Dopamine, sleep, and neuronal excitability modulate amyloid-β-mediated forgetting in Drosophila.

ABSTRACT: Alzheimer disease (AD) is one of the main causes of age-related dementia and neurodegeneration. However, the onset of the disease and the mechanisms causing cognitive defects are not well understood. Aggregation of amyloidogenic peptides is a pathological hallmark of AD and is assumed to be a central component of the molecular disease pathways. Pan-neuronal expression of Aβ42Arctic peptides in Drosophila melanogaster results in learning and memory defects. Surprisingly, targeted expression to the mushroom bodies, a center for olfactory memories in the fly brain, does not interfere with learning but accelerates forgetting. We show here that reducing neuronal excitability either by feeding Levetiracetam or silencing of neurons in the involved circuitry ameliorates the phenotype. Furthermore,

SUBMITTER: Kaldun JC 

PROVIDER: S-EPMC8523056 | biostudies-literature | 2021 Oct

REPOSITORIES: biostudies-literature