Parkinson’s – a degenerative disease of the central nervous system - develops when dopamine cells die, and reduced production of dopamine in late-stage Parkinson’s can cause difficulty in walking, restricted or delayed movement, lack of appetite and difficulty eating, ‘freezing’ or motionlessness, and head and limb tremors.  Researchers from Yale School of Medicine – supported by the Michael J Fox Foundation for Parkinson’s Research – found that ghrelin, a hormone produced in the stomach, is protective of dopamine neurons. 

“We also found that, in addition to its influence on appetite, ghrelin is responsible for direct activation of the brain’s dopamine cells. Because the hormone originates from the stomach, it is circulating normally in the body, so it could easily be used to boost resistance to Parkinson’s or it could be used to slow the development of the disease,” said Tamas Horvath, chair and professor of comparative medicine and professor of neurobiology and obstetrics & gynaecology at Yale School of Medicine. 

Horvath - who studied the action of ghrelin in mice - suggests the results could easily be translated to humans because the ghrelin system is preserved through various species. Horvath and his colleagues conducted the study in mice that received a ghrelin supplement and those that were deficient in the hormone and receptor. When compared to control mice, those with impaired ghrelin action in the brain had a greater loss of dopamine. 

Horvath and his team will now try to establish ghrelin levels in both healthy individuals and Parkinson’s patients, and determine whether altered ghrelin levels might be biomarkers of disease development and vulnerability.

Ghrelin is associated with the release of growth hormones, appetite, learning and memory, and reward circuitry for the brain that regulates food cravings.  Recent studies show that body mass index, stored fat and diabetes are linked to Parkinson’s, and obesity is a risk factor for neurodegeneration in mice.