Alzheimer's disease: a review concerning immune response and microischemia

Alzheimer's disease (AD), as we think of it today, is the idiopathic progre ssive loss of cognitive function over a period of several years. The risk o f late onset dementia increases significantly with each decade of life such that half of the population over the age of 80 is vulnerable to this disea se (1). We know that proper functioning of the central nervous system is de pendent on adequate blood flow to remove harmful metabolic products and sup ply nutrients such as glucose and oxygen to the brain. It has been suggeste d that cerebral hypoperfusion causes AD (2). Mean cerebral blood flow decre ases with age and with sclerosis of cerebral blood vessels. Blood flow appe ars to increase in stimulated areas of the brain during different activitie s. However, there is a derangement of blood flow in disease states; this ha s been documented in the temporal robes of AD patients, (3,4). English lang uage journal articles located by a MEDLINE search (1960-1999) were reviewed with consideration to the hypothesis that Alzheimer's disease is an autoim mune disease initiated by low oxygen tension and microischemia. Inflammatio n is thought to be a known contributor to the pathology of AD (5,6). Recent reports support the concept of autoimmunity as a final common pathway of n euron death, particularly for cholinergic in Alzheimer's disease (6). A mod el of Alzheimer's disease is proposed and related research and treatment mo dalities are discussed. (C) 2001 Harcourt Publishers Ltd.