Trial Report Targeting the overexpressed mitochondrial protein VDAC1 in a mouse model of Alzheimer’s disease..., 2022, Verma et al

[boolybooly]

Targeting the overexpressed mitochondrial protein VDAC1 in a mouse model of Alzheimer’s disease protects against mitochondrial dysfunction and mitigates brain pathology

...neuronal cultures and a 5 × FAD mouse model of AD were treated with VBIT-4. We addressed multiple topics related to the disease and its molecular mechanisms using immunoblotting, immunofluorescence, q-RT-PCR, 3-D structural analysis and several behavioral tests.

Conclusions
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.

https://translationalneurodegeneration.biomedcentral.com/articles/10.1186/s40035-022-00329-7

Interesting in light of the mitochondrial aspects of ME. As I understand it, VBIT-4 is basically a mitochondrial pore formation blocker, which reduces apoptosis because mitochondrial pore formation is a key step in apoptosis (aka cell death).

 

[boolybooly]

My thoughts are ...

A mouse model based on excess VDAC1 production is not quite the same as human Alzheimer's and the VDAC1 antagonist VBIT-4 is bound to put that right and represents a cure for the mouse model, not necessarily human Alzheimer's.

Secondly apoptosis evolved for a reason, to remove infected or dysfunctional cells and any therapy which blocks it will have corresponding side effects i.e. increased latent infection and possibly reduced immunological removal of precancerous cells.