KCTD20 Suppression as a Potential Therapeutic Strategy againstNeurodegenerative Tauopathies

The accumulation of tau proteins in the brain contributes to the therapeutic challenges faced by patients with Alzheimer’s disease, frontotemporal dementia, and other neurodegenerative disorders. It has been found that KCTD20 suppression is a crucial therapeutic target for preventing tau protein degeneration triggered by glutamate. KCTD20 knockdown with either siRNA or antisense oligonucleotide increases lysosomal exocytosis and suppresses tau aggregation, as well as increases the survival of neurons. To illustrate this new preclinical modality, scientists combined patient- derived organoids with animal models, a strategy that may revolutionize future clinical therapies for neurodegenerative diseases.