Abstract

The Potential Impact of Methyl Mercury Toxicity Within Alzheimer’s Disease Progression, Considering the Tau Hypothesis, Neurovascular Hypothesis as Well as The Potential Role of Dietary and Botanical Mercury Chelators and that of Pharmacologically Developed Agents for Disease Management

Highlights

  • The results showed that among the 286 autopsied brains of 544 participants, brain mercury levels positively correlated with the number of seafood meals consumed per week (ρ = 0.16; P = .02)

  • In models adjusted for age, sex, education, and total energy intake, seafood consumption (≥1 meal[s]/week) was significantly correlated with less Alzheimer disease pathology including lower density of neuritic plaques (β= −0.69 score units [95% CI, −1.34 to −0.04]), less severe and widespread neurofibrillary tangles (β= −0.77 score units [95% CI, −1.52 to −0.02]), and lower neuropathologically defined Alzheimer disease (β= −0.53 score units [95% CI, −0.96 to −0.10]) but only among apolipoprotein E (APOE ε4) carriers

  • The study concluded that in a cross-sectional analysis, moderate seafood consumption was correlated with less Alzheimer disease neuropathology

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Summary

Objectives

Objectives of Research ReviewThe objectives of this research review are to: a. Further review and enhance current literature and research surrounding both pharmacological and naturally occurring chelation for Methylmercury Toxicity, whilst linking this with ADZ progression for the purpose of dietary considerations for disease progression and or regression. B. Further enhance research into potential dietary links to chelation and ADZ progression through Methylmercury Toxicity. C. Further identify common factors in Methylmercury Toxicity and ADZ progression in relation to potential naturally occurring dietary sources. The biochemical steps of normal and abnormal physiological processing are absolutely essential in order to unwind the steps for a potential reversal process This being said, at this current time, the application of being able to unwind the Tau protein mis-fold is not possible, additional understanding could further manage and identify potential risk factors of ADZ

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