In Vivo Mitochondrial Function in Idiopathic and Genetic Parkinson’s Disease

Parkinson&#8217;s disease (PD) is associated with brain mitochondrial dysfunction. High-energy phosphates (HEPs), which rely on mitochondrial functioning, may be considered potential biomarkers for PD. Phosphorus magnetic resonance spectroscopy (<sup>31</sup>P-MRS) is a suitable tool...

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Bibliographic Details
Main Authors: Gabriele Dossi, Letizia Squarcina, Mario Rango
Format: Article
Language:English
Published: MDPI AG 2019-12-01
Series:Metabolites
Subjects:
Online Access:https://www.mdpi.com/2218-1989/10/1/19
Description
Summary:Parkinson&#8217;s disease (PD) is associated with brain mitochondrial dysfunction. High-energy phosphates (HEPs), which rely on mitochondrial functioning, may be considered potential biomarkers for PD. Phosphorus magnetic resonance spectroscopy (<sup>31</sup>P-MRS) is a suitable tool to explore in vivo cerebral energetics. We considered 10 <sup>31</sup>P-MRS studies in order to highlight the main findings about brain energetic compounds in patients affected by idiopathic PD and genetic PD. The studies investigated several brain areas such as frontal lobes, occipital lobes, temporoparietal cortex, visual cortex, midbrain, and basal ganglia. Resting-state studies reported contrasting results showing decreased as well as normal or increased HEPs levels in PD patients. Functional studies revealed abnormal PCr + &#946;ATP levels in PD subjects during the recovery phase and abnormal values at rest, during activation and recovery in one PD subject with PINK1 gene mutation suggesting that mitochondrial machinery is more impaired in PD patients with PINK1 gene mutation. PD is characterized by energetics impairment both in idiopathic PD as well as in genetic PD, suggesting that mitochondrial dysfunction underlies the disease. Studies are still sparse and sometimes contrasting, maybe due to different methodological approaches. Further studies are needed to better assess the role of mitochondria in the PD development.
ISSN:2218-1989