Abstract
Alzheimer’s disease (AD) is the most prevalent form of dementia in the aged population. Definitive diagnosis of AD is based on the presence of senile plaques and neurofibrillary tangles that are identified in postmortem brain specimens. The formation of AD specific lesions is attributed to the pathological accumulation of either extracellular amyloid beta (A) peptide or intraneuronal hyperphosphorylated Tau protein. Constituents of the lesions are prone to promoting synaptic deficits, leading to memory impairments. However, besides targeting lesions, other pathways maybe of interest to control, such as inflammatory processes. Epidemiological studies report beneficial effects of caffeine, a nonselective antagonist of adenosine receptors. In the present review, we discuss the impact of caffeine and the adenosinergic system in AD pathology as well as consequences in terms of pathology and therapeutics.
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