Open Access Short Communication

Social Pathology of Dementia

Mario D Garrett*

Professor of Gerontology, San Diego State University, USA

Corresponding Author

Received Date: February 08, 2021;  Published Date: February 23, 2021

When Alois Alzheimer first discussed his findings about plaques and tangles in dementia at the 1906-7 Psychiatric Convention of the South West German Society in Tubingen there was no discussion and no interest shown. His first attempt to publish the findings was rejected. It was already known at the time dementia results in the biological markers of plaques and tangles. It was Emil Kraepelin, Alois Alzheimer’s supervisor, that pushed for the publication of these observations and later adopted Alzheimer’s eponym for the disease. But this was all about political and not science. The argument was that although these biological markers were common, it was not common among younger people, and hence the need for a new disease. It was an ageist argument where a disease is valid because it afflicts younger people. However, even this distinction was eliminated. In 1976 Richard Katzman combined senile (“old age”) dementia with Alzheimer’s disease. He did this not to reclaim science but to gain a larger constituency for Alzheimer’s disease in order to promote the mission of the recently established United States National Institute on Aging (NIA). Again, politics won above science. But this confabulation resulted in Alzheimer’s disease research becoming confused and lacking theory. The resulting confusion has recently led the NIA to start promoting the diagnoses of Alzheimer’s disease based on biological markers and not on clinical diagnosis, For the first time in the history of medicine, there is a push to diagnose a clinical disease based on biology while ignoring clinical evidence. This is the holy grail of psychiatry. However, evidence contradicts NIA’s aspiration. These biological markers—colloquially referred to as plaques and tangles —are not consistently correlated to Alzheimer’s disease or dementia. Half of clinically diagnosed oldest-old with dementia have insufficient neuropathology to account for their dementia, while thirty to fifty percent of older adults without dementia meet the neuropathological criteria for Alzheimer’s disease, , , , , , . Among older people, the correlation between Alzheimer’s disease neuropathology and its clinical expression declines. It is disturbing that we have known this fallacy for more than a century. Yet we continue to promote this simplistic cause of dementia and the only way to change this theoretical rigidity is to think more creatively outside of the political (and funding) interests.

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