Alzheimer’s disease is the most common chronic neurodegenerative disease clinically characterized by a progressive impairment of cognitive function. The neurochemical parameter best correlated with cognitive dysfunction is the level of soluble β-amyloid peptide. Experimental evidence suggests that caffeine afford a robust protection against β-amyloid peptide toxicity. We discuss the mechanisms through which caffeine prevents cerebral β-amyloid peptide toxicity.
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