Research Article Mitochondrial Respiration in Intact Peripheral Blood Mononuclear Cells and Sirtuin 3 Activity in Patients with Movement Disorders Slawomir Michalak, 1 Jolanta Florczak-Wyspiańska, 2 Joanna Rybacka-Mossakowska, 1 Wojciech Ambrosius, 2 Krystyna Osztynowicz, 1 Aleksandra Baszczuk, 3 Wojciech Kozubski, 2 and Ewa Wysocka 3 1 Department of Neurochemistry and Neuropathology, Poznan University of Medical Sciences, Przybyszewskiego str. 49, 60-355 Poznan, Poland 2 Department of Neurology, Poznan University of Medical Sciences, Przybyszewskiego str. 49, 60-355 Poznan, Poland 3 Chair and Department of Laboratory Diagnostics, Poznan University of Medical Sciences, Szamarzewskiego str. 82/84, 60-569 Poznan, Poland Correspondence should be addressed to Slawomir Michalak; swami@ump.edu.pl Received 31 March 2017; Accepted 1 August 2017; Published 10 September 2017 Academic Editor: Leah Siskind Copyright © 2017 Slawomir Michalak et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Objective. Mitochondrial dysfunction is considered a unifying pathophysiological explanation for movement disorders. Sirtuin 3 (SIRT3) exhibits deacetylase activity and antioxidant properties. The aim of the study was to analyze the mitochondrial respiration in peripheral blood mononuclear cells (PBMCs) and the SIRT3 activity in patients with movement disorders. Methods. Mitochondrial respiration was analyzed in intact PBMCs using the ROUTINE, LEAK, electron transfer system (ETS), and residual oxygen consumption (ROX) protocol by means of high-resolution respirometry. The SIRT3 expression and PBMC activity were measured using fluorometry. Ultrasound measurements of the echogenicity of the substantia nigra and the diameter of the 3rd ventricle were also performed. Results. Patients with movement disorders exhibited a lower ROUTINE respiration than controls (P = 0.0237). Reduced oxygen fluxes in the LEAK (P =0 033) and ROX (P =0 0486) states were observed in patients with movement disorders compared with controls. Decreased ROUTINE respiration (P =0 007) and oxygen flux in the LEAK state (P =0 0203) were observed in patients with PD with substantia nigra hyperechogenicity compared with controls. Decreased SIRT 3 deacetylase activity was found in patients with movement disorders. Conclusion. Impaired mitochondrial respiration in intact PBMCs was associated with inhibited SIRT3 activity and neurodegeneration measures evaluated using ultrasound in patients with PD. 1. Introduction Movement disorders constitute a group of degenerative conditions in the central nervous system, including primarily Parkinson’s disease (PD), atypical parkinsonian syndromes, dystonia, essential tremor, and restless legs syndrome. The idiopathic form of PD affects 1% of the population over 65 years of age with the incidence of 8–18 cases per 100,000 persons per year. With a prevalence of approximately 3% in persons over 75 years of age, neurodegenerative diseases are confirmed to develop predominantly in the elderly and are a major cause of disability in this population [1]. In contrast to idiopathic PD, other movement disor- ders like progressive supranuclear palsy (PSP, Steele- Richardson-Olszewski’s disease), corticobasal degeneration (CBD), multisystem atrophy (MSA), and diffuse Lewy Hindawi Oxidative Medicine and Cellular Longevity Volume 2017, Article ID 9703574, 10 pages https://doi.org/10.1155/2017/9703574