AI Summary
The article discusses the identification of 14-3-3θ as a key player in promoting TDP-43 deposition, which is involved in ALS and FTD. The researchers devised a treatment targeting the 14-3-3θ-mediated pathology, resulting in improved outcomes in animal models of ALS/FTD. This research has implications for potential future therapies in treating these neurodegenerative diseases.
TDP-43 forms neuronal deposits in amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) due to unknown causes. Ke et al. identified the TDP-43 interactor 14-3-3θ, which promotes TDP-43 deposition. They devised a treatment harnessing 14-3-3θ’s affinity for TDP-43, mitigating deficits and neurodegeneration in ALS/FTD models with implications for future therapy.