Is Alzheimer?s Disease A Medical Notion Of Dementia Worth Keeping In Neuroscience | 12525
Journal of Alzheimers Disease & Parkinsonism
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The eponym of Alzheimer?s disease has been around for more than one century from 1910. Its diagnosis varies: from senile
dementia to senium praecox (for both pre-senile and senile dementia) to Mild Cognitive Impairment (MCI) leading to AD as
the most feared form of dementia. Such uncertainties create serious problems which most neuroscientists have refused to admit.
They prefer to: perpetuate the eponym even to 2006 in Science to keep it alive for contrast with other forms of dementia; debate
on its cause, by regarding AD as the effect to seek a one-to-one cause-effect relationship, Amyloid Beta Hypothesis, for instance,
which has dominated the field for more than 20 years, albeit to no avail; advocate the intervention or prevention, unaware of AD
as a fiction, resulting from its confusion with dementia, to the extent of using animal models to mimick the existence of AD; take
the liberty on the basis of DSM-IV to assign lesion site unaware that Auguste?s brain at autopsy had widespread atrophy, and that
pre-mortem she had four vascular disorders, one of which, decubitus angina, was the direct cause of her death. I take exception
to such predilections. Dementia can be tested and diagnosed as the effects of brain atrophy; it manifests in a cluster of behavioral
alterations; the causes can be vascular or non-vascular in origin. Thus, dementia is neither a disease nor equivalent to AD. Plaques
and tangles should be called Fischer?s disease (FD) which gradually causes brain atrophy to result progressively from simple
dementia to presbyophrenia in a dichotomy as suggested by Fischer. For this reason, MCI is a cheap reinvention of Fischer?s
dichotomy. Once AD is replaced by FD, neuroscientists and clinicians must be made to understand that: (1) As a medical notion
of dementia, it is not worth keeping; (2) dementia can start from any brain location and will spread, because its cause is wear and
tear as an on-going process of aging; (3) the cause is either vascular or non-vascular in origin, but the effect can vary, resulting in a
cluster of behavioral alterations, language disorder included, from onset of simple dementia to presbyophrenia before the patient
succumbs; and (4) there is no one-to-one cause-effect relation, as the brain atrophy spreads from cortical to cortical, cortical to
subcortical, and/or subcortical to cortical regions.
Fred C. C. Peng is a Behavioral Neuroscientist in the Department of Neurosurgery and the Neurological Institute at Taipei, VGH, Taiwan. He has a
wide range of interests in behavioral alterations caused by differing brain lesions, such as epilepsy, FD, stroke, PD, SCA (spino-cerebellar ataxia),
Pick?s Disease, aphasia, PSP (progressive supranuclear palsy), and many others.
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