Elevating acetyl-CoA levels reduces aspects of brain aging

The reason acetylation is key is that it occurs as part of the RNA Polymerase II complex. AIUI it is a very basic energy availability control on transcription. There is I think a crosstalk between transcription and DNA methylation as well which means that if transcription successfully occurs demethylation occurs.

I think one of the key questions is what happens when RNA Pol II is stalled at a particular point awaiting acetylation and the histone in the neighbourhood is deacetylated.

ACSS2 is interesting because of the acetate metabolism and it may also feed into the effects of things like cider vinegar and alcohol metabolism. However, ACLY and the relationship between SLC25A1 and nuclear acetyl-CoA seem to be the key pathways involved in affecting transcription changes and particularly those which are part of aging.

AIUI ACCS2 is inhibited by acetylation levels so that it tends not to generate acetyl-CoA when the histone is highly acetylated.

The other histone modifications will have some effects and I am sure they are important in some circumstances, but the process of acetylation and deacetylation clearly rests at the centre of transcription control.


B Vitamins impact on acetyl coA


I thought this was interesting

From X: https://x.com/helios_movement/status/1750532721779347734?s=46&t=g51H5gL_rX6JIVg_7VgkQg

No associated paper mentioned.