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Brain network markers of abnormal cerebral glucose metabolism and blood flow in Parkinson's disease

Neuroscience Bulletin 2014年第5期30卷 823-837页

作者： Shichun Peng david eidelberg Yilong Ma Center for Neurosciences The Feinstein Institute for Medical ResearchNorth Shore-Long Island Jewish Health System

Neuroimaging of cerebral glucose metabolism and blood flow is ideally suited to assay widely-distributed brain circuits as a result of local molecular events and behavioral modulation in the central nervous system. With the progress in novel analytical methodology, this endeavor has succeeded in unraveling the mechanisms underlying a wide spectrum of neurodegenerative diseases. In particular, statistical brain mapping studies have made significant strides in describing the pathophysiology of Parkinson＇s disease （PD） and related disorders by providing signature biomarkers to determine the systemic abnormalities in brain function and evaluate disease progression, therapeutic responses, and clinical correlates in patients. In this article, we review the relevant clinical applications in patients in relation to healthy volunteers with a focus on the generation of unique spatial covariance patterns associated with the motor and cognitive symptoms underlying PD. These characteristic biomarkers can be potentially used not only to improve patient recruitment but also to predict outcomes in clinical trials.

关键词： Parkinson's disease metabolism blood flow PET SPECT movement disorder network analysis imaging biomarkers

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亨廷顿病的临床前期:学习期间大脑的代偿性反应

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世界核心医学期刊文摘(神经病学分册) 2006年第4期 8-9页

作者： Feigin A. Ghilardi M.- F. D. eidelberg 江山 Institute for Medical Research North Shore-LIJ Health System 350 Community Drive Manhasset NY 11030 United States.Dr

Motor sequence learning is abnormal in presymptomatic Huntington's disease (p-HD). The neural substrates underlying this early manifestation of HD are poorly understood. To study the mechanism of this cognitive abnormality in p-HD, we used positron emission tomography to record brain activity during motor sequence learning in these subjects. Eleven p-HD subjects (age, 45.8 ± 11.0 years; CAG repeat length, 41.6 ± 1.8) and 11 agematched control subjects (age, 45.3 ± 13.4 years) underwent H215O positron emission tomography while performing a set of kinematically controlled motor sequence learning and execution tasks. Differences in regional brain activation responses between groups and conditions were assessed. In addition, we identified discrete regions in which learning-related activity correlated with performance. We found that sequence learning was impaired in p-HD subjects despite normal motor performance. In p-HD, activation responses during learning were abnormally increased in the left mediodorsal thalamus and orbitofrontal cortex (OFC; BA 11/47). Impaired learning performance in these subjects was associated with increased activation responses in the precuneus (BA 18/31). These data suggest that enhanced activation of thalamocortical pathways during motor learning can compensate for caudate degeneration in p-HD. Nonetheless, this mechanism may not be sufficient to sustain a normal level of task performance, even during the presymptomatic stage of the disease.

关键词：亨廷顿病反应患者运动序列临床前期序列学习

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肌张力障碍DYT1突变非显性携带者纹状体D_2受体结合位点减少

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世界核心医学期刊文摘（神经病学分册） 2005年第6期1卷 46-46页

作者： Asanuma K. Okulski J. D. eidelberg 姚庆和 Center for Neurosciences N. Shore- Long Isl. Jewish Res. Inst. 350 Community Drive Manhasset NY 11030 United States Dr.

To determine whether reduced striatal D2 receptor binding reported in patients with idiopathic torsion dystonia is associated with the genotype, the authors used PET and [11C]- raclopride to assess non- manifesting carriers of the DYT1 mutation. D2 receptor binding was reduced by approximately 15% in caudate and putamen (p < 0.005). These results suggest that striatal D2 binding reductions are a trait feature of the DYT1 genotype.

关键词：肌张力障碍 DYT1 D2 受体结合位点携带者纹状体壳核尾状核

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