The Putative role of Environmental Aluminium in the Development of Chronic Neuropathology in Adults and Children
Metabolic Brain Disease, July 2017
The conceptualisation of autistic spectrum disorder and Alzheimer’s disease has undergone something of a paradigm shift in recent years and rather than being viewed as single illnesses with a unitary pathogenesis and pathophysiology they are increasingly considered to be heterogeneous syndromes with a complex multifactorial aetiopathogenesis, involving a highly complex and diverse combination of genetic, epigenetic and environmental factors. One such environmental factor implicated as a potential cause in both syndromes is aluminium, as an element or as part of a salt, received, for example, in oral form or as an adjuvant. Such administration has the potential to induce pathology via several routes such as provoking dysfunction and/or activation of glial cells which play an indispensable role in the regulation of central nervous system homeostasis and neurodevelopment. Other routes include the generation of oxidative stress, depletion of reduced glutathione, direct and indirect reductions in mitochondrial performance and integrity, and increasing the production of proinflammatory cytokines in both the brain and peripherally. The mechanisms whereby environmental aluminium could contribute to the development of the highly specific pattern of neuropathology seen in Alzheimer’s disease are described. Also detailed are several mechanisms whereby significant quantities of aluminium introduced via immunisation could produce chronic neuropathology in genetically susceptible children. Accordingly, it is recommended that the use of aluminium salts in immunisations should be discontinued and that adults should take steps to minimise their exposure to environmental aluminium.
Evidence of the neurotoxicity of aluminium cations (Al3+) includes: an association between chronic aluminium exposure and the development of AD; the involvement of aluminium adjuvants in the development of ASIA; and epidemiological evidence pointing to an association between the use of aluminium adjuvants and ASD. There is good evidence to suggest that immunisation may accelerate or precipitate the transition between subclinical and overt symptomatic autoimmune conditions within the first 30 days post-immunisation, particularly in those younger than 50 years of age. The immune response to immunisation may be influenced by variations in HLA, TLR and cytokine genes. Moreover, aluminium exposure is associated with the production of pro-inflammatory cytokines and chemokines and with the development of chronic oxidative stress, mitochondrial dysfunction and glial activation or dysfunction; these changes in turn are associated with ASD.