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Aluminium in Alzheimer's disease: Are we still at a crossroad?
journal contribution
posted on 2005-01-01, 00:00 authored by Veer GuptaVeer Gupta, S Anitha, M L Hegde, L Zecca, R M Garruto, R Ravid, S K Shankar, R Stein, P Shanmugavelu, K S Jagannatha RaoAluminium, an environmentally abundant non-redox trivalent cation has long been implicated in the pathogenesis of Alzheimer's disease (AD). However, the definite mechanism of aluminium toxicity in AD is not known. Evidence suggests that trace metal homeostasis plays a crucial role in the normal functioning of the brain, and any disturbance in it can exacerbate events associated with AD. The present paper reviews the scientific literature linking aluminium with AD. The focus is on aluminium levels in brain, region-specific and subcellular distribution, its relation to neurofibrillary tangles, amyloid beta, and other metals. A detailed mechanism of the role of aluminium in oxidative stress and cell death is highlighted. The importance of complex speciation chemistry of aluminium in relation to biology has been emphasized. The debatable role of aluminium in AD and the cross-talk between aluminium and genetic susceptibility are also discussed. Finally, it is concluded based on extensive literature that the neurotoxic effects of aluminium are beyond any doubt, and aluminium as a factor in AD cannot be discarded. However, whether aluminium is a sole factor in AD and whether it is a factor in all AD cases still needs to be understood.
History
Journal
Cellular and Molecular Life SciencesVolume
62Issue
2Pagination
143 - 158Publisher DOI
ISSN
1420-682XPublication classification
C1.1 Refereed article in a scholarly journalUsage metrics
Keywords
Science & TechnologyLife Sciences & BiomedicineBiochemistry & Molecular BiologyCell BiologyAlzheimer's diseaseneurofibrillary tanglesamyloid betaaluminiumoxidative stresscell deathgeneticsINDUCED NEUROFIBRILLARY DEGENERATIONDIALYSIS-ASSOCIATED ENCEPHALOPATHYAMYLOID PRECURSOR PROTEINDRINKING-WATERBRAIN ALUMINUMTRANSFERRIN C2A-BETASENILE PLAQUESTRACE-ELEMENTSINDUCED NEURODEGENERATIONPhysiology
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