Prä- und postprandiale Ghrelinkonzentration bei Patienten mit Multisystematrophie und Progressiver Supranukleärer Blickparese

The gastrointestinal peptide hormone ghrelin, besides its numerous functions in the human body, has been proven to be neuroprotective in a rodent toxin model of Parkinson’s disease. Therefore ghrelin is of great interest in Parkinson’s research, especially after Unger et al. (2011) could show a reduced postprandial ghrelin response in Parkinson’s disease patients which has been explained by dorsal vagal nucleus neurodegeneration. On the basis of these results the postprandial ghrelin secretion of desacyl- and acylghrelin in patients with atypical parkinsonism, MSA and PSP, was studied. Neuropathologically MSA is, like Parkinson’s disease considered as a synucleinopathy, whereas PSP in comparison is a tauopathy. 13 PSP- and 15 MSA-patients were compared to 23 healthy controls. Decrease and increase of AG and DAG (ratio 60 min/baseline; ratio 180 min/60 min) as well as AUCG and AUCI were calculated. Because of the small group sizes relative AG and DAG values to the basic ghrelin concentration were analysed as well. The overall acylghrelin concentration (AUCG) in PSP was lower compared to controls. Relative values in PSP patients (in regard to the basic ghrelin concentration) showed a significant difference to both of the other groups. MSA patients did not show any significant differences compared to control. Regulation of ghrelin secretion is not well understood yet. A neurohumoral impact is possible. The Vagal nerve is likely influencing ghrelin secretion during cephalic-phase of nutrition. Postprandial changes were considered to be regulated differently. There is growing evidence for autonomic dysfunction in PSP. Neurodegeneration of the dorsal vagal nucleus is not seen in PSP. Though, several autonomic regions of the brainstem are included in the neuropathologic spread of the disease. This may explain a disturbed ghrelin-secretion, as a result of autonomic dysfunction in PSP and point towards a much more complex regulation of ghrelin-concentration.