Parkinson hastalığında sempatik sinirlerde artmış alfa-sinüklein birikiminin patolojik önemi: Ölüm sonrası gözlemsel bir çalışma

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Abstract Background: Parkinson disease (PD) is characterized by intra-neuronal deposition of the protein α-synuclein (α-syn) and by deficiencies of the catecholamines dopamine and norepinephrine (NE) in the brain and heart. Accumulation of α-syn in sympathetic noradrenergic nerves may provide a useful PD biomarker; however, whether α-syn buildup is pathophysiological has been unclear. If it were, one would expect associations of intra-neuronal α-syn deposition with catecholaminergic denervation and with decreased NE contents in the same samples. Methods: We assayed immunoreactive α-syn and tyrosine hydroxylase (TH, a marker of catecholaminergic innervation) concurrently with catecholamines in coded post-mortem scalp skin, submandibular gland (SMG), and apical left ventricular myocardial tissue samples from 14 patients with autopsy-proven PD and 12 age-matched control (CTRL) subjects who did not have a neurodegenerative disease. Results: PD patients had increased α-syn in sympathetic noradrenergically innervated arrector pili muscles (5.7 times CTRL, pConclusions: PD entails increased α-syn in skin, SMG, and myocardial tissues. In skin and SMG augmented α-syn deposition in sympathetic nerves does not seem to be pathogenic. The pathophysiological significance of intra-neuronal α-syn deposition appears to be organ-selective and prominent in the heart.

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