Message: Think green
The natural antioxidants in green tea are candidates to be qualified as neuroprotective drugs because of their pharmacological activities. Green tea is particularly rich in flavanols named catechins and, compared to black tea, contains four times more of the catechin fraction.
Source: J Agric Food Chem 2002, 50, 565-570
Caffeine, the most widely consumed behaviourally active substance in the western world (Pharmacol Rev 51 1999: 83–133), has neuroprotective effects in cases of hypoxia and ischaemia (Brain Res Rev 33 2000: 258–274). Does caffeine protect against neurodegeneration in Alzheimer’s disease as it does in Parkinson’s? Researchers from Faculty of Medicine of Lisbon, Portugal, tested the hypothesis that average daily caffeine intake in the period of 20 years before the diagnosis could be lower than caffeine intake in age- and sex-matched healthy people and showed that indeed, people who was diagnosed with Alzheimer’s consumed an average 74 mg (less than one cup) while the controls had about 200 mg. ”These results, if confirmed with future prospective studies, may have a major impact on the prevention of Alzheimer’s,” concluded the researchers (Eur J Neurology, V 9, Issue 4, 2002: 377–382).
In a Canadian study, daily coffee intake decreased the risk of Alzheimer’s by 31% during a 5-year followup in 65-year old people (Am J Epidemiol 2002, 156, 445-453.). The Finland, Italy and the Netherlands Elderly (FINE) Study showed that elderly men drinking three cups of coffee daily had the least cognitive decline (Eur J Clin Nutr 2007, 61, 226-232). Tea drinking (Am J Epidemiol, 2004, 159, 959-967.), or flavonoid intake from tea has not been associated with a reduced risk of dementia. The low coffee consumers in mid-life had the highest occurrence of dementia and Alzheimer’s at late-life, and the highest scores on the depression scale (J Alzheimer’s Disease 16: 2009, 85–91).
One possible mechanism could involve insulin and degrading enzyme that degrades both insulin and amyloid-beta, the most suspected cause of Alzheimer’s (CNS Drugs 17, 2009, 27-45). Another mechanism is via adenosine receptors (caffein mimics effects of adenosine). It has been shown in mice that both caffeine and adenosine prevent amyloid-beta induced cognitive decline (Exp Neurol 203, 2007, 241-245).