Growing evidence points to a metabolic impairment in Alzheimer’s disease (AD) patients, whose number worldwide is projected to reach 135 million by 2050, according to Jerusalem Post.
Neurology researchers say AD starts to develop several decades before the onset of dementia and the deterioration of cognitive function.
Reduced metabolism results from a dysfunction of the mitochondria, which produce most of the energy in cells. It is also involved in cell death, inflammation and immune response. Even though AD is linked to mitochondrial dysfuntion, there are no current drug candidats that target this aspect. Researchers at Ben-Gurion University of the Negev in Beersheba are proposing a new treatment approach by targeting the mitochondrial gatekeeper – the voltage-dependent anion channel-1 (VDAC1) – which controls mitochondrial activity and cell life and death.
The new proposed target and therapy demonstrated significant improvement across multiple parameters in mouse models. The research was recently reported in the prestigious journal Translational Neurodegeneration under the title “Targeting the overexpressed mitochondrial protein VDAC1 in a mouse model of Alzheimer’s disease protects against mitochondrial dysfunction and mitigates brain pathology.”