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Parkinson Disease: HELP
Articles by Y. Wang
Based on 11 articles published since 2009
(Why 11 articles?)
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Between 2009 and 2019, Y. Wang wrote the following 11 articles about Parkinson Disease.
 
+ Citations + Abstracts
1 Article Comprehensive MRI quantification of the substantia nigra pars compacta in Parkinson's disease. 2018

Takahashi, H / Watanabe, Y / Tanaka, H / Mihara, M / Mochizuki, H / Takahashi, K / Yamamoto, K / Liu, T / Wang, Y / Tomiyama, N. ·Department of Diagnostic and Interventional Radiology, Osaka University Graduate School of Medicine, 2-2 Yamadaoka Suita, Osaka 565-0871, Japan. Electronic address: hiroto.takahashi07@gmail.com. · Department of Diagnostic and Interventional Radiology, Osaka University Graduate School of Medicine, 2-2 Yamadaoka Suita, Osaka 565-0871, Japan. · Department of Neurology, Osaka University Graduate School of Medicine, 2-2 Yamadaoka Suita, Osaka 565-0871, Japan. · Department of Medical Statistics, Osaka City University Graduate School of Medicine, 3-3-138 Sugimoto Sumiyoshi-ku, Osaka, 558-8585, Japan. · Departments of Biomedical Engineering and Radiology, Cornell University, MedImageMetric LLC, New York, NY, 10044, USA. ·Eur J Radiol · Pubmed #30527311.

ABSTRACT: PURPOSE: To quantify dopaminergic neurodegeneration and iron overload in the substantia nigra pars compacta (SNpc) to evaluate Parkinson's disease (PD) using both quantitative susceptibility mapping (QSM) and neuromelanin imaging. MATERIALS AND METHODS: We studied 39 PD patients (PD group) and 25 healthy controls (HC group) who underwent brain MRI with QSM and neuromelanin imaging. QSM and neuromelanin values of the SNpc were obtained using a voxel-based automated region segmentation system. The signal-to-noise ratio (SNR) of the SNpc in the neuromelanin images was calculated based on the mean value for the background region. The neuromelanin value was defined as the neuromelanin volume with an SNR higher than that of the background. The significance of the intergroup differences, and according to the severity stages in the PD group was tested for each QSM and neuromelanin value. Receiver-operating characteristic (ROC) analysis for diagnosing PD was performed for QSM and neuromelanin values. RESULTS: The QSM value was significantly higher in the PD group than in the HC group (P < 0.05). The neuromelanin value was significantly smaller in the PD group than in the HC group (P < 0.05). The areas under the ROC curve were 0.68 and 0.86 for QSM and neuromelanin values, respectively. Using QSM and neuromelanin imaging to classify the PD stage was difficult. CONCLUSIONS: Quantifying the SNpc alterations with our region-based approach is useful for the diagnosis of PD.

2 Article Lateral Asymmetry and Spatial Difference of Iron Deposition in the Substantia Nigra of Patients with Parkinson Disease Measured with Quantitative Susceptibility Mapping. 2016

Azuma, M / Hirai, T / Yamada, K / Yamashita, S / Ando, Y / Tateishi, M / Iryo, Y / Yoneda, T / Kitajima, M / Wang, Y / Yamashita, Y. ·From the Departments of Diagnostic Radiology (M.A., M.T., Y.I., M.K., Y.Y.) coralcommunity@yahoo.co.jp. · Department of Radiology (T.H.), Faculty of Medicine, University of Miyazaki, Miyazaki, Japan. · Neurosurgery (K.Y.). · Neurology (S.Y., Y.A.), Graduate School of Medical Sciences. · From the Departments of Diagnostic Radiology (M.A., M.T., Y.I., M.K., Y.Y.). · Department of Medical Physics in Advanced Biomedical Sciences (T.Y.), Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan. · Department of Radiology (Y.W.), Weill Cornell Medical College, New York, New York. ·AJNR Am J Neuroradiol · Pubmed #26822728.

