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
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