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Alzheimer's Disease

Published: 2020
SYNOPSIS

It is critical to address biological etiologies such as mercury toxicity in the elderly population diagnosed with Alzheimer’s, but end organ damage may not be reversible.

TITLE

One man’s swordfish story: The link between Alzheimer’s disease and mercury exposure

CITATION

Foley MM, Seidel I, Sevier J, Wendt J, Kogan M. One man’s swordfish story: The link between Alzheimer’s disease and mercury exposure. Complement Ther Med. 2020 Aug;52:102499. doi: 10.1016/j.ctim.2020.102499. Epub 2020 Jul 2. PMID: 32951747.

SUMMARY

It is well-documented that when mercury levels surpass the permissible value, individuals experience a myriad of symptoms that include chronic fatigue, dizziness, and loss of appetite. Mercury is also known to be one of the most potent neurotoxins. This case study depicts a 91- year-old who presented with cognitive decline diagnosed as Alzheimer’s disease. This patient was found to have severely elevated mercury levels caused by consuming high mercury containing fish. Following diet adjustment and detoxification, this patient’s cognitive impairment significantly improved in proportion to the decline in methylmercury level. One year later, his cognition and functional status rapidly and unexpectedly declined. A computed tomography (CT) scan revealed multiple new lacunar subacute strokes. Thus, it is critical to address biological etiologies such as mercury toxicity in the elderly population diagnosed with Alzheimer’s, but end organ damage may not be reversible.

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Published: 2020
SYNOPSIS

Quantitative analyses suggest increased brain aluminium content in a number of neurodegenerative diseases including familial Alzheimer’s disease, congophilic amyloid angiopathy, epilepsy and autism.

TITLE

Imaging of aluminium and amyloid β in neurodegenerative disease

CITATION

C. Exley, M.J. Mold; Imaging of aluminium and amyloid β in neurodegenerative disease. Heliyon 6 21 April 2020; https://doi.org/10.1016/j.heliyon.2020.e03839.

SUMMARY

Recent research has confirmed the presence of aluminium in human brain tissue. Quantitative analyses suggest increased brain aluminium content in a number of neurodegenerative diseases including familial Alzheimer’s disease, congophilic amyloid angiopathy, epilepsy and autism. Complementary aluminium-specific fluorescence microscopy identifies the location of aluminium in human brain tissue and demonstrates significant differences in distribution between diseases. Herein we combine these approaches in investigating associations between aluminium in human brain tissue and specific disease-associated neuropathologies.

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