Dan R Laks, M.S.
UCLA Neuroscience Research Center
6/21/09
The brain is a main target of aluminum exposure and effect[1] where it induces
neurodegeneration[2-4]. At high levels, aluminum has been demonstrated to inhibit prenatal and postnatal neurodevelopment in humans and animals[5-11]. Aluminum has been shown to target and accumulate in the hippocampus, the primary area of the brain associated with memory
formation[12-14]. Aluminum exposure in human populations has been associated with deficits in cognitive function[15]. Aluminum neurotoxicity in children manifests symptoms of verbal impairment and regression[16]. Although the relationship between aluminum exposure and associated disease such as Alzheimer’s disease[13, 17-23], amyotrophic lateral sclerosis[24], and Parkinson’s disease[24, 25] remains to be fully elucidated, the specific toxicology of aluminum exposure on the endocrine system has been firmly established[26-31]. Aluminum deposits in the pituitary, parathyroid, and adrenals[32] and has been demonstrated to interfere with parathyroid hormone secretion[33-36], insulin like growth factor and T3 levels[37], and the reproductive system[28, 29, 31, 38].
It is thought that inflammation resulting from aluminum exposure may induce learning and memory deficits[39]. Certainly, targeted effects on the endocrine system may affect immune-modulation and produce a pro-inflammatory cascade that responds to targeted aluminum deposition in the hippocampus with resultant neurotoxicity.
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