Aluminium in Alzheimer's disease: are we still at a crossroad? Review uri icon

Overview

abstract

  • 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.

publication date

  • January 1, 2005

Research

keywords

  • Aluminum
  • Alzheimer Disease
  • Brain

Identity

Scopus Document Identifier

  • 19944433257

Digital Object Identifier (DOI)

  • 10.1007/s00018-004-4317-3

PubMed ID

  • 15666086

Additional Document Info

volume

  • 62

issue

  • 2