Early Aβ42 Exposure Causes Learning Impairment in Later Life.

ABSTRACT: Amyloid cascade hypothesis proposes that amyloid β (Aβ) accumulation is the initiator and major contributor to the development of Alzheimer's disease (AD). However, this hypothesis has recently been challenged by clinical studies showing that reduction of Aβ accumulation in the brain does not accompany with cognitive improvement, suggesting that therapeutically targeting Aβ in the brain may not be sufficient for restoring cognitive function. Since the molecular mechanism underlying the progressive development of cognitive impairment after Aβ clearance is largely unknown, the reason of why there is no behavioral improvement after Aβ clearance remains elusive. In the current study, we demonstrated that transient Aβ expression caused learning deficit in later life, despite the accumulated Aβ

SUBMITTER: Cheng KC 

PROVIDER: S-EPMC9116909 | biostudies-literature | 2022 Jun

REPOSITORIES: biostudies-literature