O-GlcNAc impacts mitophagy via the PINK1-dependent pathway.

ABSTRACT:

Background

The accumulation of dysfunctional mitochondria is an early feature of Alzheimer's disease (AD). The impaired turnover of damaged mitochondria increases reactive oxygen species production and lowers ATP generation, leading to cellular toxicity and neurodegeneration. Interestingly, AD exhibits a disruption in the global post-translational modification β-N-acetylglucosamine (O-GlcNAc). O-GlcNAc is a ubiquitous single sugar modification found in the nuclear, cytoplasmic, and mitochondrial proteins. Cells maintain a homeostatic level of O-GlcNAc by cycling the addition and removal of the sugar by O-GlcNAc transferase (OGT) or O-GlcNAcase (OGA), respectively.

Methods

We used patient-derived induced pluripotent stem cells, a transgenic mouse model of AD, SH-SY5Y neurobla

SUBMITTER: Alghusen IM 

PROVIDER: S-EPMC11339348 | biostudies-literature | 2024

REPOSITORIES: biostudies-literature