A new study, published earlier this week in the Journal of Alzheimer’s Disease, supports a 40-year theory suggesting an association between human exposure to aluminum and Alzheimer’s disease. According to the study, previous research measured a high content of aluminum in brain tissues from donors with familial Alzheimer’s disease (AD). To confirm and elaborate upon prior research, this team measured aluminum in the brain tissues of a cohort of Colombian donors with familial AD who shared a specific mutation.
The mutation shared by the Colombian cohorts is PS1-E280A, which, according to the study, results in elevated cortical levels of amyloid-beta, early-onset disease, and aggressive disease etiology. The aluminum levels in these brain tissues were compared to control brain tissues from donors with no neuropathological disease.
Using aluminum-specific fluorescence microscopy imaging, the researchers discovered that 42% of the tissues from the Colombian cohort had an aluminum concentration pathologically significant above the standard accepted level. Every tissue sampled featured aluminum deposits. The study reports that approximately two-thirds of aluminum deposits were identified in grey matter. The deposits were located in addition to amyloid-beta in senile plaques and within brain vasculature. Additionally, aluminum was found apart from amyloid-beta in intracellular compartments, including glia and neuronal axons. There were no significant differences in aluminum content between lobes and no significant relationship between the age of donor and aluminum content. There was, however, a significant difference between genders, with females having higher aluminum content than males.
The researchers suggest that aluminum and amyloid-beta are linked in the neuropathology of familial AD. In a news release from IOS Press regarding the study, lead investigator Christopher Exley, Ph.D. stated, “This is the second study confirming significantly high brain accumulation in familial Alzheimer’s disease, but it is the first to demonstrate an unequivocal association between the location of aluminum and amyloid-beta in the disease. It shows that aluminum and amyloid-beta are intimately woven in the neuropathology.”
The results of this study also suggest that genetic predispositions known to increase amyloid-beta, such as the mutation featured in this study, may also predispose individuals to accumulate and retain aluminum in brain tissue. Dr. Exley also said, “One could envisage increased amyloid-beta in brain tissue as a response to high levels of aluminum content, or that aluminum fosters the accumulation of amyloid-beta. Either way, the new research confirms my resolve that within the normal lifespan of humans, there would not be any AD if there were no aluminum in the brain tissue. No aluminum, no AD.”