Metal Chelation In Alzheimers
ironjustice
novel Alzheimer therapy.
Liu G, Men P, Perry G, Smith MA.
Methods Mol Biol. 2010;610:123-44.
Department of Radiology, University of Utah,
Salt Lake City, Utah, USA.
Current therapies for Alzheimer disease (AD) such
as the acetylcholinesterase inhibitors and the
latest NMDA receptor inhibitor, Namenda, provide
moderate symptomatic delay at various stages of the
disease, but do not arrest the disease progression
or bring in meaningful remission.
New approaches to the disease management are urgently
needed.
Although the etiology of AD is largely unknown, oxidative
damage mediated by metals is likely a significant
contributor since metals such as iron, aluminum, zinc,
and copper are dysregulated and/or increased in AD brain
tissue and create a pro-oxidative environment.
This role of metal ion-induced free radical formation
in AD makes chelation therapy an attractive means of
dampening the oxidative stress burden in neurons.
The chelator desferrioxamine, FDA approved for iron
overload, has shown some benefit in AD, but like many
chelators, it has a host of adverse effects and
substantial obstacles for tissue-specific targeting.
Other chelators are under development and have shown
various strengths and weaknesses.
Here, we propose a novel system of chelation therapy
through the use of nanoparticles.
Nanoparticles conjugated to chelators show unique
ability to cross the blood-brain barrier (BBB),
chelate metals, and exit through the BBB with their
corresponding complexed metal ions.
This method may provide a safer and more effective
means of reducing the metal load in neural tissue,
thus attenuating the harmful effects of oxidative
damage and its sequelae.
Experimental procedures are presented in this
chapter.
PMID: 20013176
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