|| Checking for direct PDF access through Ovid
Alzheimer disease (AD) is a progressive and irreversible dementia syndrome characterized by loss of intellectual capacity in many domains, altered behavior, inability to care for oneself, and, ultimately, neurologic abnormalities. AD results from a cascade of events that leads to the formation of neuritic plaques (containing amyloid proteins) and neurofibrillary tangles (paired, helical filaments containing tau proteins) in the cortex and hippocampus. The cognitive impairments of AD can be traced, in part, to neurotrans-mitter deficits, primarily the loss of chemicals involved in acetylcholine synthesis in the brain; this is known as the cholinergic hypothesis. Risk factors for the disease include age, head injuries, family history of AD or Down's syndrome, sex (i.e., more common in women), and vascular disease. The exact cause of AD is still unknown. Etiologic hypotheses suggest that AD may be caused by genetic abnormalities (primarily on chromosomes 14, 21, and 19), environmental toxins (e.g., aluminum), inflammations due to viruses or infections, defective neuronal plastic capability, or disrupted oxidative metabolism. At present, treatment of AD is limited to addressing the symptoms of the disease. As the mechanisms of AD pathology become better understood, it is hoped that strategies for interfering with those mechanisms can be developed and implemented as treatments to thwart the development or progress of the disease.