Targeting the overexpressed mitochondrial protein VDAC1 in a mouse model of Alzheimer ’s disease protects against mitochondrial dysfunction and mitigates brain pathology

ConclusionsThe study suggests that mitochondrial dysfunction with its gatekeeper VDAC1 is a promising target for AD therapeutic intervention, and VBIT-4 is a promising drug candidate for AD treatment.
Source: Translational Neurodegeneration - Category: Neurology Source Type: research