ABSTRACT: BACKGROUND AND PURPOSE: Quantitative susceptibility mapping is useful for assessing iron deposition in the substantia nigra of patients with Parkinson disease. We aimed to determine whether quantitative susceptibility mapping is useful for assessing the lateral asymmetry and spatial difference in iron deposits in the substantia nigra of patients with Parkinson disease. MATERIALS AND METHODS: Our study population comprised 24 patients with Parkinson disease and 24 age- and sex-matched healthy controls. They underwent 3T MR imaging by using a 3D multiecho gradient-echo sequence. On reconstructed quantitative susceptibility mapping, we measured the susceptibility values in the anterior, middle, and posterior parts of the substantia nigra, the whole substantia nigra, and other deep gray matter structures in both hemibrains. To identify the more and less affected hemibrains in patients with Parkinson disease, we assessed the severity of movement symptoms for each hemibrain by using the Unified Parkinson's Disease Rating Scale. RESULTS: In the posterior substantia nigra of patients with Parkinson disease, the mean susceptibility value was significantly higher in the more than the less affected hemibrain substantia nigra (P < .05). This value was significantly higher in both the more and less affected hemibrains of patients with Parkinson disease than in controls (P < .05). Asymmetry of the mean susceptibility values was significantly greater for patients than controls (P < .05). Receiver operating characteristic analysis showed that quantitative susceptibility mapping of the posterior substantia nigra in the more affected hemibrain provided the highest power for discriminating patients with Parkinson disease from the controls. CONCLUSIONS: Quantitative susceptibility mapping is useful for assessing the lateral asymmetry and spatial difference of iron deposition in the substantia nigra of patients with Parkinson disease.

3 Article White matter differences between multiple system atrophy (parkinsonian type) and Parkinson's disease: A diffusion tensor image study. 2015

Ji, L / Wang, Y / Zhu, D / Liu, W / Shi, J. ·Department of Neurology, Nanjing Brain Hospital, Nanjing Medical University, No. 264 Guangzhou Road, Nanjing 210029, PR China. · Division of Developmental Medicine, Department of Medicine, Boston Children's Hospital, 300 Longwood Avenue, Boston, MA 02115, United States. · Department of Radiology, Nanjing Brain Hospital, Nanjing Medical University, No. 264 Guangzhou Road, Nanjing 210029, PR China. · Department of Neurology, Nanjing Brain Hospital, Nanjing Medical University, No. 264 Guangzhou Road, Nanjing 210029, PR China; Department of Neurology, School of Medicine, Nanjing University, No. 22 Hankou Road, Nanjing 210093, PR China. Electronic address: profshijp@163.com. ·Neuroscience · Pubmed #26215920.

ABSTRACT: The clinical differential diagnosis between the Parkinson variant of multiple system atrophy (MSA-P) and Parkinson's disease (PD) is difficult in early stages. To identify objective markers for differential diagnosis, we combined the novel tract-based spatial statistics (TBSS) and region of interest (ROI) analyses for the first time to investigate three groups (15 MSA-P, 20 PD patients and 20 controls) with diffusion tensor imaging data. By TBSS, we performed pairwise comparisons of fractional anisotropy (FA), mean diffusivity, radial diffusivity (RD) and axial diffusivity maps. The clusters with significant differences between MSA-P and PD were used as ROIs for further analyses. FA/RD values in bilateral corticospinal tract (CST) and left anterior thalamic radiation (ATR) in MSA-P were significantly different from PD or controls, and significantly correlated with clinical data. These findings indicated that the abnormalities of left ATR and bilateral CST were specific for MSA-P relative to PD or controls, and seemed to be promising for differential diagnosis. Furthermore, it may be useful for severity assessment of MSA-P.

