The mTOR pathway - do dissociatives make you live longer (or die earlier)!?

[dopamimetic]

Just happened yesterday to read a really interesting journal article at the library about rapamycin and the related research about ageing and the prevention / reversal thereof. Of course had to think of the ketamine-related antidepressant activity that seems to be, at least partially, mediated through that mechanistic target of rapamycin (mTOR) pathway and dissociatives / NMDA antagonists in general.

Seems to be a somewhat complex matter, as always, and things aren't that clearly understandable at least for me - that rapamycin tends to make organisms like yeasts or the fruit fly to live longer, but also probably increases the cancer risk or at least growth of already existing cancers etc. because it dampens parts of the immune response.

So do dissociatives now potentially rejuvenate you or keep your cells vital but increase the risk of getting cancer a bit or the opposite (oversimplified)?

mTOR is a key modulator of ageing and age-related disease
The TOR pathway comes of age
Ketamine modifies mood through mTOR

 

[Sturnam]

If you notice, Ketamine is shown to enhance mTOR activity at neurogenic doses. However, rapamycin is an inhibitor of mTOR; the idea is that slowing down mTOR activity may prolong life. Ketamine would seem to do the exact opposite (although the doses for neurogenesis are usually much lower than recreational doses of ketamine).

For depression, increased activity of mTOR would increase protein synthesis rates, which is added as new dendritic spines. How this exactly means that it relieves depression is unknown.

 

[serotonin2A]

That is an oversimplification because ketamine only has effects on a small number of cells in your body. It isn't altering mTor in your lungs or a whole host of other organs. The effects of ketamine on mTor are indirect, and are mediated by Glu activation of AMPA receptors. Ketamine is only altering Glu release in the brain, and only in certain brain regions.