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 MonsonegoNoga VardiShira KnafoVarda Shoshan-Barmaz

Published 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.

Keyphrases

mouse model
randomized controlled trial
oxidative stress
resting state
white matter
emergency department
cancer therapy
amino acid
small molecule
protein protein
functional connectivity
binding protein
multiple sclerosis
mild cognitive impairment