4 Article Nrf2-ARE signals mediated the anti-oxidative action of electroacupuncture in an MPTP mouse model of Parkinson's disease. 2015

Lv, E / Deng, J / Yu, Y / Wang, Y / Gong, X / Jia, J / Wang, X. ·a Departments of Neurobiology and Physiology , Key Laboratory for Neurodegenerative Disorders of the Ministry of Education, Beijing Key Laboratory for Parkinson's Disease, Capital Medical University; Beijing Institute for Brain Disorders , Beijing , 100069 , China. ·Free Radic Res · Pubmed #26118717.

ABSTRACT: Oxidative stress and neuroinflammation are early events associated with dopaminergic neuronal degeneration in Parkinson's disease (PD). Previous studies indicated that electroacupuncture (EA) stimulation is effective in protecting dopaminergic neurons from degeneration in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of PD. In this study, we further characterized the effect of EA on MPTP-induced oxidative responses in the mouse dopamine system. We found that subacute administration of MPTP enhanced lipid and protein oxidation and reduced expression of endogenous antioxidant enzymes (such as superoxide dismutase and catalase) in the striatum. MPTP also reduced expression of an antioxidant transcription factor, nuclear factor-E2-related factor-2 (Nrf2), and Nrf2-regulated antioxidant enzymes (nicotinamide adenine dinucleotide phosphate quinone oxidoreductase-1 and heme oxygenase-1) in the striatum and/or midbrain. Using human placental alkaline phosphatase (hPAP) as a reporter of Nrf2-regulated gene expression in hPAP transgenic mice, we found that MPTP suppressed hPAP expression in the striatum and midbrain. Application of EA at an effective frequency (100 Hz) was sufficient to reverse these changes induced by MPTP. In addition, EA reduced microglia activation and astrogliosis in the striatum and midbrain, increased tyrosine hydroxylase levels in the striatum, and improved vertical movement in MPTP mice. These results provide further evidence supporting that EA produces a series of anti-oxidative effects that effectively counteract with the oxidative stress in the nigrostriatal dopamine system induced by MPTP in a mouse model of PD.

5 Article Usefulness of quantitative susceptibility mapping for the diagnosis of Parkinson disease. 2015

Murakami, Y / Kakeda, S / Watanabe, K / Ueda, I / Ogasawara, A / Moriya, J / Ide, S / Futatsuya, K / Sato, T / Okada, K / Uozumi, T / Tsuji, S / Liu, T / Wang, Y / Korogi, Y. ·From the Departments of Radiology (Y.M., S.K., K.W., I.U., A.O., J.M., S.I., K.F., T.S., Y.K.). · From the Departments of Radiology (Y.M., S.K., K.W., I.U., A.O., J.M., S.I., K.F., T.S., Y.K.) kakeda@med.uoeh-u.ac.jp. · Neurology (K.O., T.U., S.T.), University of Occupational and Environmental Health, School of Medicine, Kitakyushu, Japan. · Departments of Biomedical Engineering and Radiology (T.L., Y.W.), Cornell University, New York, New York. ·AJNR Am J Neuroradiol · Pubmed #25767187.

