In a recent post – A role for aluminium in multiple sclerosis, we highlighted that individuals with multiple sclerosis excrete high amounts of aluminium in their urine.
It was also demonstrated that regular drinking of a silicon-rich mineral water (Why-everyone-should-drink-silicon-rich-mineral-water) facilitated the urinary excretion of aluminium. Elevated urinary excretion of aluminium exacerbated in the short term by drinking silicon-rich mineral water is indicative of a high body burden of aluminium (http://pubs.rsc.org/en/content/articlelanding/2013/em/c3em00374d#!divAbstract).
However, the systemic origin of excreted aluminium in multiple sclerosis remained unknown though we speculated that it might be brain tissue, reflecting known intimate associations between aluminium and myelin. The latter being the primary target biomolecule in the aetiology of multiple sclerosis.
To understand if aluminium is present in brain tissue in multiple sclerosis we obtained, from the Multiple Sclerosis Society Brain Bank, samples of frozen cortex from 14 individuals who died with diagnosis of multiple sclerosis. Further, we obtained fixed tissues from two of these individuals to investigate the location of any aluminium found in the brain. The results of this research are now published in the International Journal of Environmental Research and Public Health (http://www.mdpi.com/1660-4601/15/8/1777 ).
Aluminium was found in all tissues investigated. We consider a concentration of aluminium above 2g/g dry wt. (2ppm) to be of concern and one third of all tissues examined (332 in total) had a concentration of aluminium above this level. As has been previously observed in familial AD (https://www.hippocraticpost.com/ageing/no-aluminium-no-alzheimers-disease/) and autism https://www.hippocraticpost.com/infection-disease/aluminium-and-autism/) some tissues in multiple sclerosis contained significant deposits of aluminium, probably reflecting the known focal distribution of aluminium in brain tissue. There were no statistically significant differences in aluminium content between lobes (frontal, temporal, occipital and parietal) and similarly for gender and age of donor. The quantitative data do suggest that brain tissue is both a sink for aluminium in multiple sclerosis and one possible source of the high levels of aluminium measured in urine of individuals suffering from the disease.
Quantitative data were supported by aluminium-specific fluorescence microscopy that showed aluminium associated with both extracellular and intracellular compartments in grey and white matter. Specifically, aluminium was found associated with diffuse, plaque-like structures, glial-like cells and corpora amylacea. The latter may be of significance in that they are known to be depositories of both neuronal and non-neuronal degeneration, including myelin, which is known to be a target of aluminium-induced tissue damage.
While it is too early to confirm a role for human exposure to aluminium in the aetiology of multiple sclerosis the significant observations of elevated urinary excretion of aluminium in individuals suffering the disease and excessive accumulation of aluminium in brain tissue post mortem suggest that it cannot be ignored. In addition, burgeoning anecdotal evidence of the benefits of silicon-rich mineral waters in individuals with multiple sclerosis may suggest a future non-invasive therapy.