The 12th edition of Synapse is now available at Dr. Deborah Serani’s blog.

One of my favorite includes the recent prion-like nucleation-polymerization reaction that has been found in beta Amyloid proteins (whose aggregation results in plaques in Alzheimer’s). Although, the polymerization reaction and spread-by-shape mechanism was seen only in those who were genetically susceptible to Alzheimer’s and the effect was very specific (thus ruling out infection hypothesis), yet this spread-by-shape may explain some of the prognosis of the illness following the initial trigger.

With some recent new studies indicating that some picornavirus strains my affect memory, an infection triggering hypothesis, followed by malignant spread due to spread-by-shape-mechanism-of-prions in those genetically susceptible may help explain the disease etiology.

Prion mechanism, has been hypothesized as having evolved to prevent cannibalism. Thus, the genes that confer vulnerability to TSE seem to have been fixated in humans; in the case of Alzheimer’s the evolutionary rationale may be similar and may have arisen to prevent cannibalism of old family members or even old animals in general. If an infected senile animal, on consumption, confers disease vulnerability on the human who has consumed the meat, then this sort of behavior too may be selected against. As in India (a predominantly vegetarian country), the prevalence of Alzheimer’s disease among 70- to 79-year olds is 4.4-fold less than that of the United States, I am tempted to consider the possibility that some of the triggering of Alzheimer’s may be due to infected senile-animal food consumption.

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