Alzheimer's disease (AD) is the commonest cause of dementia. Although its ethology is unknown, there is increasing evidence in support of the view that an abnormal degradation of the amyloid precursor protein (APP), perhaps influenced by a number of genetic, tisular or environmental factors, may be the primary cause of the many biochemical and morphological disorders that exist in the associative areas of the brain of these patients. Histopathologically it can be shown by the presence of extracellular senile plaques, intraneuronal fibrilar tangles and neuronal loss. There is no specific pharmacological treatment at present to prevent the disease or its development, in spite of the numerous and diverse drugs studied. Many of these studies are methodologically inadequate. The attempt of activating the cholinergic system has deserved special attention. A reversible inhibitor of acetylcholinesterase, tacrine, has been approved in the United States and other countries for the symptomatic treatment of mild to moderate AD, but its use still arises many questions. Different drug and non drug related interventions may be of great value in the care of these patients, and may influence the specific pharmacological treatments. The complexity and heterogeneity of AD and the multiple factors which may take part in its evolution make it necessary to place special attention on the methodological aspects of the clinical trials with new drugs for the treatment of this disease.
|Journal||Revista de neurologia|
|Publication status||Published - 1 Jan 1995|