Rapamycin Up-regulates Genes Associated with Increased Max Lifespan (MLS)

An interesting new presentation by professor Vera Gorbunova where she discusses her research on profiling the genetic action of lifespan-improving therapeutics so that they can screen for new drugs and compounds that do the same.

And, as is usually the case when looking at anti-aging drugs and interventions, Rapamycin is at the top of the list.

They looked at rapamycin, 17-alpha estradiol, caloric restriction, etc. and found that some interventions work to decrease the activity, or down-regulate the genes associated with shorter maximum lifespans, while up-regulating the genes associated with longer maximum lifespans (MLS). Others, like calorie restriction do a mix of both.

Strangely, some, like protandim and acarbose operate opposite to what we would expect, increasing the function of genes associated with decreased maximum lifespan, while decreasing the genes associated with increased maximum lifespan.

See the YouTube video here: From long-lived animal species to human interventions | Prof Vera Gorbunova


There are many CR upregulates that rapamycin does not upregulate. What are some examples?

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I look forward to research about the potential overlap of the effects of rapamycin and 17-alpha estradiol. Are we better off using both for MLS?


Curious what that may mean for a acarbose/metformin. Any thoughts?