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Potential risk factor identified for
Parkinson's
Newswise — A new study demonstrates that high levels of MAO-B, an
enzyme that regulates nerve activity in the
brain, cause Parkinson’s-like symptoms in
mice genetically engineered to overexpress
the protein.
Furthermore, drugs currently used as an adjunct therapy for
Parkinson’s in humans prevented the
development of Parkinson’s symptoms in these
same animals.
The findings, by scientists at the Buck Institute for Age Research,
raise the possibility that humans could be
tested to see if they have a risk factor for
the progressive, incurable neurodegenerative
disorder that affects 1.5 million Americans
and receive preventive treatment.
The study appears in the February 20 issue of the open-access,
online Journal, PLoS One.
Levels of measurable MAO-B vary 50-fold in humans and tend to
increase with age. Several studies have
suggested that increases in MAO-B contribute
to the neurodegeneration associated with PD,
but direct proof of a causative role for the
enzyme has been lacking.
The drug deprenyl, which inhibits MAO-B, is a longstanding therapy
for Parkinson’s used together with drugs
that boost the level of dopamine, an
important neurotransmitter that is
preferentially depleted in the disease.
Clinical studies that suggest that deprenyl treatment alone does
not impact mortality associated with
Parkinson’s have cast doubt on the role of
MAO-B in the disease itself. Buck faculty
member Julie Andersen, PhD, who led the
study says that may not be the case.
“Those studies were targeted to patients who already had symptoms
of Parkinson’s -- by the time Parkinson’s is
symptomatically detectable, dopamine loss is
usually at least 60%,” said Andersen.
“Therefore the lack of effectiveness of MAO-B inhibition in these
patients does not negate a role for MAO-B
increase in disease development.”
Andersen added, “We have demonstrated that elevations in MAO-B
result in selective loss of neurons
associated with Parkinson’s in a mouse model
and that the severity of this loss is
age-dependent.”
Tests to measure levels of MAO-B are not currently available to the
general public, although enzyme levels are
tracked in clinical trials. Andersen says
MAO-B testing could be akin to current
practices involving cholesterol, which is
measured and monitored as a risk factor for
cardiovascular disease.
“However, it is important to note that Parkinson’s is a
multi-factor disease,” said Andersen. “The
fact that someone has high levels of MAO-B
does not necessarily mean they are fated to
develop Parkinson’s.”
Andersen said results of the study point to the need for an early
diagnostic test for Parkinson’s.
"Currently, by the time people are diagnosed with the disease they
have already lost 60% of the
neurotransmitter levels implicated in
Parkinson’s; treatment with a drug like
deprenyl would likely be most effective if
taken before symptoms appear in order to
halt disease progression."
The novel transgenic mouse line created for this study provides a
new model for exploring molecular pathways
involved in the initiation or early
progression of several key features
associated with Parkinson’s pathology
including dopaminergic midbrain cell loss.
The mouse line also allows for additional
therapeutic drug testing.
Joining Andersen in the study were Jyothi K. Mallajosyula,
Deepinder Kaur, Shankar J. Chinta,
Subramanian Rajagopalan, Anand Rane, and
David G. Nicholls of the Buck Institute,
along with Dino DiMonte of the Parkinson’s
Institute and Heather Macarthur of the Saint
Louis University School of Medicine. The
work was funded by the National Institutes
of Health (R01 NS40057-04) and the National
Parkinson’s Foundation.
The Buck Institute is an independent non-profit organization
dedicated to extending the healthspan, the
healthy years of each individual’s life.
The National Institute of Aging designated the Buck a Nathan Shock
Center of Excellence in the Biology of
Aging, one of just five centers in the
country.
Buck Institute scientists work in an innovative, interdisciplinary
setting to understand the mechanisms of
aging and to discover new ways of detecting,
preventing and treating age-related diseases
such as Alzheimer’s and Parkinson’s disease,
cancer, stroke, and arthritis.
Collaborative research at the Institute is supported by genomics,
proteomics and bioinformatics technology.
For more information:
www.buckinstitute.org.
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