Illuminating the association between aluminium and familial Alzheimer’s disease

Researchers at Keele University have found aluminium co-located with phosphorylated tau protein, which is an early initiator of familial Alzheimer’s disease.

The new study published in the Journal of Alzheimer’s Disease Reports builds on two previously published studies of familial Alzheimer’s disease (AD) from the same group. The research, which looked at the brain tissue of a cohort of Colombian donors with familial AD, reveals that aluminium is co-located with phosphorylated tau protein, present as tangles within neurons in the brains of patients with early-onset or familial Alzheimer’s disease.

“The presence of these tangles is associated with neuronal cell death, and observations of aluminium in these tangles may highlight a role for aluminium in their formation,” explained lead investigator Matthew John Mold, PhD, Birchall Centre, Lennard-Jones Laboratories, Keele University, Staffordshire, UK.

The previous research indicated extensive co-localisation of aluminium and amyloid-β in brain tissue in familial Alzheimer’s disease.

In the most recent study, the scientists used a highly selective method of immunolabelling, carried out in combination with aluminium-specific fluorescence microscopy.

Co-author, Professor Christopher Exley, commented: “It is of interest and perhaps significance with respect to aluminium’s role in AD that its unequivocal association with tau is not as easily recognisable as with amyloid-β. There are many more aggregates of aluminium with amyloid-β than with tau in these tissues and the latter are predominantly intracellular.”

Dr George Perry, Editor-in-Chief of the Journal of Alzheimer’s Disease, commented: “Aluminium accumulation has been associated with Alzheimer’s disease for nearly half a century, but it is the meticulously specific studies of Drs Mold and Exley that are defining the exact molecular interaction of aluminium and other multivalent metals that may be critical to formation of the pathology of Alzheimer’s disease.”

Dr Mold explained: “The new data may suggest that the association of aluminium with extracellular senile plaques precedes that with intracellular aggregates of tau. These relationships with both amyloid-β and tau may account for the high levels of aluminium observed in the brain tissue of donors with familial AD versus those without a diagnosis of neurodegenerative disease,” concluding that, “tau and amyloid-beta are known to act in synergy to produce neurotoxicity in AD and our data provide new evidence for a role of aluminium in this process.”

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