Journal
AUTOPHAGY
Volume 8, Issue 1, Pages 147-151Publisher
TAYLOR & FRANCIS INC
DOI: 10.4161/auto.8.1.18331
Keywords
progerin; rapamycin; autophagy; aging; neurodegeneration; progeria
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Funding
- NIA NIH HHS [R00 AG029761] Funding Source: Medline
- NATIONAL HUMAN GENOME RESEARCH INSTITUTE [ZIAHG200305] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [R00AG029761] Funding Source: NIH RePORTER
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While rapamycin has been in use for years in transplant patients as an antirejection drug, more recently it has shown promise in treating diseases of aging, such as neurodegenerative disorders and atherosclerosis. We recently reported that rapamycin reverses the cellular phenotype of fibroblasts from children with the premature aging disease Hutchinson-Gilford progeria syndrome (HGPS). We found that the causative aberrant protein, progerin, was cleared through autophagic mechanisms when the cells were treated with rapamycin, suggesting a new potential treatment for HGPS. Recent evidence shows that progerin is also present in aged tissues of healthy individuals, suggesting that progerin may contribute to physiological aging. While it is intriguing to speculate that rapamycin may affect normal aging in humans, as it does in lower organisms, it will be important to identify safer analogs of rapamycin for chronic treatments in humans in order to minimize toxicity. In addition to its role in HGPS and normal aging, we discuss the potential of rapamycin for the treatment of age-dependent neurodegenerative diseases.
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