Stomach Hormone Can Boost Resistance To Or Slow Down Parkinson's, Study

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Main Category: Parkinson's Disease
Also Included In: Neurology / Neuroscience;  Endocrinology;  GastroIntestinal / Gastroenterology
Article Date: 30 Nov 2009 - 2:00 PDT

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US researchers report finding that ghrelin, a hormone produced in the stomach that regulates appetite and how the body deposits fat, may be used to boost resistance to or slow the development of Parkinson's disease.

The study is the work of Dr Tamas Horvath, chair and professor of comparative medicine and professor of neurobiology and obstetrics and gynecology at the Yale University School of Medicine, New Haven, Connecticut, and colleagues and was published earlier this month in The Journal of Neuroscience.

Parkinson's disease is a neurodegenerative disorder where dopamine neurons in an area of the midbrain known as the substantia nigra, which is responsible for dopamine production, start to die off.

As less dopamine is produced, the symptoms become more severe, so that eventually people with the disease have difficulty walking, have restricted and delayed movements, get tremors in their head and limbs, lose their appetite, can't eat properly, and have periods of immobility or "freezing".

We already know that ghrelin targets the hypothalamus and affects appetite, food intake and how the body deposits fat. The authors wrote that ghrelin receptors at sites outside of the hypothalamus also "promote circuit activity associated with learning and memory, and reward seeking behavior". And recent human studies have shown that body mass index (BMI), stored fat and diabetes are linked to Parkinson's disease.

In this study, Horvath and colleagues discovered that ghrelin also protects the neurons that make dopamine.

"We also found that, in addition to its influence on appetite, ghrelin is responsible for direct activation of the brain's dopamine cells," said Horvath. He explained that because the hormone is made in the stomach, it circulates normally in the bloodstream, "so it could easily be used to boost resistance to Parkinson's or it could be used to slow the development of the disease".

For the study, which was supported by the Michael J Fox Foundation for Parkinson's Research, Horvath and colleagues gave one group of mice extra ghrelin, and while another group were genetically engineered to lack the hormone and its receptor.

When compared to a group of control mice, the mice that had impaired ghrelin action in the brain had more dopamine loss.

The authors explained that the mice that were given extra ghrelin lost fewer substantia nigra pars compacta dopamine cells and showed "restricted striatal dopamine loss", while the mice that were genetically engineered to lack the hormone and its receptors lost more substantia nigra pars compacta dopamine cells and showed "lowered striatal dopamine levels". The effect in the genetically engineered mice was reversed when they switched the ghrelin receptor on.

They concluded that their study supports the idea that ghrelin could be a new therapeutic strategy to fight neurodegeneration, loss of appetite and body weight linked with Parkinson's disease.

Horvath said they could see these results being applicable to humans because the ghrelin system is preserved through various species.

The researchers are now planning to find out how ghrelin levels differ between healthy people and people with Parkinsons disease, and whether changes in ghrelin levels might serve as a biomarker of disease susceptibility and development.

"Ghrelin Promotes and Protects Nigrostriatal Dopamine Function via a UCP2-Dependent Mitochondrial Mechanism.
Zane B. Andrews, Derek Erion, Rudolph Beiler, Zhong-Wu Liu, Alfonso Abizaid, Jeffrey Zigman, John D. Elsworth, Joseph M. Savitt, Richard DiMarchi, Matthias Tschöp, Robert H. Roth, Xiao-Bing Gao, and Tamas L. Horvath.
The Journal of Neuroscience, November 11, 2009, 29(45):14057-14065.
DOI:10.1523/JNEUROSCI.3890-09.2009

Additional source: Yale University.

Written by: Catharine Paddock, PhD
Copyright: Medical News Today
Not to be reproduced without permission of Medical News Today

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