Aluminium in Alzheimer's disease: Are we still at a crossroad?

Veer Bala Gupta, S. Anitha, M. L. Hegde, L. Zecca, R. M. Garruto, R. Ravid, S. K. Shankar, R. Stein, P. Shanmugavelu, K. S. Jagannatha Rao

Research output: Contribution to journalReview articlepeer-review

280 Scopus citations


Aluminium, 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.

Original languageEnglish (US)
Pages (from-to)143-158
Number of pages16
JournalCellular and Molecular Life Sciences
Issue number2
StatePublished - Jan 1 2005


  • Aluminium
  • Alzheimer's disease
  • Amyloid beta
  • Cell death
  • Genetics
  • Neurofibrillary tangles
  • Oxidative stress

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Cell Biology


Dive into the research topics of 'Aluminium in Alzheimer's disease: Are we still at a crossroad?'. Together they form a unique fingerprint.

Cite this