Moderate coffee consumption may reduce the risk of developing Alzheimer’s Disease by up to 27%Print this page
Updated report contains latest scientific research into coffee consumption and Alzheimer’s Disease
21 September 2016 – In support of World Alzheimer’s Day, the Institute for Scientific Information on Coffee (ISIC) today reviews the scientific evidence surrounding coffee consumption and its potential to reduce the risk of Alzheimer’s Disease.
Approximately 26 million people suffer from Alzheimer’s Disease worldwide. Specifically in the EU, an aging population is likely to correlate with a rise in the disease1. Epidemiological studies have suggested that there may be an association between moderate coffee consumption and a reduced risk of developing Alzheimer’s Disease.
The scientific literature to date suggests that moderate, regular and lifelong coffee consumption (with moderate consumption defined as 3-5 cups per day2) is the optimal intake to benefit from this suggested association.
ISIC has today published the third edition of its report The good things in life: can coffee consumption reduce the risk of developing Alzheimer’s Disease? The newly-updated report provides a comprehensive overview of the latest research into coffee, caffeine and Alzheimer’s Disease.
Key research findings highlighted in the report include:
- Research published this year suggests that moderate coffee consumption can reduce the risk of developing Alzheimer’s by up to 27%3.
- The role of the Mediterranean diet: certain fruits, vegetables and beverages – including coffee – contain polyphenols. These compounds act on the brain to reduce inflammation, reduce neuronal deaths and preserve levels of acetylcholine, which is an organic chemical that functions in the brain and body as a neurotransmitter – a chemical released by nerve cells to send signals to other cells. Ferulic acid is another polyphenol found in coffee and this has been shown to protect against cognitive defect4-8.
- The caffeine in coffee reduces two hallmarks of Alzheimer’s: reducing the accumulation of beta amyloid peptide, and reducing the hyperphosphorylation of tau protein9. Caffeine also reduces the extent of neuronal deaths, especially in the areas of the brain involved in memory10. As a neuro-stimulant, caffeine promotes higher levels of acetylcholine11.
- New research suggests that another compound in coffee – quercetin – may also help protect key cells in the brain, although further research is needed to confirm this finding12.
Further research is required to fully understand the nature of the relationship between coffee consumption and Alzheimer’s Disease. To read ISIC’s report, please click here.
More information on coffee consumption and neurodegenerative disorders is available here.
- Alzheimer Europe (2010) ‘The impact of Alzheimer’s disease in Europe’. Available at: alzheimer-europe.org/EN/Research/PharmaCog/Why-Pharmacog/(language)/eng-GB
- EFSA (2015) Scientific Opinion on the Safety of Caffeine. EFSA Journal, 13(5):4102.
- Liu Q.-P. et al. (2016) Habitual coffee consumption and risk of cognitive decline/dementia: A systematic review and meta-analysis of prospective cohort studies. Nutr, 32(6):628-36.
- Perez-Jimenez et al. (2011) Dietary intake of 337 polyphenols in French adults. Am J Clin Nutr, 93(6):1220-1228.
- Kim H.S. et al. (2004) Inhibitory effects of long-term administration of ferulic acid on microglial activation induced by intracerebroventricular injection of beta-amyloid peptide (1-42) in mice. Biol Pharm Bull, 27:120-1.
- Cho J.Y. et al. (2005) Inhibitory effects of long-term administration of ferulic acid on astrocyte activation induced by intracerebroventricular injection of beta-amyloid peptide (1-42) in mice. Prog Neuropsychopharmacol Biol Psychiatry, 29:901-7.
- Wenk G.L. et al. (2004) Attenuation of chronic neuroinflammation by a nitric oxide-releasing derivative of the antioxidant ferulic acid. J Neurochem, 89:484–493.
- Yan J.J. et al. (2001) Protection against beta-amyloid peptide toxicity in vivo with long-term administration of ferulic acid. Br J Pharmacol, 133(1):89-96.
- Laurent C. et al. (2014) Beneficial effects of caffeine in a transgenic model of Alzheimer’s disease-like tau pathology. Neurobiol Aging, 35(9):2079-90.
- Dall’Igna O.P. et al. (2003) Neuroprotection by caffeine and adenosine A2A receptor blockade of β-amyloid neurotoxicity. J. Pharmacol, 138:1207–1209.
- Fredholm B. et al. (1999) Actions of caffeine in the brain with special reference to factors that contribute to its widespread use. Pharmacol Rev, 51:83–133.
- Lee M. et al. (2016) Quercetin, not caffeine, is a major neuroprotective component in coffee. Neurobiol Aging, 46:113-123.
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