Proteostasis co-founder, Andrew Dillin, Ph.D., Howard Hughes Medical Institute Investigator and associate professor of molecular and cell biology at the Salk Institute for Biological Studies, said, Our research not only demonstrates that an important pathway may be involved in protecting against Alzheimer ™s disease, but also that this pathway can be regulated and manipulated. Dr. Dillin is the author of the publication, which appears in the December 11, 2009 issue of Cell, and co-founder Jeffery Kelly, Ph.D., Lita Annenberg Hazen Professor of Chemistry at the Scripps Research Institute, is a co-author.

The team of researchers led by Dr. Dillin were able slow the cellular aging process in Alzheimer ™s mice. By modulating the activity of a PN aggregase pathway which plays an important role in regulating lifespan, the scientists showed that Alzheimer ™s mice were able to live up to 35% longer than controls. The experimental mice were chronologically old but biologically young and had nearly normal cognition and behavior. The study also showed that by modulating the pathway to delay the cellular aging process, the mice became more efficient at dealing with toxic beta amyloid accumulations.

Online copies of the article can be obtained at cell.

SOURCE Proteostasis Therapeutics