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Alzheimer’s disease is the most common subtype of dementia. This disease is diagnosed in approximately two thirds of all cases of dementia (1). According to current diagnostic criteria, a diagnosis of Alzheimer’s disease is considered probable when alternative causes of dementia have been excluded (2, 3). A clinical diagnosis of dementia is often made according to the Diagnostic and Statistical Manual of Mental Disorders, Third Edition, Revised (DSM-III-R) criteria for dementia, with a subdiagnosis of Alzheimer’s disease made according to the National Institute of Neurological and Communicative Disorders and Stroke–Alzheimer’s Disease and Related Disorders Association (NINCDS-ADRDA) criteria (2). The pathogenesis of Alzheimer’s disease is largely unknown. In short, the most frequently used explanation is that unknown genetic or environmental factors initiate a cascade of neuropathologic events that feature accumulation of β-amyloid and neurofibrillary tangles. This process is clinically characterized by a long latent phase, then a prodromal stage with a gradual and progressive decline in long-term episodic memory and impairment of other cognitive domains of mental functioning (4). Eventually, the person crosses a threshold of cognitive loss, after which the full syndrome is evident (5).

Pharmacologic Agents Associated with a Preventive Effect on Alzheimer's Disease: A Review of the Epidemiologic Evidence