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

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

Abstract

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.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Aging / drug effects*
  • Alzheimer Disease / chemically induced
  • Alzheimer Disease / genetics
  • Alzheimer Disease / prevention & control*
  • Animals
  • Animals, Genetically Modified
  • Caenorhabditis elegans / genetics
  • Caenorhabditis elegans / growth & development
  • Caenorhabditis elegans / metabolism
  • Caenorhabditis elegans Proteins / antagonists & inhibitors
  • Caenorhabditis elegans Proteins / genetics
  • Caenorhabditis elegans Proteins / metabolism*
  • Disease Models, Animal
  • Drug Approval*
  • Forkhead Transcription Factors
  • Glucose / toxicity*
  • Histone Acetyltransferases / antagonists & inhibitors
  • Histone Acetyltransferases / genetics
  • Histone Acetyltransferases / metabolism*
  • Humans
  • Neurons / cytology
  • Neurons / drug effects*
  • Pharmaceutical Preparations / administration & dosage*
  • RNA, Small Interfering / genetics
  • Signal Transduction / drug effects
  • Survival Rate
  • Transcription Factors / antagonists & inhibitors
  • Transcription Factors / genetics
  • Transcription Factors / metabolism*
  • United States
  • United States Food and Drug Administration

Substances

  • Caenorhabditis elegans Proteins
  • Forkhead Transcription Factors
  • Pharmaceutical Preparations
  • RNA, Small Interfering
  • Transcription Factors
  • daf-16 protein, C elegans
  • CBP-1 protein, C elegans
  • Histone Acetyltransferases
  • Glucose