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 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The history of senile dementia begins in the Greco-Roman period with basic concepts of senility by Pythagoras and Hippocrates. During the Middle Ages, the main contribution was by Roger Bacon in 1290. The first textbook of neurology, De cerebri morbis, by Jaso de Pratis (1549), included a chapter on dementia ("De memoriae detrimento"). In the 17th century, Thomas Willis recognized intellectual loss with aging. In the 19th century, Philippe Pinel removed chains from the mentally ill; his student Esquirol wrote the first modern classification of mental disease, including senile dementia. In 1860, Morel recognized brain atrophy with aging. The modern history of vascular dementia began in 1896, when Emil Kraepelin in his textbook Psychiatrie included "arteriosclerotic dementia" among the senile dementias, following the ideas of Otto Binswanger and Alois Alzheimer, who had differentiated clinically and pathologically arteriosclerotic brain lesions from senile dementia and from neurosyphilitic general paresis of the insane. Binswanger's and Alzheimer's contributions are reviewed in detail.
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PMID:A historical review of the concept of vascular dementia: lessons from the past for the future. 1060 75

Senile dementia was the third most common admission diagnosis for New York psychiatric hospitals at the start of the twentieth century and the distinction between vascular and senile dementia was understood by psychiatrists even then. The term Alzheimer's disease (AD) was originally introduced to distinguish a pre-senile dementia from the common general paresis, but Alzheimer raised the possibility that pre-senile AD might not be distinguishable in clinical or histological terms from senile dementia. By the late 1970s it had become clear that the most common disorder producing dementia in elderly people was clinically and pathologically identical to pre-senile AD. AD is malignant, reducing remaining life expectancy by almost half and raising the risk of death over five years threefold (cancer raises it fourfold). Synapse loss associated with beta amyloid oligomers is a strong determinant of cognitive decline in patients with AD. Tau-containing neurofibrillary tangles usefully track disease severity. Unmodifiable risk factors include mutations in three genes which affect the production or metabolism of beta amyloid, the risk factor gene for Apolipoprotein [see symol in text]4 and female gender. The overriding risk factor is age, the prevalence of AD doubling with every five years of age until 90. Low education, head injury and low folate levels are examples of potentially modifiable risk factors. Since a delay of onset of five years would halve the number of patients with the disease, clinical trials for such putative protective factors as estrogens, folic acid, vitamin E, statins, and NSAIDs have begun. Cognitive and leisure activity may be protective against the development of AD but any protective function can only be confirmed by clinical trials.
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PMID:Luigi Amaducci memorial award winner's paper 2003. A neurologist's view of Alzheimer's disease and dementia. 1555 52