The etiology of Alzheimer’s disease (AD) is totally unknown, despite the vigorous efforts in several laboratories during recent years to solve this mystery. The lack of success in delineating one or more underlying etiologies for AD may be due to the fact that there are no animal models directly derived from this disease. Further, almost all investigative studies of AD concentrate on end stages of disease where fully developed lesions are apparent. In searching for potential etiologies of AD, such fully developed cases might represent the wrong end of the disease spectrum and be relatively uninformative with respect to original inciting events (E.E. Manuelidis 1985). In autopsy brains of individuals with AD, there is clear evidence of a neuronal cemetery, with neuronal devastation and gliosis in selected brain regions. Tangles and more widespread plaques and amyloid deposits are the remaining skeletons and bushes associated with end stage neuronal degeneration. We have postulated that these very important cardinal lesions are the end result rather than the originating causes of AD. Although these sequelae and their associated biochemical processes may play a role in the progression of AD, the initial inciting events are not known. Without underestimating the value of the data generated by our colleagues on the biochemistry and histology of these lesions, we concentrate, rightly or wrongly, on the concept that a transmissible agent may underlie AD during very early stages of disease.
Buffy Coat Spongiform Change Select Brain Region Transmissible Agent Fresh Buffy Coat
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