Pyk2 overexpression in postsynaptic neurons blocks amyloid β_1-42-induced synaptotoxicity in microfluidic co-cultures.

ABSTRACT: Recent meta-analyses of genome-wide association studies identified a number of genetic risk factors of Alzheimer's disease; however, little is known about the mechanisms by which they contribute to the pathological process. As synapse loss is observed at the earliest stage of Alzheimer's disease, deciphering the impact of Alzheimer's risk genes on synapse formation and maintenance is of great interest. In this article, we report a microfluidic co-culture device that physically isolates synapses from pre- and postsynaptic neurons and chronically exposes them to toxic amyloid β peptides secreted by model cell lines overexpressing wild-type or mutated (V717I) amyloid precursor protein. Co-culture with cells overexpressing mutated amyloid precursor protein exposed the synapses of primary hippo

SUBMITTER: Kilinc D 

PROVIDER: S-EPMC7941669 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature