HDAC6 inhibition as a mechanism to prevent neurodegeneration in the mSOD1^G93A mouse model of ALS.

ABSTRACT: The loss of upper and lower motor neurons, and their axons is central to the loss of motor function and death in amyotrophic lateral sclerosis (ALS). Due to the diverse range of genetic and environmental factors that contribute to the pathogenesis of ALS, there have been difficulties in developing effective therapies for ALS. One emerging dichotomy is that protection of the neuronal cell soma does not prevent axonal vulnerability and degeneration, suggesting the need for targeted therapeutics to prevent axon degeneration. Post-translational modifications of protein acetylation can alter the function, stability and half-life of individual proteins, and can be enzymatically modified by histone acetyltransferases (HATs) and histone deacetyltransferases (HDACs), which add, or remove acetyl gro

SUBMITTER: Phipps AJ 

PROVIDER: S-EPMC11315133 | biostudies-literature | 2024 Jul

REPOSITORIES: biostudies-literature