Abnormal Iron Deposits May Cause Some
Brain Disorders
NEW YORK, January 30, 2001 (Reuters Health) - New research suggests
that abnormal handling of iron by the body could lead
to the development of brain disorders such as Parkinson's disease.
"Researchers have long debated whether the characteristic iron deposits
of these diseases are the cause or the result of the disease process.
This (research) is a strong clue that iron may play a causative role in
Parkinson's and similar disorders,'' said National Institute of Child
Health and Human Development (NICHD) director, Dr. Duane Alexander, in a
statement released by NICHD.
Dr. Tracey Rouault from NICHD in Bethesda, Maryland and colleagues made
their discovery while studying mice bred to lack iron regulatory protein
2 (IRP2), which plays a key role in managing the intake and output of
iron by cells. The findings are reported in the February issue of Nature
Genetics.
Once they reached 6 months of age, mice without IRP2 developed a
progressive brain disorder marked by uncoordinated walking, trembling,
moving slowly, and weakness--features also seen in human diseases like
Parkinson's, the authors report. Mice missing one of their two IRP2
genes developed a less severe form of the disorder and developed it
later in life.
The lack of IRP2 resulted in high levels of ferritin (another protein
responsible for controlling iron storage), along with clusters of iron
in selected areas of the mice's brains, the report indicates.
These collections of iron matched the regions of the brain where brain
cells were degenerating, the researchers note, and, in fact, iron
accumulation began even before the degeneration took place.
"The implications are that disorders of iron metabolism may be primary
causes of late-onset neurodegenerative disease,'' Rouault told Reuters
Health.
"Since the cause of these diseases is almost never understood, it would
be possible to define a population of humans with mutations in this
gene, and then attempt to correct the problems with iron metabolism,
using our mice as a disease model,'' the researcher explained.
"Basic research pays off,'' Rouault added. ``We can hope that causes and
treatments will be found for neurodegenerative disease.''
SOURCE: Nature Genetics 2001;27:209-214.
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Judith Richards, London, Ontario, Canada
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