TDP-43 loss of function drives aberrant splicing in Parkinson's disease
Demonstrated that TDP-43 loss of function drives aberrant splicing events in Parkinson's disease.
james-w.-brenton
Demonstrated that TDP-43 loss of function drives aberrant splicing events in Parkinson's disease.
Demonstrated that AAV-delivered chimeric TDP-43 repressor (CTR) achieves broad brain biodistribution, restores TDP-43 splicing function, rescues neurons, and mitigates FTD-like …
TDP-43 depletion exacerbates tauopathy-dependent brain atrophy by sensitizing neurons to caspase 3-mediated tau cleavage in a multiple etiology dementia mouse model.
Conference abstract presented at ASGCT 2024 on validating TDP-43 splicing repression as a therapeutic strategy for ALS and FTD.