A logical therapeutic target to retard iron accumulation in specific brain regions would be chelation therapy. The problem is to get metal chelators to reach the appropriate target regions in the brain, where they will complex the iron and diffuse back out as the metal-chelate, without either interfering with the iron-dependent enzymes or by redistributing brain iron such that previously nontoxic iron becomes toxic by being moved to a different brain compartment.

We showed some years ago, in iron-loaded rats, that while chelators were able to cross the blood-brain barrier, and reduce the levels of iron in specific brain regions, some of them also interfered with the metabolism of the neurotransmitter dopamine [97]. Increasing efforts are being made to target chelators, or to use the more sophisticated term, metal-protein-attenuating compounds (MPACs), to cross the blood-brain barrier. Recent examples include incorporating chelators in nanoparticles [167] and the use of lipophilic brain-permeable molecules and polyphenols (reviewed in [2]). Some success has been reported with the copper chelator clioquinol (5-chloro-7-iodo-8-hydroxyquinoline) in a phase 2 clinical trial in Alzheimer's disease [168].

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