Neuronal Rubicon Represses Extracellular APP/Amyloid β Deposition in Alzheimer's Disease.

ABSTRACT: Alzheimer's disease (AD) is the most prevalent age-associated neurodegenerative disease. A decrease in autophagy during aging contributes to brain disorders by accumulating potentially toxic substrates in neurons. Rubicon is a well-established inhibitor of autophagy in all cells. However, Rubicon participates in different pathways depending on cell type, and little information is currently available on neuronal Rubicon's role in the AD context. Here, we investigated the cell-specific expression of Rubicon in postmortem brain samples from AD patients and 5xFAD mice and its impact on amyloid β burden in vivo and neuroblastoma cells. Further, we assessed Rubicon levels in human-induced pluripotent stem cells (hiPSCs), derived from early-to-moderate AD and in postmortem samples from severe AD

SUBMITTER: Espinoza S 

PROVIDER: S-EPMC9221152 | biostudies-literature | 2022 Jun

REPOSITORIES: biostudies-literature