A study has confirmed the association between aluminum exposure and Alzheimer’s disease. There is a growing body of research linking aluminum exposure to Alzheimer’s disease. In the current study, researchers discovered considerable amounts of aluminum in brain tissue from donors who had familial Alzheimer’s disease. A high degree of aluminum located together with the amyloid-beta protein was also discovered, leading to early onset of Alzheimer’s. This is the 2nd study which confirms significantly high accumulation of aluminum in the brain’s of individuals with familial Alzheimer’s disease, but it’s the 1st study to reveal a clear link between the location of aluminum and amyloid-beta in Alzheimer’s, showing how intimately woven aluminum and amyloid-beta are in the neuropathology.
An aluminum and amyloid-beta association was suggested more than 40 years ago. A prior study revealed significant accumulations of aluminum brain tissue from donors diagnosed with familial Alzheimer’s disease. Researchers from the current study wanted to further understand this relationship by measuring aluminum in the brain tissue of a group of donors who had familial Alzheimer’s disease with a specific mutation. This mutation results in elevated amyloid-beta levels, early onset of Alzheimer’s disease, and an aggressive disease etiology. A comparison was then made of aluminum levels from a control set of brain tissues from donors without neuropathological disease diagnosis. Aluminum-specific fluorescence microscopy imaging was also used for investigating the aluminum amyloid-beta relationship in familial Alzheimer’s disease.
The study results showed that the donors with the genetic mutation had brain tissue with universally high aluminum content, with 42% of tissues having an aluminum level that is considered as pathologically significant, and significantly higher levels in comparison to the control group. Aluminum deposits were identified with the imaging studies in all brain tissues examined. They were mainly located together with amyloid-beta in senile plaques and sometimes in the brain vasculature. Aluminum was also discovered in intracellular compartments independently from amyloid-beta which include neuronal and glia axons. The outcomes strongly indicate that genetic predispositions which are known to increase amyloid-beta in brain tissue also predispose people to accumulate and retain aluminum in brain tissue.
Researcher Dr. Exley said that the localization of aluminum together with amyloid-beta strengthens the association of aluminum to Alzheimer’s pathogenesis. Increased amyloid-beta in brain tissue could be envisaged as a response to high aluminum content levels, or the accumulation of amyloid-beta is promoted by aluminum.