Theories on the aetiology and pathogenesis of Alzheimer's disease (AD) are revised. After discussing senile involution, the principal characteristic alterations of AD are presented. These pathological changes include involutive morphological phenomena (neurofibrillar tangles, senile neuritic plaques with varying = amyloid content) and functional phenomena (alterations in energy metabolism, in protein synthesis, and in the neurotransmitter metabolism). Currently it is assumed that the neurons most affected seem to be primarily those of the ascending cholinergic activating system, whose somas are situated in Meinert's basal nucleus. Serotoninergic, adrenergic and peptidergic brainstem neurons and serotoninergic neurons of the cerebral cortex are also affected. Secondary to these, the main pathological alterations, triggered by these disfunctions, are observed in neurons of the neocortex, hippocampus and amygdala. These changes are responsible for the symptoms of AD. The aetiology of these changes may be genetic = (related to chromosoma 21), toxic (aluminium) or infective (slow agents similar to those that cause Creutzfeldt-Jakob disease, kuru and scrapie). Various aetiopathological theories emphasized on immunological or vascular phenomena, altered protein synthesis, etc. It seems to be important that certain neurons are affected in most of degenerative diseases: the high-risk neurons. These neurons could be affected by toxic and environmental factors.