Brain energy metabolism in early MSA-P: A phosphorus and proton magnetic resonance spectroscopy study.
作者信息
Stamelou M, Pilatus U, Reuss A, Respondek G, Knake S, Oertel W H, Höglinger G U
机构信息
Department of Neurology, Philipps University Marburg, Germany; Second Department of Neurology, University of Athens, Greece; Movement Disorders Department, Hygeia Hospital, Athens, Greece.
Institute of Neuroradiology, Goethe-University Frankfurt, Frankfurt, Germany.
出版信息
Parkinsonism Relat Disord. 2015 May;21(5):533-5. doi: 10.1016/j.parkreldis.2015.03.001. Epub 2015 Mar 12.
INTRODUCTION
Recently, mutations in the COQ2 gene, encoding for an enzyme involved in coenzyme Q10 biosynthesis, have been suggested to confer susceptibility risk for multiple system atrophy (MSA). Thus, the possible role of mitochondrial dysfunction in the pathophysiology of MSA has emerged. Here, we studied brain energy metabolism in vivo in early MSA-parkinsonism (MSA-P) patients and compared to healthy controls.
METHODS
We have used combined phosphorus and proton magnetic resonance spectroscopy to measure high- and low-energy phosphates in the basal ganglia of early (Hoehn and Yahr stage I-III), probable MSA-P patients (N = 9) compared to healthy controls (N = 9).
RESULTS
No significant changes in the high energy phosphates and other parameters reflecting the energy status of the cells were found in the basal ganglia of MSA-P patients compared to healthy controls. N-acetylaspartate was significantly reduced in MSA-P compared to healthy controls and correlated with the Unified Multiple System Atrophy Rating Scale.
CONCLUSION
Brain energy metabolism in early MSA-P is not impaired, despite the presence of impaired neuronal integrity. This may imply that mitochondrial dysfunction may not play a primary role in the pathophysiology of MSA, at least in European populations.
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