There has been a strong link between human exposure to aluminium and the incidence of Alzheimer's disease for half a century or more.
The aluminium content of brain tissue in late-onset or sporadic Alzheimer's disease is significantly higher than is found in age-matched controls.
Even higher levels of aluminium have been found in individuals, diagnosed with an early-onset form of sporadic (usually late onset) Alzheimer's disease, who have experienced an unusually high exposure to aluminium through the environment (e.g. Camelford) or through their workplace.
Researchers have now shown that some of the highest levels of aluminium ever measured in human brain tissue are found in individuals who have died with a diagnosis of familial Alzheimer's disease.
The levels of aluminium in brain tissue from individuals with familial Alzheimer's disease are similar to those recorded in individuals who died of an aluminium-induced encephalopathy while undergoing renal dialysis.
Familial Alzheimer's disease is extremely rare, perhaps 2-3% of all cases of Alzheimer's disease. Its bases are genetic mutations associated with a protein called amyloid-beta, a protein which has been heavily linked with the cause of all forms of Alzheimer's disease.
Individuals with familial Alzheimer's disease produce more amyloid beta and the onset of the symptoms of Alzheimer's disease are much earlier in life.
This new research may suggest that these genetic predispositions to early onset Alzheimer's disease are linked in some way to the accumulation of aluminium (through 'normal' everyday human exposure) in brain tissue.
Since aluminium is a known neurotoxin its accumulation in human brain tissue can only contribute to any ongoing disease state or toxicity.
The paper has been published in the Journal of Trace Elements in Medicine and Biology.
Article: Aluminium in brain tissue in familial Alzheimer's disease, Ambreen Mirza, Andrew King, Claire Troakes, Christopher Exley, Journal of Trace Elements in Medicine and Biology, doi: 10.1016/j.jtemb.2016.12.001, published online 9 December 2016.