| Abstrakt: |
A recent study from the University of Oxford explores the role of mitochondrial dysfunction in amyotrophic lateral sclerosis (ALS) and its impact on axonal transport in motor neurons. The research highlights how mutations in TDP-43 lead to deficiencies in mitochondrial functions, affecting axonal transport, which can be partially rescued by overexpression of dynactin-1. This study sheds light on the complex determinants of ALS, including genetic and non-genetic factors, and offers insights into potential therapeutic interventions. [Extracted from the article] |
