Neurochemical hypothesis: participation by aluminum in producing critical mass of colocalized errors in brain leads to neurological disease.
1. Aluminum is an established neurotoxin. Prolonged exposure to even low levels of aluminum permit its chelation and subsequent transport to brain where it is non-uniformly distributed. 2. Available evidence suggests that (i) aluminum interferes with glucose metabolism by inhibiting hexokinase and glucose-6-phosphate dehydrogenase; (ii) it binds to calmodulin and affects numerous phosphorylation-dephosphorylation reactions; (iii) it binds to transferrin and ferritin, affects the function of these proteins which in turn affect iron metabolism. 3. Thus accumulation of aluminum-induced metabolic errors colocalized in specific areas of the brain may lead to neurological disorders.
Joshi
J G
JG
Department of Biochemistry, University of Tennessee, Knoxville 37996-0840.
D000535:Aluminum / Q000633:toxicity*; D000544:Alzheimer Disease / Q000139:chemically induced* / Q000378:metabolism; D000818:Animals; D001921:Brain / Q000187:drug effects* / Q000378:metabolism; D004734:Energy Metabolism / Q000187:drug effects; D005609:Free Radicals; D006801:Humans; D007501:Iron / Q000378:metabolism; D008670:Metals / Q000378:metabolism; D010766:Phosphorylation / Q000187:drug effects
D005609:Free Radicals; D008670:Metals; D000535:Aluminum; D007501:Iron