ABSTRACT: BACKGROUND AND PURPOSE: Quantitative susceptibility mapping allows overcoming several nonlocal restrictions of susceptibility-weighted and phase imaging and enables quantification of magnetic susceptibility. We compared the diagnostic accuracy of quantitative susceptibility mapping and R2* (1/T2*) mapping to discriminate between patients with Parkinson disease and controls. MATERIALS AND METHODS: For 21 patients with Parkinson disease and 21 age- and sex-matched controls, 2 radiologists measured the quantitative susceptibility mapping values and R2* values in 6 brain structures (the thalamus, putamen, caudate nucleus, pallidum, substantia nigra, and red nucleus). RESULTS: The quantitative susceptibility mapping values and R2* values of the substantia nigra were significantly higher in patients with Parkinson disease (P < .01); measurements in other brain regions did not differ significantly between patients and controls. For the discrimination of patients with Parkinson disease from controls, receiver operating characteristic analysis suggested that the optimal cutoff values for the substantia nigra, based on the Youden Index, were >0.210 for quantitative susceptibility mapping and >28.8 for R2*. The sensitivity, specificity, and accuracy of quantitative susceptibility mapping were 90% (19 of 21), 86% (18 of 21), and 88% (37 of 42), respectively; for R2* mapping, they were 81% (17 of 21), 52% (11 of 21), and 67% (28 of 42). Pair-wise comparisons showed that the areas under the receiver operating characteristic curves were significantly larger for quantitative susceptibility mapping than for R2* mapping (0.91 versus 0.69, P < .05). CONCLUSIONS: Quantitative susceptibility mapping showed higher diagnostic performance than R2* mapping for the discrimination between patients with Parkinson disease and controls.

6 Article Genetic overlap between Alzheimer's disease and Parkinson's disease at the MAPT locus. 2015

Desikan, R S / Schork, A J / Wang, Y / Witoelar, A / Sharma, M / McEvoy, L K / Holland, D / Brewer, J B / Chen, C-H / Thompson, W K / Harold, D / Williams, J / Owen, M J / O'Donovan, M C / Pericak-Vance, M A / Mayeux, R / Haines, J L / Farrer, L A / Schellenberg, G D / Heutink, P / Singleton, A B / Brice, A / Wood, N W / Hardy, J / Martinez, M / Choi, S H / DeStefano, A / Ikram, M A / Bis, J C / Smith, A / Fitzpatrick, A L / Launer, L / van Duijn, C / Seshadri, S / Ulstein, I D / Aarsland, D / Fladby, T / Djurovic, S / Hyman, B T / Snaedal, J / Stefansson, H / Stefansson, K / Gasser, T / Andreassen, O A / Dale, A M / Anonymous2101224. ·Department of Radiology, University of California, San Diego, La Jolla, CA, USA. · Department of Cognitive Science, University of California, San Diego, La Jolla, CA, USA. · Department of Neurosciences, University of California, San Diego, La Jolla, CA, USA. · NORMENT; Institute of Clinical Medicine, University of Oslo and Division of Mental Health and Addiction, Oslo University Hospital, Oslo, Norway. · Department for Neurodegenerative Diseases, Hertie Institute for Clinical Brain Research University of Tubingen, Tubingen, Germany. · Institute for Clinical Epidemiology and Applied Biometry, University of Tübingen, Tübingen, Germany. · Department of Psychiatry, University of California, San Diego, La Jolla, CA, USA. · Medical Research Council Centre for Neuropsychiatric Genetics and Genomics, Institute of Psychological Medicine and Clinical Neurosciences, Cardiff University School of Medicine, Wales, UK. · The John P. Hussman Institute for Human Genomics, University of Miami, Miami, FL, USA. · Department of Neurology, Taub Institute on Alzheimer's Disease and the Aging Brain, and Gertrude H. Sergievsky Center, Columbia University, New York, NY, USA. · Department of Molecular Physiology and Biophysics, Vanderbilt Center for Human Genetics Research, Vanderbilt University, Nashville, TN, USA. · Departments of Medicine (Biomedical Genetics), Neurology, Ophthalmology, Biostatistics, and Epidemiology, Boston University Schools of Medicine and Public Health, Boston, MA, USA. · Department of Pathology and Laboratory Medicine, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA, USA. · German Center for Neurodegenerative Diseases (DZNE)-Tübingen, Paul-Ehrlich-Straße 15, Tübingen, Germany. · Laboratory of Neurogenetics, National Institute on Aging, Bethesda, MD, USA. · Sorbonne Université, UPMC Univ Paris 06, Paris, France. · UCL Genetics Institute and Department of Molecular Neuroscience, UCL Institute of Neurology, London, UK. · Department of Molecular Neuroscience, UCL Institute of Neurology, London, UK. · INSERM UMR1043, CPTP, CHU Purpan, Toulouse, France. · Department of Biostatistics, School of Public Health, Boston University, Boston, MA, USA. · The National Heart Lung and Blood Institute's Framingham Heart Study, Framingham, MA, USA. · Deparment of Epidemiology, Erasmus MC University Medical Center, Rotterdam, Netherlands. · Deparment of Internal Medicine, University of Washington, Seattle, WA, USA. · Icelandic Heart Association, Kopavogur, Iceland. · Department of Epidemiology, University of Washington, Seattle, WA, USA. · Laboratory of Epidemiology, Demography and Biometry, Intramural Research Program, National Institute on Aging, Washington, DC, USA. · Department of Neurology, Boston University School of Medicine, Boston, MA, USA. · Norwegian Centre for Dementia Research, Department of Old Age Psychiatry, Oslo University Hospital, Oslo, Norway. · Department of Geriatric Psychiatry, Akershus University Hospital, Oslo, Norway. · Centre for Age-Related Medicine, Stavanger University Hospital, Stavanger, Norway. · Alzheimer's Disease Research Centre, Department of Neurobiology, Care Sciences and Society, Karolinska Institute, Stockholm, Sweden. · Institute of Clinical Medicine, University of Oslo, Oslo, Norway. · Department of Neurology, Akershus University Hospital, Oslo, Norway. · Department of Neurology, Massachusetts General Hospital, Boston, MA, USA. · Department of Geriatric Medicine, University Hospital Reykjavik, Reykjavik, Iceland. · deCODE Genetics/Amgen, Reykjavik, Iceland. · Faculty of Medicine, University of Iceland, Reykjavik, Iceland. ·Mol Psychiatry · Pubmed #25687773.

