Moderate coffee consumption may lower the risk of Alzheimer’s Disease by up to 20 per cent

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An Alzheimer Europe session report by the Institute for Scientific Information on Coffee highlights the potential role of coffee consumption in reducing the risk of Alzheimer’s Disease

 27 November, 2014 Drinking 3-5 cups of coffee per day may help to protect against Alzheimer’s Disease, according to research highlighted in an Alzheimer Europe session report published by the Institute for Scientific Information on Coffee (ISIC), a not-for-profit organisation devoted to the study and disclosure of science related to coffee and health.

The number of people in Europe aged over 65 is predicted to rise from 15.4% of the population to 22.4% by 20251 and, with an aging population, neurodegenerative diseases such as Alzheimer’s Disease are of increasing concern. Alzheimer’s Disease affects one person in twenty over the age of 65, amounting to 26 million people world-wide1

Recent scientific evidence has consistently linked regular, moderate coffee consumption with a possible reduced risk of developing Alzheimer’s Disease2,3. An overview of this research and key findings were presented during a satellite symposium at the 2014 Alzhemier Europe Annual Congress.

The session report from this symposium highlights the role nutrition can play in preserving cognitive function, especially during the preclinical phase of Alzhemier’s, before symptoms of dementia occur4. The report notes that a Mediterranean diet, consisting of fish, fresh fruit and vegetables, olive oil and red wine, has been associated with a reduced risk for development of Alzheimer’s Disease5,6,7. Research suggests that compounds called polyphenols are responsible for this protective effect, these compounds are also found in high quantities in coffee6.

Epidemiological studies have found that regular, life-long moderate coffee consumption is associated with a reduced risk of developing Alzheimer’s Disease2,3, with the body of evidence suggesting that coffee drinkers can reduce their risk of developing the disease by up to 20%3. A recent paper, suggested that moderate coffee consumption was associated with a lower risk of developing dementia over a four year follow-up period, however the effect diminished over longer follow up period9.

Finally, the report explores the compounds within coffee, which may be responsible for this protective effect, identifying caffeine and polyphenols as key candidates. Caffeine helps prevent the formation of amyloid plaques and neurofibrulary tangles in the brain10 – two hallmarks of Alzheimer’s Disease.  In addition to this, both caffeine and polyphenols reduce inflammation and decrease the deterioration of brain cells – especially in the hippocampus and cortex, areas of the brain involved in memory11,12,13,14.

Dr. Arfan Ikram, an assistant professor in neuroepidemiology at Erasmus Medical Centre Rotterdam, presented his findings at the symposium. He commented: “The majority of human epidemiological studies suggest that regular coffee consumption over a lifetime is associated with a reduced risk of developing Alzheimer’s Disease, with an optimum protective effect occurring with three to five cups of coffee per day.”

Dr. Iva Holmerova, vice chairperson of Alzheimer Europe, commented:  “The findings presented in this report are very encouraging and help to develop our understanding of the role nutrition can play in protecting against Alzheimer’s Disease. Coffee is a very popular beverage enjoyed by millions of people around the world and I’m pleased to know that moderate, lifelong consumption can have a beneficial effect on the development of Alzheimer’s Disease.”

The session report details the key scientific research presented by Dr. Neville Vassallo, Dr. Arfan Ikram and Dr. Astrid Nehlig during a session entitled: Nutrition and Cognitive Function, which took place on the 23rd October in Glasgow, UK.

For more information on coffee and neurodegenerative diseases please visit www.coffeeandhealth.org.

To read the full report, click here.

References

  1. Alzheimer Europe (2010). The impact of Alzheimer’s disease in Europe. Available at http://www.alzheimer-europe.org/EN/Research/PharmaCog/Why-Pharmacog/(language)/eng-GB
  2. Barranco Quintana J.L. et al. (2007) Alzheimer’s disease and coffee: a quantitative review. Neurol Res, 29:91-5
  3. Santos C. et al. (2010) Caffeine intake and dementia: systematic review and meta-analysis. J Alzheimers Dis, 20(1):187-204.
  4. Lansbury & Lashuel. (2006) Review Article: A century-old debate on protein aggregation and neurodegeneration enters the clinic. Nature, 443:774-779
  5. Scarmeas N. et al. (2006) Mediterranean diet and risk for Alzheimer’s disease. Ann Neurol, 59:912–21
  6. Scarmeas N. et al. (2009) Physical activity, diet and Alzheimer’s disease risk. JAMA, 302(6):627-37
  7. Gu Y. et al. (2010) Food Combination and Alzheimer Disease Risk: A Protective Diet. Arch Neurol, 67(6):699-706
  8. Perez-Jimenez et al. (2011) Dietary intake of 337 polyphenols in French adults. Am J Clin Nutr, 93(6):1220-1228 .
  9. Mirza S.S. et al. (2014) Coffee consumption and incident dementia. European Journal of Epidemiology, published online ahead of print.
  10. Laurent et al. (2014) Beneficial effects of caffeine in a transgenic model of Alzheimer’s disease-like tau pathology. Neurobiol Aging, 35(9):2079-90.
  11. Dall’Igna O.P. et al. (2003) Neuroprotection by caffeine and adenosine A2A receptor blockade of β-amyloid neurotoxicity. Br. J. Pharmacol, 138:1207–1209.
  12. 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.
  13. 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.
  14. 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.

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