Iron metabolism in Parkinsonian syndromes.
Berg D, Hochstrasser H
Mov Disord. 2006 Jun 30;

Growing evidence suggests an involvement of iron in the pathophysiology
of neurodegenerative diseases. Several of the diseases are associated
with parkinsonian syndromes, induced by degeneration of basal ganglia
regions that contain the highest amount of iron within the brain. The
group of neurodegenerative disorders associated with parkinsonian
syndromes with increased brain iron content can be devided into two
groups: (1) parkinsonian syndromes associated with brain iron
accumulation, including Parkinson's disease, diffuse Lewy body disease,
parkinsonian type of multiple system atrophy, progressive supranuclear
palsy, corticobasal ganglionic degeneration, and Westphal variant of
Huntington's disease; and (2) monogenetically caused disturbances of
brain iron metabolism associated with parkinsonian syndromes, including
aceruloplasminemia, hereditary ferritinopathies affecting the basal
ganglia, and panthotenate kinase associated neurodegeneration type 2.
Although it is still a matter of debate whether iron accumulation is a
primary cause or secondary event in the first group, there is no doubt
that iron-induced oxidative stress contributes to neurodegeneration.
Parallels concerning pathophysiological as well as clinical aspects can
be drawn between disorders of both groups. Results from animal models
and reduction of iron overload combined with at least partial relief of
symptoms by application of iron chelators in patients of the second
group give hope that targeting the iron overload might be one
possibility to slow down the neurodegenerative cascade also in the
first group of inevitably progressive neurodegenerative disorders. (c)
2006 Movement Disorder Society.

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