The environmental presence of aluminium (Al) is widespread and a significant human absorption of Al salts occurs by way of diet and drinking water. Whether this can affect the incidence and progression of age-related neurological diseases, notably Alzheimers disease remains controversial. However, there are increasing indications that Al can cause inflammatory changes within the central nervous system both in humans and in experimental animals. It is also known that basal levels of immune activation are elevated within the aging brain even in the absence of recognized inflammatory stimuli. Since, following activation, the immune system of the brain is unable to rapidly return to basal levels, this may in part reflect an accumulation of the lifespan history of the organisms immune responses. Even greater levels of inflammatory activity are found in brains of those suffering from several types of distinct neurodegenerative disorders. Since most of these disorders are idiopathic and not strongly linked to a specific genetic trait, it must be assumed that environmental factors can initiate or advance the development of such disorders. Data from experimental animals and from post-mortem human tissue, together with epidemiological evidence, make Al a strong candidate for being a significant contributor to overall incidence of more than one neurodegenerative disorder.
Keywords: Aluminium, aging, neurotoxicity, neurodegenerative diseases, ALUMINIUM EXPOSURE, ANIMAL STUDIES, encephalopathy, dopaminergic neurotoxin, accumulate evidence
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