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Caffeine synergizes with another coffee component to increase plasma GCSF: linkage to cognitive benefits in Alzheimer's mice.
J Alzheimers Dis. 2011; 25(2):323-35.JA

Abstract

Retrospective and prospective epidemiologic studies suggest that enhanced coffee/caffeine intake during aging reduces risk of Alzheimer's disease (AD). Underscoring this premise, our studies in AD transgenic mice show that long-term caffeine administration protects against cognitive impairment and reduces brain amyloid-β levels/deposition through suppression of both β- and γ-secretase. Because coffee contains many constituents in addition to caffeine that may provide cognitive benefits against AD, we examined effects of caffeinated and decaffeinated coffee on plasma cytokines, comparing their effects to caffeine alone. In both AβPPsw+PS1 transgenic mice and non-transgenic littermates, acute i.p. treatment with caffeinated coffee greatly and specifically increased plasma levels of granulocyte-colony stimulating factor (GCSF), IL-10, and IL-6. Neither caffeine solution alone (which provided high plasma caffeine levels) or decaffeinated coffee provided this effect, indicating that caffeine synergized with some as yet unidentified component of coffee to selectively elevate these three plasma cytokines. The increase in GCSF is particularly important because long-term treatment with coffee (but not decaffeinated coffee) enhanced working memory in a fashion that was associated only with increased plasma GCSF levels among all cytokines. Since we have previously reported that long-term GCSF treatment enhances cognitive performance in AD mice through three possible mechanisms (e.g., recruitment of microglia from bone marrow, synaptogenesis, and neurogenesis), the same mechanisms could be complimentary to caffeine's established ability to suppress Aβ production. We conclude that coffee may be the best source of caffeine to protect against AD because of a component in coffee that synergizes with caffeine to enhance plasma GCSF levels, resulting in multiple therapeutic actions against AD.

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Authors+Show Affiliations

Cao C
Department of Molecular Pharmacology & Physiology, The USF/Byrd Alzheimer's Institute, Tampa, FL 33613, USA. ccao@health.usf.edu
Wang L
No affiliation info available
Lin X
No affiliation info available
Mamcarz M
No affiliation info available
Zhang C
No affiliation info available
Bai G
No affiliation info available
Nong J
No affiliation info available
Sussman S
No affiliation info available
Arendash G
No affiliation info available

MeSH

Alzheimer DiseaseAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAnalysis of VarianceAnimalsCaffeineCoffeeCognition DisordersCytokinesDisease Models, AnimalGranulocyte Colony-Stimulating FactorHumansMemory, Short-TermMiceMice, Inbred C57BLMice, TransgenicMutationNeuropsychological TestsPeptide FragmentsPhosphodiesterase InhibitorsPresenilin-1TheophyllineTime Factors

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

21422521

Citation

Cao, Chuanhai, et al. "Caffeine Synergizes With Another Coffee Component to Increase Plasma GCSF: Linkage to Cognitive Benefits in Alzheimer's Mice." Journal of Alzheimer's Disease : JAD, vol. 25, no. 2, 2011, pp. 323-35.
Cao C, Wang L, Lin X, et al. Caffeine synergizes with another coffee component to increase plasma GCSF: linkage to cognitive benefits in Alzheimer's mice. J Alzheimers Dis. 2011;25(2):323-35.
Cao, C., Wang, L., Lin, X., Mamcarz, M., Zhang, C., Bai, G., Nong, J., Sussman, S., & Arendash, G. (2011). Caffeine synergizes with another coffee component to increase plasma GCSF: linkage to cognitive benefits in Alzheimer's mice. Journal of Alzheimer's Disease : JAD, 25(2), 323-35. https://doi.org/10.3233/JAD-2011-110110
Cao C, et al. Caffeine Synergizes With Another Coffee Component to Increase Plasma GCSF: Linkage to Cognitive Benefits in Alzheimer's Mice. J Alzheimers Dis. 2011;25(2):323-35. PubMed PMID: 21422521.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Caffeine synergizes with another coffee component to increase plasma GCSF: linkage to cognitive benefits in Alzheimer's mice. AU - Cao,Chuanhai, AU - Wang,Li, AU - Lin,Xiaoyang, AU - Mamcarz,Malgorzata, AU - Zhang,Chi, AU - Bai,Ge, AU - Nong,Jasson, AU - Sussman,Sam, AU - Arendash,Gary, PY - 2011/3/23/entrez PY - 2011/3/23/pubmed PY - 2011/11/5/medline SP - 323 EP - 35 JF - Journal of Alzheimer's disease : JAD JO - J Alzheimers Dis VL - 25 IS - 2 N2 - Retrospective and prospective epidemiologic studies suggest that enhanced coffee/caffeine intake during aging reduces risk of Alzheimer's disease (AD). Underscoring this premise, our studies in AD transgenic mice show that long-term caffeine administration protects against cognitive impairment and reduces brain amyloid-β levels/deposition through suppression of both β- and γ-secretase. Because coffee contains many constituents in addition to caffeine that may provide cognitive benefits against AD, we examined effects of caffeinated and decaffeinated coffee on plasma cytokines, comparing their effects to caffeine alone. In both AβPPsw+PS1 transgenic mice and non-transgenic littermates, acute i.p. treatment with caffeinated coffee greatly and specifically increased plasma levels of granulocyte-colony stimulating factor (GCSF), IL-10, and IL-6. Neither caffeine solution alone (which provided high plasma caffeine levels) or decaffeinated coffee provided this effect, indicating that caffeine synergized with some as yet unidentified component of coffee to selectively elevate these three plasma cytokines. The increase in GCSF is particularly important because long-term treatment with coffee (but not decaffeinated coffee) enhanced working memory in a fashion that was associated only with increased plasma GCSF levels among all cytokines. Since we have previously reported that long-term GCSF treatment enhances cognitive performance in AD mice through three possible mechanisms (e.g., recruitment of microglia from bone marrow, synaptogenesis, and neurogenesis), the same mechanisms could be complimentary to caffeine's established ability to suppress Aβ production. We conclude that coffee may be the best source of caffeine to protect against AD because of a component in coffee that synergizes with caffeine to enhance plasma GCSF levels, resulting in multiple therapeutic actions against AD. SN - 1875-8908 UR - https://www.unboundmedicine.com/medline/citation/21422521/Caffeine_synergizes_with_another_coffee_component_to_increase_plasma_GCSF:_linkage_to_cognitive_benefits_in_Alzheimer's_mice_ L2 - https://content.iospress.com/openurl?genre=article&id=doi:10.3233/JAD-2011-110110 DB - PRIME DP - Unbound Medicine ER -