Mitochondrial Disruption by Amyloid Beta 42 Identified by Proteomics and Pathway Mapping.

ABSTRACT: Alzheimer's disease (AD) is marked by chronic neurodegeneration associated with the occurrence of plaques containing amyloid β (Aβ) proteins in various parts of the human brain. An increase in several Aβ fragments is well documented in patients with AD and anti-amyloid targeting is an emerging area of therapy. Soluble Aβ can bind to various cell surface and intracellular molecules with the pathogenic Aβ₄₂ fragment leading to neurotoxicity. Here we examined the effect of Aβ₄₂ on network adaptations in the proteome of nerve growth factor (NGF) differentiated PC12 cells using liquid-chromatography electrospray ionization mass spectrometry (LC-ESI MS/MS) proteomics. Whole-cell peptide mass fingerprinting was coupled to bioinformatic gene set enrichment analysis (GSEA) in

SUBMITTER: Sinclair P 

PROVIDER: S-EPMC8468661 | biostudies-literature | 2021 Sep

REPOSITORIES: biostudies-literature