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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.
The lack of a gene called IRP2 in mice resulted in high levels
of ferritin, a protein responsible for controlling iron storage,
along with clusters of iron in selected areas of the mice's
brains.
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.
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 the mice as a disease model.
Nature Genetics February,
2001;27:209-214
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