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Subject:
From:
Meir Weiss <[log in to unmask]>
Reply To:
Cerebral Palsy List <[log in to unmask]>
Date:
Thu, 25 Aug 2011 13:01:47 -0400
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-----Original Message-----
From: NIH news releases and news items [mailto:[log in to unmask]] On
Behalf Of NIH OLIB (NIH/OD)
Sent: August 25, 2011 12:15
To: [log in to unmask]
Subject: PROTEIN LINKED TO PARKINSON'S DISEASE MAY REGULATE FAT METABOLISM

U.S. Department of Health and Human Services 
NATIONAL INSTITUTES OF HEALTH NIH News 
National Heart, Lung, and Blood Institute (NHLBI)
<http://www.nhlbi.nih.gov/>
Embargoed for Release: Thursday, August 25, 2011, 12 p.m. EDT

CONTACT: NHLBI Office of Communications, 301-496-4236,
<e-mail:[log in to unmask]>


PROTEIN LINKED TO PARKINSON'S DISEASE MAY REGULATE FAT METABOLISM
Preliminary NIH study may have implications for early onset of the disease

National Institutes of Health researchers have found that Parkin, an
important protein linked with some cases of 

early-onset Parkinson's disease, regulates how cells in our bodies take up
and process dietary fats.

Parkinson's disease is a complex, progressive, and currently incurable
neurological disorder characterized by 

shaking, stiffness, slowed movement, and impaired balance. Parkinson's
primarily affects people over 50, but in 

about 5 to10 percent of cases it occurs in people as young as their 20s.
This form of the disease, which affects 

actor, author, and Parkinson's activist Michael J. Fox, is known as
early-onset Parkinson's. 

Parkin mutations are present in as many as 37 percent of early-onset
Parkinson's cases. However, laboratory mice 

with defective Parkin do not display obvious signs of the disease. 

This preliminary study, which will appear online in the Journal of Clinical
Investigation on Aug. 25, suggests 

defective Parkin may indirectly contribute to the development of some
early-onset Parkinson's by changing the 

amount and types of fat in people's bodies.

"This discovery shows that the clues to understand Parkinson's disease may
not necessarily be in the brain," said 

study leader Michael Sack, M.D., chief of the Laboratory of Mitochondrial
Biology in Cardiometabolic Syndromes at 

the NIH's National Heart, Lung, and Blood Institute. 

The research team, composed of scientists from the NHLBI and the NIH's
National Institute of Neurological 

Disorders and Stroke, observed that mice with defective Parkin did not gain
weight in response to a high-fat 

laboratory diet, as regular mice typically do. 

When the researchers examined several organs of the Parkin-defective mice,
they noticed that the cells contained 

low levels of certain proteins that transport fat in the body. In contrast,
normal mice that were fed the same 

high-fat diet had high levels of these fat-carrying proteins, as well as
high levels of Parkin, suggesting that 

Parkin is involved in fat transportation.

The researchers saw a similar pattern when they analyzed blood cells from
patients enrolled at the NIH 

Parkinson's Clinic. In lab tests, cells from people with Parkin mutations
had less ability to absorb fat. These 

results provide evidence that the findings could be relevant in humans.

As to how fat may be important in Parkinson's, Dr. Sack notes that the brain
cells destroyed during the course of 

the disease are found in a region called the substantia nigra, which
controls movement, among other roles. "The 

neurons in this part of the brain are extremely active. Each one has over
300,000 connections and is continuously 

transmitting information," he said. "These neurons require good support in
the form of their fat and cholesterol 

membrane. If the right types of fat aren't available, then cell integrity
will be sub-par and they could be prone 

to damage."

Dr. Sack and his colleagues plan some early-stage clinical studies on the
connection between fat metabolism and 

Parkinson's. They will continue working with the NIH Parkinson's Clinic and
encourage patients to participate in 

the research as it moves forward.  

To schedule an interview with Dr. Sack or learn more about the study,
contact the NHLBI Office of Communications 

at 301-496-4236 or <email:[log in to unmask]>.

The National Heart, Lung, and Blood Institute (NHLBI) is a component of the
National Institutes of Health. NHLBI 

plans, conducts, and supports research related to the causes, prevention,
diagnosis, and treatment of heart, 

blood vessel, lung, and blood diseases; and sleep disorders. The Institute
also administers national health 

education campaigns on women and heart disease, healthy weight for children,
and other topics. NHLBI press 

releases and other materials are available online at: <www.nhlbi.nih.gov>.

NINDS <www.ninds.nih.gov> is the nation's leading funder of research on the
brain and nervous system. The NINDS 

mission is to reduce the burden of neurological disease -- a burden borne by
every age group, by every segment of 

society, by people all over the world.  

About the National Institutes of Health (NIH): NIH, the nation's medical
research agency, includes 27 Institutes 

and Centers and is a component of the U.S. Department of Health and Human
Services. NIH is the primary federal 

agency conducting and supporting basic, clinical, and translational medical
research, and is investigating the 

causes, treatments, and cures for both common and rare diseases. For more
information about NIH and its programs, 

visit <www.nih.gov>.
---------------------------
RESOURCES: 
 -- Parkinson's Disease: Hope Through Research
 -- Parkinson's Disease: Challenges, Progress and Promise 
 -- NHLBI Intramural Research Program

##

This NIH News Release is available online at:
<http://www.nih.gov/news/health/aug2011/nhlbi-25.htm>.

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<http://service.govdelivery.com/service/subscribe.html?code=USNIH_1>.
If you subscribed via the NIH Listserv, go to
<https://list.nih.gov/cgi-bin/wa.exe?A0=nihpress>.

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