ABSTRACT
Alois Alzheimer (1898) felt that senile dementia was the most frequent neuropsychiatric disorder. Alzheimer and several other authors knew that a small proportion of patients developed signs of a ‘senium praecox’ (Gowers 1902). He stated: ‘In some people a premature ageing or degeneration occurs, preferably affecting the central nervous system.’ When Alzheimer published his famous first case of ‘Alzheimer’s disease’ (AD) he was intrigued by the early onset of a dementia syndrome and the abundant intraneuronal neurofibrillary tangles in the patient’s neocortex, which had never been seen before in a patient with such early onset of illness. In this patient, the clinical course and the neuropathological changes, particularly the neuronal loss in the superficial layers of the neocortex were excessively severe. Kraepelin (1910) decided that this presenile form of degenerative dementia with plaques and neurofibrillary tangles should bear Alzheimer’s name. Initially this term was reserved for severe forms of presenile dementia with abundant plaques and neurofibrillary tangles, until a number of researchers felt that the clinical and neuropathological differences between the presenile and the senile manifestations of primary degenerative dementia were insufficient to define separate diagnostic entities (Albert, 1963; Lauter and Meyer, 1968; Corsellis, 1969). This new unitarian concept had a number of important implications. The concept of Alzheimer’s disease, originally having a narrow focus, now became extended and softened. Senile dementia could no longer be accepted as the inevitable consequence of normal ageing, but became a disease. The number of patients with AD increased enormously. The economic burden and
obligation became obvious. The main risk factor was identified: age.
