Both studies show that rapamycin reduces the level of amyloid-beta-42 (A? or Abeta, the main constituent of amyloid plaques in the brains of Alzheimer’s disease sufferers). As the amyloid-beta-42 levels dropped in the mice studied, they showed showed marked improvement in memory, learning and cognition. Given the two different mouse models used in the two studies, the studies’ authors hypothesis that rapamycin may produce a similar positive effect in humans with Alzheimer’s.
Rapamycin may sound familiar to Crohn’s disease patients — it has demonstrated effectiveness in the treatment of Crohn’s disease in patients who haven’t responded to other treatments3 and has seen use as an “off-label” treatment for Crohn’s.
Rapamycin was originally discovered over 30 years ago in a soil sample from Easter Island. In 1999, the U.S. FDA (Food and Drug Administration) approved its use as an immunosuppressant in kidney transplant patients. Since then, rapamycin has been found to have other benefits as well (treating diseases as diverse as pancreatic cancer and epilepsy), causing some medical professionals to label it a “medical breakthrough drug.”
- “Molecular interplay between mTOR, A? and tau: Effects on cognitive impairments”, Antonella Caccamo, Smita Majumder, Arlan Richardson, Randy Strong and Salvatore Oddo, Journal of Biological Chemistry, April 1, 2010 [↩]
- “Inhibition of mTOR by Rapamycin Abolishes Cognitive Deficits and Reduces Amyloid-? Levels in a Mouse Model of Alzheimer’s Disease”, Patricia Spilman, Natalia Podlutskaya, Matthew J. Hart, Jayanta Debnath, Olivia Gorostiza, Dale Bredesen, Arlan Richardson, Randy Strong, Veronica Galvan, PLoS One, April 1, 2010 [↩]
- “Use of sirolimus (rapamycin) to treat refractory Crohn’s disease”, Massey, Bredin, Parkes, GUT, May 18, 2008 [↩]