ABSTRACT: We investigated the genetic overlap between Alzheimer's disease (AD) and Parkinson's disease (PD). Using summary statistics (P-values) from large recent genome-wide association studies (GWAS) (total n=89 904 individuals), we sought to identify single nucleotide polymorphisms (SNPs) associating with both AD and PD. We found and replicated association of both AD and PD with the A allele of rs393152 within the extended MAPT region on chromosome 17 (meta analysis P-value across five independent AD cohorts=1.65 × 10(-7)). In independent datasets, we found a dose-dependent effect of the A allele of rs393152 on intra-cerebral MAPT transcript levels and volume loss within the entorhinal cortex and hippocampus. Our findings identify the tau-associated MAPT locus as a site of genetic overlap between AD and PD, and extending prior work, we show that the MAPT region increases risk of Alzheimer's neurodegeneration.

7 Article Different iron-deposition patterns of multiple system atrophy with predominant parkinsonism and idiopathetic Parkinson diseases demonstrated by phase-corrected susceptibility-weighted imaging. 2012

Wang, Y / Butros, S R / Shuai, X / Dai, Y / Chen, C / Liu, M / Haacke, E M / Hu, J / Xu, H. ·Department of Radiology, Union Hospital, Wuhan, China. ·AJNR Am J Neuroradiol · Pubmed #22051807.

ABSTRACT: BACKGROUND AND PURPOSE: MSA-P and IPD have similar clinical presentations that may complicate accurate clinical diagnosis. Different iron-deposition patterns of those 2 diseases have been demonstrated in histopathology. The aim was to demonstrate the different iron-deposition patterns of MSA-P and IPD by using SWI phase images. MATERIALS AND METHODS: Sixteen patients with IPD, 8 with MSA-P, and 44 age-matched healthy controls underwent SWI of brain. The different phase shifts as well as the high iron percentage of the area in several gray nuclei were statistically evaluated. The putamen was divided into 4 subregions for further analysis. RESULTS: Patients with MSA-P had significantly higher iron deposition in the putamen and PT compared with those with IPD (P < .05). Moreover, ROC curves indicated slightly more sensitivity in differentiating MSA-P from IPD, by means of the high-iron-deposition-percentage area than the average phase shift (putamen: AUC = 0.88 versus 0.78; PT: AUC = 0.79 versus 0.62). Moreover, the lower inner region of the putamen was the most valuable subregion in differentiating MSA-P from IPD among the 4 subregions (AUC = 0.92 and 0.91 for high-iron-percentage area and average phase shift, respectively). CONCLUSIONS: Higher iron deposition in the putamen and PT may differentiate MSA-P from IPD, but the lower inner region of the putamen may be better compared with the PT and other subregions of the putamen. Moreover, the high iron percentage makes it possible to detect smaller increases in iron content more confidently in comparison with average phase shift.

