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By Satkari Mookerjee

An Exposition of the Philosophy of severe Realism as Expounded via the varsity of Dignaga

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This was accomplished for the first time in 1971 and then over the followed couple of years by several research groups starting with efforts headed by George Glenner and Earl Benditt. These investigators found that the proteins were not the same, but rather each one amyloid protein was unique to the disease associated with their presence. The primary structure, that is, the amino acid sequences, of the amyloidogenic proteins found in different tissues and organs had little resemblance to one another; they normally fold into a diverse set of 3D structures, and unlike the amyloids are soluble.

Figlewicz, D. , et al. (1983). Mutations in Cu/Zn superoxide dismutase gene are associated with familial amyotrophic lateral sclerosis. Nature, 362, 59–62. Spillantini, M. , Crowther, R. , & Goedert, M. (1998). α-Synuclein in filamentous inclusions of Lewy bodies from Parkinson’s disease and dementia with Lewy bodies. Proceedings of the National Academy of Sciences of the United States of America, 95, 6469–6473. St. George-Hyslop, P. , Tanzi, R. , Polinsky, R. , Haines, J. , Watkins, P. , et al.

These susceptibility findings provide valuable information on how the diseases develop. How these data all fit together to produce the various PMDs remain a great unsolved challenge in the field today. Lastly, it must be pointed out that sporadic cases of AD are far-more prevalent than familial ones. They account for more than 95 % of all the cases of Alzheimer’s disease! In these instances, there is no family history of the disease and, thus, a specific gene that is responsible cannot be identified.

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