Targeting the overexpressed mitochondrial protein VDAC1 in a mouse model of Alzheimer's disease protects against mitochondrial dysfunction and mitigates brain pathology.
Ankit VermaAnna Shteinfer-KuzmineNikita KamenetskySrinivas PittalaAvijit PaulEdna Nahon CrystalAlberto OuroVered Chalifa-CaspiSwaroop Kumar PandeyAlon MonsengoNoga VardiShira KnafoVarda Shoshan-BarmazPublished in: Translational neurodegeneration (2022)
The 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.