Mechanisms of aluminium neurotoxicity in oxidative stress-induced ...

INTRODUCTION
3.5 mg may be increased by the frequent use of aluminium-containing antiperspirants
and non-prescription drugs (Weburg and Berstad 1986, Flarend et al. 2001), as well as
by occupational exposure to this metal (Meyer-Baron et al. 2007).
Putative mechanisms of aluminium neurotoxicity
No biological function has yet been attributed to aluminium, for which reason it
is considered a nonessential metal (Yokel 2002a). However, aluminium neurotoxicity
was first outlined by Dölken in 1897. Since then, aluminium accumulation in the brain
has been repetitively linked to various neurodegenerative diseases (Yokel 2000, Zatta et
al. 2003, Kawahara 2005). As a matter of fact, this non-redox active metal has been
demonstrated to be a toxicant that is implicated in dialysis encephalopathy (Alfrey et al.
1976), osteomalacia (Parkinson et al. 1979), non-iron responsible anemia (Elliot et al.
1978), and also linked to many other diseases including AD (Exley 1999, Flaten 2001,
Gupta et al. 2005), amyotrophic lateral sclerosis (Kurland 1988), and PD (Dexter et al.
1989, Yasui et al. 1992, Good et al. 1992). Aluminium was shown to be
overaccumulated in the brain of post-mortem patients compared to healthy individuals
(Perl et al. 1982, Yasui et al. 1992, Ward and Mason 1987)
Many reviews have been published on the toxic effects of aluminium.
Nevertheless, and despite all hitherto reported data concerning aluminium neurotoxicity,
no single unifying mechanism responsible for its neurotoxicity has been identified.
Therefore, several interlinked hypotheses have been proposed, highlighting distinct
events as a basis for the beginning of aluminium toxic brain damage.
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