1. PLoS One. 2011;6(11):e27762. doi: 10.1371/journal.pone.0027762. Epub 2011 Nov 16.

FDA-approved drugs that protect mammalian neurons from glucose toxicity slow
aging dependent on cbp and protect against proteotoxicity.

Lublin A(1), Isoda F, Patel H, Yen K, Nguyen L, Hajje D, Schwartz M, Mobbs C.

Author information: 
(1)Fishberg Center for Neurobiology, Mount Sinai School of Medicine, New York,
New York, United States of America.

Screening a library of drugs with known safety profiles in humans yielded 30
drugs that reliably protected mammalian neurons against glucose toxicity.
Subsequent screening demonstrated that 6 of these 30 drugs increase lifespan in
C. elegans: caffeine, ciclopirox olamine, tannic acid, acetaminophen, bacitracin,
and baicalein. Every drug significantly reduced the age-dependent acceleration of
mortality rate. These protective effects were blocked by RNAi inhibition of cbp-1
in adults only, which also blocks protective effects of dietary restriction. Only
2 drugs, caffeine and tannic acid, exhibited a similar dependency on DAF-16.
Caffeine, tannic acid, and bacitracin also reduced pathology in a transgenic
model of proteotoxicity associated with Alzheimer's disease. These results
further support a key role for glucose toxicity in driving age-related
pathologies and for CBP-1 in protection against age-related pathologies. These
results also provide novel lead compounds with known safety profiles in human for
treatment of age-related diseases, including Alzheimer's disease and diabetic
complications.

DOI: 10.1371/journal.pone.0027762 
PMCID: PMC3218048
PMID: 22114686  [Indexed for MEDLINE]