ears of symptom onset). At autopsy neuropathological findings were even more unusual. One quarter to one third of cerebral cortical neurons had disappeared, and many of the remaining neurons contained thick, coiled masses of fibers within their cytoplasm (Beach, 1987). Alzheimer speculated that a chemical change had occurred in the neurofibrils. Thus Alzheimer described for the first time neurofibrillary tangles (NFT), which togther with SP are considered to be the neuropathologocal halmarks of AD (See Appendix 1 for Alzheimer's original drawing of NFT). Alzheimer concluded that he discovered a unique entity separate from senile dementia as it was known at that time. However, it was not until 1910 when Kraepelin discussed the condition in the 8th edition of his textbook Psychiatrie that AD gained official recognition.The second decade of the twentieth century witnessed the end of the golden period in dementia research (this only lasted until the 1960's when a renaissance occurred). U'Ren cites two reasons as the principal causes (Pitt, 6). First the rise of Freud's Psychodynamic theory caused American psychiatry to swerve in the direction of psychological explanations. Second Kraepelin's descriptions and classifications seemed to leave little room for therapeutic efforts or optimism.Notwithstanding, several key contributions have been made in the 'Dark Ages' of dementia research. In 1920 Creutzfeldt, and in 1921 Jakob, described cases of dementia with pyramidal and extrapyramidal signs. Although it is now thought that only Jakob's case was typical of the disease the Creutzfeldt-Jakob disease (CJD) was given to the world. The year 1936 saw an important change with regards to the diagnosis of AD. Before 1936 it was common practice to provide a diagnosis based on both clinical and pathological characteristics. However, when it became clear that many non-demented people had some senile plaques and neurofibrillary tangles, Je...
