From the pathological point of view, there is spread of atrophy of the cerebral cortex with secondary enlargement of the ventricular system, with characteristic lesions: neuritic plaques (containing amyloid AB), or neurofibrillary tangles and amyloid accumulation in cerebral arterial wall AB.
There also, the loss of neurons. Alzheimer is the most common cause of mental disorders in the Western world and constitutes 75% of all dementia. The incidence (number of new cases) and prevalence (the proportion represented in population) increases almost exponentially with age (40-90 years old, from the point where the increase is moderate). The prevalence of Alzheimer is about 1% in the decade of 60, but more than in 80 years reached 20-40%.
Alzheimer disease is a disease of long evolution, and multicausal, it involved in heredity (genetics) and environmental factors. Genetic factors: the specific genetic changes have been observed in patients with this disease and has been attributed at least in part with the origin of and the same generation. Among them are: Gene amyloid precursor protein (APP) located on chromosome 21 gene for presenilin 1 (PS-1) located on chromosome 14, Gene presenilin 2 (PS-2) located on chromosome 1 and Gene Epsilon Rev. Other genes that change can be attributed to EA, can be found on chromosomes 10, 12 and 17, and HLA-A2.
