2 influences age-progressive amyloid β and tau pathologies in distinctive ways

Abstract excerpt

Abstract Background The S209F variant of Abelson Interactor Protein 3 ( ABI3 ) increases risk for Alzheimer’s disease (AD), but little is known about its function in relation to AD pathogenesis. Methods Here, we use a mouse model that is deficient in Abi3 locus to study how the loss of function of Abi3 impacts two cardinal neuropathological hallmarks of AD—amyloid β plaques and tau pathology. Our study employs...

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