8 Article Enhanced survival of dopaminergic neuronal transplants in hemiparkinsonian rats by the p53 inactivator PFT-α. 2011

Chou, J / Greig, N H / Reiner, D / Hoffer, B J / Wang, Y. ·National Institute on Drug Abuse, Baltimore, MD 21224, USA. ·Cell Transplant · Pubmed #21294958.

ABSTRACT: A key limiting factor impacting the success of cell transplantation for Parkinson's disease is the survival of the grafted cells, which are often short lived. The focus of this study was to examine a novel strategy to optimize the survival of exogenous fetal ventromesencephalic (VM) grafts by treatment with the p53 inhibitor, pifithrin-α (PFT-α), to improve the biological outcome of parkinsonian animals. Adult male Sprague-Dawley rats were given 6-hydroxydopamine into the left medial forebrain bundle to induce a hemiparkinsonian state. At 7 weeks after lesioning, animals were grafted with fetal VM or cortical tissue into the lesioned striatum and, thereafter, received daily PFT-α or vehicle injections for 5 days. Apomorphine-induced rotational behavior was examined at 2, 6, 9, and 12 weeks after grafting. Analysis of TUNEL or tyrosine hydroxylase (TH) immunostaining was undertaken at 5 days or 4 months after grafting. The transplantation of fetal VM tissue into the lesioned striatum reduced rotational behavior. A further reduction in rotation was apparent in animals receiving PFT-α and VM transplants. By contrast, no significant reduction in rotation was evident in animals receiving cortical grafts or cortical grafts + PFT-α. PFT-α treatment reduced TUNEL labeling and increased TH(+) cell and fiber density in the VM transplants. In conclusion, our data indicate that early postgrafting treatment with PFT-α enhances the survival of dopamine cell transplants and augments behavioral recovery in parkinsonian animals.

9 Article Sensitive and specific detection of α-synuclein in human plasma. 2010

Tinsley, R B / Kotschet, K / Modesto, D / Ng, H / Wang, Y / Nagley, P / Shaw, G / Horne, M K. ·Florey Neuroscience Institutes, University of Melbourne, Melbourne, Victoria 3010, Australia. rogan.tinsley@florey.com.au ·J Neurosci Res · Pubmed #20648655.

ABSTRACT: alpha-Synuclein (alphasyn) mutations, overexpression, misfolding, and aggregation are associated with Parkinson's disease. This protein has been intensively studied in neuronal systems. However, alphasyn is also present in extracellular fluids, such as cerebrospinal fluid and blood plasma. Recent studies have attempted to quantify its levels and compare these in various extracellular fluids of control and Parkinson's disease subjects. Data from these studies have been difficult to interpret, suggesting that more sensitive, standardized, and well-characterized assays of larger cohorts are required. Here, we describe the development of a new ELISA specifically for quantifying alphasyn in human plasma. An initial assay, using a commercial anti-alphasyn monoclonal antibody (211; Santa Cruz Biotechnology, Santa Cruz, CA) and based on a published protocol, was adapted for use in human plasma. In addition, we have developed a novel alphasyn-specific antibody for the assay that has very high sensitivity and signal:noise characteristics. Assays with either antibody showed high specificity for alphasyn, and detected it in a variety of sample types, including plasma. These assays can now be employed on large cohorts of patients and control subjects to determine whether plasma levels are altered in disease. Although measuring extracellular alphasyn levels may prove to be a useful biomarker of Parkinson's disease, it should also be a powerful tool for basic research aimed at understanding the normal and pathological physiology of alphasyn secretion. .

