02 December 2009

Ghrelin – a cure for parkinsonism?

Hunger hormone may slow the development of Parkinson's diseaseABC Magazine
American scientists led by an expert in the field of evidence-based medicine, neurobiology, obstetrics and gynecology from the Medical School at Yale University, Dr. Tamas Horvath, report that the hormone ghrelin, which is responsible for a person's sense of appetite, can be used to delay or slow down the development of Parkinson's disease.

(Ghrelin Promotes and Protects Nigrostriatal Dopamine Function via a UCP2-Dependent Mitochondrial Mechanism – The Journal of Neuroscience, Vol. 29(45):14057-14065, 11.11.2009.)

Parkinson's disease is a chronic progressive degenerative disease of the central nervous system caused by damage to the midbrain region – substantia nigra. There are neurons responsible for the production of the neurotransmitter dopamine. It is its lack that leads to the development of Parkinson's disease. Patients develop and progress motor disorders: they have difficulty walking, their movements are limited and cannot be controlled by them, periods of immobility often occur. (On brain scans of a healthy person and a patient with Parkinson's disease, the dopamine level is shown in red.)

Ghrelin is responsible for seemingly completely unrelated to movement actions: it regulates appetite, interest in various dishes, and also regulates the deposition of fat reserves in the body, acting on the hypothalamus. Activation of ghrelin receptors located outside the hypothalamus triggers a cycle of operations related to memory, learning, and the search behavior of positive reinforcement. In addition, a recent study showed that body mass index, body fat deposition and diabetes are closely related to Parkinson's disease.

In their report, Horvath and his colleagues report that ghrelin, among other things, protects dopamine-producing neurons. The experiments were carried out on three groups of mice: a control group; groups of animals that received ghrelin additionally; groups of mice whose organisms were genetically deficient in ghrelin – the loss of dopamine in the latter was much greater than in mice from the control group. Mice from the "ghrelin" group, on the contrary, showed minimal loss of dopamine.

Thus, scientists believe that the use of ghrelin can become the basis for the development of a new method of treating Parkinson's disease. At the next stage, it is planned to find out how ghrelin levels differ in healthy people and in patients with Parkinson's disease, and also to clarify whether ghrelin can serve as a biological marker of predisposition to this disease.

Portal "Eternal youth" http://vechnayamolodost.ru02.12.2009

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