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Increased Cerebral Oxidative Stress In Amyotrophic Lateral Sclerosis: A 62Cu-ATSM PET Study (P7.006)

OBJECTIVE: To evaluate cerebral oxidative stress in amyotrophic lateral sclerosis (ALS), we applied positron emission tomography (PET) with [ 62 Cu]diacetyl-bis( N 4 -methylthiosemicarbazone) ( 62 Cu-ATSM) to ALS patients.
 BACKGROUND: The effects of oxidative stress and mitochondrial dysfunction on neurodegeneration in the pathogenesis of ALS in living patients remain unknown. High-level accumulation of 62 Cu-ATSM indicates an over-reduction state mainly caused by mitochondrial dysfunction, which leads to oxidative stress.
 DESIGN/METHODS: Twelve ALS patients (7 males/5 females, mean age 65.2±9.4) and 9 age-matched healthy controls (6 males/3 females, mean age 61.3±8.6) underwent 62 Cu-ATSM PET. The severity of symptoms was evaluated employing the revised ALS Functional Rating Scale (ALSFRS-R). Dynamic PET data acquisition was performed, and standardized uptake value (SUV) images were created from each of early and delayed images. The delayed images were normalized globally after anatomical standardization using the individual parameters which were determined from the early images using Statistical Parametric Mapping 2 (SPM2). Accumulations in the delayed images of the patients were compared with those of the controls using SPM2, and SUVs of each region where SPM map showed significant increase in the patients were calculated by region of interest analysis.
 RESULTS: SPM map demonstrated that the accumulations in the bilateral motor cortex and right parietal cortex of patients were significantly increased compared with those observed in the controls. SUVs in the bilateral motor cortex of patients (92.0±4.6) were significantly increased compared with those of the controls (83.4±5.2) ( P r =-0.64, P <0.05).
 CONCLUSIONS: 62 Cu-ATSM PET imaging demonstrated that oxidative stress in the motor cortex was enhanced in ALS patients compared with controls and increased especially in patients with mild in the severity, indicating that oxidative stress associates with initiation of neurodegeneration in ALS.
 Study Supported by: This study was supported in part by Grants-in-Aid for Japan Advanced Molecular Imaging Program from JST, and Scientific Research on Innovative Areas and Scientific Research (C) from JSPS. Disclosure: Dr. Ikawa has nothing to disclose. Dr. Okazawa has nothing to disclose. Dr. Tsujikawa has nothing to disclose. Dr. Muramatsu has nothing to disclose. Dr. Kishitani has nothing to disclose. Dr. Kamisawa has nothing to disclose. Dr. Matsunaga has nothing to disclose. Dr. Yamamura has nothing to disclose. Dr. Mori has nothing to disclose. Dr. Hamano has nothing to disclose. Dr. Kiyono has nothing to disclose. Dr. Nakamoto has nothing to disclose. Dr. Yoneda has nothing to disclose.