10 Article In vivo modulation of the firing activity of putative slow- and fast-spiking interneurons in the medial prefrontal cortex by 5-HT3 receptors in 6-hydroxydopamine-induced Parkinsonian rats. 2010

Gui, Z H / Zhang, Q J / Liu, J / Ali, U / Li, L B / Wang, Y / Wang, T / Chen, L / Hou, C / Fan, L L. ·Department of Physiology and Pathophysiology, School of Medicine, Xi'an Jiaotong University, Xi'an 710061, PR China. ·Neuroscience · Pubmed #20576497.

ABSTRACT: In the present study, we examined changes in the firing rate and firing pattern of putative slow-spiking (SS) and fast-spiking (FS) interneurons in medial prefrontal cortex (mPFC) and the effect of 5-hydroxytryptamine-3 (5-HT(3)) receptor agonist SR 57227A on the neuronal firing in rats with 6-hydroxydopamine lesions of the substantia nigra pars compacta (SNc) by using extracellular recording. The lesion of the SNc in rats decreased the firing rate of FS interneurons and the firing pattern of both SS and FS interneurons changed towards a more burst-firing. Systemic administration of SR 57227A (40-640 microg/kg, i.v.) increased the firing rate of SS interneurons, and decreased FS interneurons in sham-operated and the lesioned rats, respectively. The doses producing excitation or inhibition in the lesioned rats were higher than sham-operated rats. The local application of SR 57227A (0.01 microg) in mPFC excited SS interneurons, and inhibited FS interneurons in sham-operated rats, while having no effects on firing rate in the lesioned rats. Systemic administration of GABA(A) receptor antagonist bicuculline (2 mg/kg, i.v.) excited FS interneurons in sham-operated rats, whereas bicuculline did not change the activity of FS interneurons in the lesioned rats. Our findings indicate that the putative SS and FS interneurons activity is modulated through activation of 5-HT(3) receptor by direct or indirect action, and the lesion of the SNc leads to changes in firing activity of the SS and FS interneurons and decreased response of these interneurons to SR 57227A, suggesting dysfunction and/or down-regulation of 5-HT(3) receptor on interneurons in the 6-hydroxydopamine-lesioned rats.

11 Article The GIGYF2 variants are not associated with Parkinson's disease in the mainland Chinese population. 2010

Cao, L / Zhang, T / Zheng, L / Wang, Y / Wang, G / Zhang, J / Fei, Q Z / Cui, P J / Wang, X J / Ma, J F / Xiao, Q / Chen, S D. ·Department of Neurology and Institute of Neurology, Rui Jin Hospital affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China. ·Parkinsonism Relat Disord · Pubmed #20044296.

ABSTRACT: In order to determine the prevalence of GIGYF2 (Grb10-Interacting GYF Protein 2) variants in the Chinese population and to better understand the association between GIGYF2 and Parkinson's disease (PD), we conducted the genetic screening of GIGYF2 in the Chinese population. Twelve exonic variants were identified in 52 familial PD probands and 56 healthy controls. Non-synonymous point variants (Thr25Ala, Asn457Th and Pro460Th) were analyzed in 510 PD patients and 481 healthy controls of Chinese Han ethnicity. The insertion and deletion variants in Exon 25 (Ins Q 1212, Ins QQ 1217, Del Q 1210, Del Q 1216 and Del PPQ1217_1219) are not related to the onset of familial PD. Our data indicate the GIGYF2 variants are not associated with PD in the mainland Chinese Population.