Caffeine and alzheimer's disease

Abstract

Caffeine is a commonly used, unregulated psychoactive substance in use by up to 90% of adults in North America on a daily basis. Caffeine acts by competitively inhibiting the inhibitory effects of adenosine, thus enhancing the action of other neurotransmitters i.e. epinephrine, norepinephrine, acetylcholine, dopamine and serotonin. A1 and A2a Adenosine receptors in the basal ganglia are inhibited specifically, and competitively by caffeine. In both animal and human studies, 300-500 mg per day of caffeine consumption has been shown to both acutely and chronically reduce blood plasma, and brain levels of amyloid-beta protein, a central player in the development of Alzheimer's Disease. Cognitive decline, dementia and Parkinson's Disease are also positively affected by long term caffeine consumption. Evidence also exists demonstrating improvement of already lost memory and cognitive function of Alzheimer's Patients. The various individually active metabolites of Caffeine (paraxanthine, theophylline and theobromine) have physiological activity yet their administration alone does not produce similar cognitive benefits, nor alter blood and brain levels of amyloid-beta, indicating the key importance of caffeine itself.