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-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
white matter
multiple sclerosis
emergency department
radiation therapy
binding protein
adverse drug
brain injury
cerebral ischemia
drug induced