Senile dementia of the Alzheimer type

Abstract

The etiology, pathophysiology, neurochemistry, diagnosis, clinical presentation, and management of senile dementia of the Alzheimer type (SDAT) are discussed. The etiology of SDAT is unclear. The pathophysiologic changes in the brain tissue of patients with SDAT are quantitative rather than qualitative in comparison to normal age-matched controls. The number of neuritic plaques and neurofibrillary tangles are positively correlated to the severity of clinical symptoms and cognitive impairment. There is overwhelming evidence that SDAT is associated with a loss of cholinergic function. Reduction of choline acetyltransferase activity, a cholinergic marker, has been significantly correlated to the severity of dementia. The diagnosis of SDAT is one of exclusion and is based upon clinical presentation and neurological, psychological, and laboratory testing. The clinical presentation of SDAT involves the progressive deterioration of intellectual capabilities. Management of SDAT primarily involves supportive care and symptom control. Attempts to treat the disease with cerebral vasodilators, metabolic enhancers, and neurotransmitter manipulation have been largely unsuccessful. Drug therapy aimed at reversing or retarding the progression of the disease is not recommended. Behavioral disturbances represent the main indication for drug use in patients with SDAT. The antipsychotic agents are considered the drugs of choice. SDAT remains an enigma. The successes in the treatment of the disease are few, but as more information is gathered on the neurochemical abnormalities involved, there is hope that early detection can prevent the disease or at least slow its progression.