Tatsuhiro Terada1, Masamichi Yokokura2, Etsuji Yoshikawa3, Masami Futatsubashi3, Satoshi Kono4, Takashi Konishi4, Hiroaki Miyajima4, Takanori Hashizume5, Yasuomi Ouchi6. 1. Department of Biofunctional Imaging, Medical Photonics Research Center, Hamamatsu University School of Medicine, 1-20-1 Handayama, Hamamatsu, 431-3192, Japan. 2. Department of Psychiatry, Hamamatsu University School of Medicine, Hamamatsu, Japan. 3. Central Research Laboratory, Hamamatsu Photonics K.K., Hamamatsu, Japan. 4. First Department of Medicine, Hamamatsu University School of Medicine, Hamamatsu, Japan. 5. Osaka Ohtani University, Tondabayashi, Japan. 6. Department of Biofunctional Imaging, Medical Photonics Research Center, Hamamatsu University School of Medicine, 1-20-1 Handayama, Hamamatsu, 431-3192, Japan. ouchi@hama-med.ac.jp.
Abstract
BACKGROUND: The neuroinflammatory glial response contributes to the degenerative process in Parkinson's disease (PD). However, the pattern of microglial progression remains unclear. METHODS: We evaluated microglial activation in early stage PD patients by quantifying changes in neuroinflammation using PET with [(11)C]DPA713, a selective PET tracer for microglial activation. Eleven PD patients (Hoehn and Yahr stages 1-2) without dementia underwent the [(11)C]DPA713 PET scan two times with 1 year apart. The binding potential (BPND) was estimated with the simplified reference tissue model. Voxelwise and regions of interest analyses were used to compare the regional BPND among groups. RESULTS: Significant increase in [(11)C]DPA713 BPND was found extrastriatally in the occipital, temporal and parietal cortex in PD patients, and the degree of BPND became much higher over the brain regions predominantly in the temporal and occipital cortex 1 year later. CONCLUSION: The current results indicated that an extrastriatal spreading of microglial activation reflects one of PD pathophysiology occurring at an early stage.
BACKGROUND: The neuroinflammatory glial response contributes to the degenerative process in Parkinson's disease (PD). However, the pattern of microglial progression remains unclear. METHODS: We evaluated microglial activation in early stage PDpatients by quantifying changes in neuroinflammation using PET with [(11)C]DPA713, a selective PET tracer for microglial activation. Eleven PDpatients (Hoehn and Yahr stages 1-2) without dementia underwent the [(11)C]DPA713 PET scan two times with 1 year apart. The binding potential (BPND) was estimated with the simplified reference tissue model. Voxelwise and regions of interest analyses were used to compare the regional BPND among groups. RESULTS: Significant increase in [(11)C]DPA713 BPND was found extrastriatally in the occipital, temporal and parietal cortex in PDpatients, and the degree of BPND became much higher over the brain regions predominantly in the temporal and occipital cortex 1 year later. CONCLUSION: The current results indicated that an extrastriatal spreading of microglial activation reflects one of PD pathophysiology occurring at an early stage.
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