- Aluminum and Amyloid-β in Familial Alzheimer’s Disease

Note: One wonders why this isn't front page news, instead of a new virus in China (for which is a vaccine is in the works) and rare Ebola (for which a vaccine is coming out.) Alzheimer's affects at least three generations at a pop.  When a grandparent succumbs, Mom and Dad (the sandwich generation) may race through savings and certainly face exhaustion finding care.  Their children pay a price. The parallels in care and behavior to an autism diagnosis are heart breaking. Yet aluminum is prevalent in day to day living and in bolus presence in many vaccines. Deodorants and antacids tout being aluminum free as a selling point.  Still, the topic is verboten when an adjuvant in vaccines.  Vaping and e-Cigs were ripped in headlines quickly for safety concerns. Just last week, I got 3 fliers in the mail from my daughters CT Medicaid talking about the dangers of vaping.  Imagine the expense, and vaping isn't mandated or pushed by doctors, stores, the media. It's a legal product one chooses.   Doctors tell women to have genetic tests for breast cancer, and many women choose preventive mastectomy to prevent the disease. With aluminum and Alzheimers, the aluminum is foisted upon us and we're ridiculed if we say, NO.

Here is a study  that includes Professor Chris Exley that should chill every reader, if the media would only publish it.

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Article type: Research Article

Authors: Mold, Matthewa | Linhart, Carolineb | Gómez-Ramírez, Johanac | Villegas-Lanau, Andrésc | Exley, Christophera; *

Affiliations: [a] The Birchall Centre, Lennard-Jones Laboratories, Keele University, Staffordshire, United Kingdom | [b] Institute of Pharmacy/Pharmacognosy, University of Innsbruck, Innsbruck, Austria | [c] Grupo de Neurociencias de Antioquia, Sede de Investigación Universitaria SIU, Medellín, Colombia

Correspondence: [*] Correspondence to: Professor Christopher Exley, The Birchall Centre, Lennard-Jones Laboratories, Keele University, Staffordshire, ST5 5BG, United Kingdom. E-mail: [email protected].

Keywords: Aluminum in human brain tissue, amyloid-β, familial Alzheimer’s disease, human exposure to aluminum

DOI: 10.3233/JAD-191140

Journal: Journal of Alzheimer's Disease, vol. Pre-press, no. Pre-press, pp. 1-9, 2019
Accepted 16 December 2019
| Published: 13 January 2020

Abstract

Genetic predispositions associated with metabolism of the amyloid-β protein precursor underlie familial Alzheimer’s disease; a form of dementia characterized by early disease onset and elevated levels of cortical amyloid-β. Human exposure to aluminum is linked to the etiology of Alzheimer’s disease and recent research measured a high content of aluminum in brain tissue in familial Alzheimer’s disease. To elaborate upon this finding, we have obtained brain tissues from a Colombian cohort of donors with familial Alzheimer’s disease. We have used established methods to measure the aluminum content of these tissues and we have compared the data with a recently measured dataset for control brain tissues. We report significantly higher levels of aluminum in brain tissues in donors with familial Alzheimer’s disease than in control tissues from donors without neurological impairment or neurodegeneration. We have used aluminum-specific fluorescence microscopy along with complementary imaging for amyloid-β to demonstrate a very high degree of co-localization of these two risk factors in brain tissue in familial Alzheimer’s disease. Aluminum and amyloid-β were co-located in senile plaques as well as vasculature, the latter resembling cerebral amyloid angiopathy. Aluminum was also found separately from amyloid-β in intracellular compartments including glia and neuronal axons. The research has identified an arguably unique association between high brain aluminum content and amyloid-β and allows postulation that genetic predispositions defining familial Alzheimer’s disease underlie this relationship.

INTRODUCTION

An association between aluminum and amyloid-β in Alzheimer’s disease has been postulated for 40 years [1]. It has not been without controversy [2] though a consensus does now support the co-localization if not co-deposition of these two major risk factors in Alzheimer’s disease [3]. Familial Alzheimer’s disease, fAD, is characterized by genetic mutations affecting the expression and metabolism of the amyloid-β protein precursor (AβPP), leading to early onset of disease [4, 5]. One fAD mutation is PS1-E280A (Glu280Ala), a mutation that occurs in a significant cohort of individuals in Colombia. The mutation results in elevated cortical levels of amyloid-β, early disease onset (<50 years of age) and an aggressive disease etiology [6].

Previous research on brain tissue from 12 donors diagnosed as fAD [7] demonstrated significant accumulations of aluminum with 11 of the 12 brains having at least one tissue sample where the concentration of aluminum was defined as pathologically concerning (≥3.00 μg/g dry wt.). Aluminum-specific fluorescence microscopy [8] confirmed the presence of aluminum in these tissues and suggested that the majority of deposits of aluminum were extracellular associated with neuronal and cellular debris. A tentative suggestion was made that aluminum and amyloid-β were co-located in a senile plaque-like structure. Herein we have measured aluminum in brain tissue in Colombian donors carrying the fAD mutation PS1-E280A and compared the data with data for control brains. We have also used aluminum-specific fluorescence microscopy to investigate interrelationships between aluminum and amyloid-β in fAD.

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