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Genetic mechanisms of coffee extract protection in a Caenorhabditis elegans model of β-amyloid peptide toxicity.
Genetics. 2010 Nov; 186(3):857-66.G

Abstract

Epidemiological studies have reported that coffee and/or caffeine consumption may reduce Alzheimer's disease (AD) risk. We found that coffee extracts can similarly protect against β-amyloid peptide (Aβ) toxicity in a transgenic Caenorhabditis elegans Alzheimer's disease model. The primary protective component(s) in this model is not caffeine, although caffeine by itself can show moderate protection. Coffee exposure did not decrease Aβ transgene expression and did not need to be present during Aβ induction to convey protection, suggesting that coffee exposure protection might act by activating a protective pathway. By screening the effects of coffee on a series of transgenic C. elegans stress reporter strains, we identified activation of the skn-1 (Nrf2 in mammals) transcription factor as a potential mechanism of coffee extract protection. Inactivation of skn-1 genetically or by RNAi strongly blocked the protective effects of coffee extract, indicating that activation of the skn-1 pathway was the primary mechanism of coffee protection. Coffee also protected against toxicity resulting from an aggregating form of green fluorescent protein (GFP) in a skn-1-dependent manner. These results suggest that the reported protective effects of coffee in multiple neurodegenerative diseases may result from a general activation of the Nrf2 phase II detoxification pathway.

Authors+Show Affiliations

Institute for Behavioral Genetics, University of Colorado, Boulder, Colorado 80309, USA.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural

Language

eng

PubMed ID

20805557

Citation

Dostal, Vishantie, et al. "Genetic Mechanisms of Coffee Extract Protection in a Caenorhabditis Elegans Model of Β-amyloid Peptide Toxicity." Genetics, vol. 186, no. 3, 2010, pp. 857-66.
Dostal V, Roberts CM, Link CD. Genetic mechanisms of coffee extract protection in a Caenorhabditis elegans model of β-amyloid peptide toxicity. Genetics. 2010;186(3):857-66.
Dostal, V., Roberts, C. M., & Link, C. D. (2010). Genetic mechanisms of coffee extract protection in a Caenorhabditis elegans model of β-amyloid peptide toxicity. Genetics, 186(3), 857-66. https://doi.org/10.1534/genetics.110.120436
Dostal V, Roberts CM, Link CD. Genetic Mechanisms of Coffee Extract Protection in a Caenorhabditis Elegans Model of Β-amyloid Peptide Toxicity. Genetics. 2010;186(3):857-66. PubMed PMID: 20805557.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Genetic mechanisms of coffee extract protection in a Caenorhabditis elegans model of β-amyloid peptide toxicity. AU - Dostal,Vishantie, AU - Roberts,Christine M, AU - Link,Christopher D, Y1 - 2010/08/30/ PY - 2010/9/1/entrez PY - 2010/9/2/pubmed PY - 2011/2/16/medline SP - 857 EP - 66 JF - Genetics JO - Genetics VL - 186 IS - 3 N2 - Epidemiological studies have reported that coffee and/or caffeine consumption may reduce Alzheimer's disease (AD) risk. We found that coffee extracts can similarly protect against β-amyloid peptide (Aβ) toxicity in a transgenic Caenorhabditis elegans Alzheimer's disease model. The primary protective component(s) in this model is not caffeine, although caffeine by itself can show moderate protection. Coffee exposure did not decrease Aβ transgene expression and did not need to be present during Aβ induction to convey protection, suggesting that coffee exposure protection might act by activating a protective pathway. By screening the effects of coffee on a series of transgenic C. elegans stress reporter strains, we identified activation of the skn-1 (Nrf2 in mammals) transcription factor as a potential mechanism of coffee extract protection. Inactivation of skn-1 genetically or by RNAi strongly blocked the protective effects of coffee extract, indicating that activation of the skn-1 pathway was the primary mechanism of coffee protection. Coffee also protected against toxicity resulting from an aggregating form of green fluorescent protein (GFP) in a skn-1-dependent manner. These results suggest that the reported protective effects of coffee in multiple neurodegenerative diseases may result from a general activation of the Nrf2 phase II detoxification pathway. SN - 1943-2631 UR - https://www.unboundmedicine.com/medline/citation/20805557/Genetic_mechanisms_of_coffee_extract_protection_in_a_Caenorhabditis_elegans_model_of_β_amyloid_peptide_toxicity_ L2 - http://www.genetics.org/cgi/pmidlookup?view=long&pmid=20805557 DB - PRIME DP - Unbound Medicine ER -