In a recent study published online in the Journal of Biological Chemistry, researchers at Georgetown University Medical Center have uncovered a surprising potential therapeutic target for both frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS). Often in both FTD and ALS, the normally nuclear TDP-43 protein is sequestered in cytoplasmic protein inclusions, which many researchers believe contributes to neuronal toxicity. However, new research out of Dr. Charbel E-H Moussa’s group suggests that it may not be the cytoplasmic TDP-43 inclusions that are toxic, instead toxicity might stem from dysregulated levels of TDP-43 in the nucleus. Dr. Moussa found that increasing the levels of the E3-ubiquitin ligase, parkin, facilitated TDP-43 degradation and slowed disease progressions in TDP-43 mouse and rat models. Read the full story here.
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