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Parkinson Disease: HELP
Articles by Hirokazu Iwamuro
Based on 3 articles published since 2008
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Between 2008 and 2019, Hirokazu Iwamuro wrote the following 3 articles about Parkinson Disease.
 
+ Citations + Abstracts
1 Review [Deep Brain Stimulation for Parkinson Disease:Mechanisms and New Technology]. 2017

Umemura, Atsushi / Shimo, Yasushi / Iwamuro, Hirokazu / Oyama, Genko / Hattori, Nobutaka / Arai, Hajime. ·Department of Research and Therapeutics for Movement Disorders, Juntendo University Graduate School of Medicine. ·No Shinkei Geka · Pubmed #28100856.

ABSTRACT: -- No abstract --

2 Clinical Trial Long-term safety and tolerability of ProSavin, a lentiviral vector-based gene therapy for Parkinson's disease: a dose escalation, open-label, phase 1/2 trial. 2014

Palfi, Stéphane / Gurruchaga, Jean Marc / Ralph, G Scott / Lepetit, Helene / Lavisse, Sonia / Buttery, Philip C / Watts, Colin / Miskin, James / Kelleher, Michelle / Deeley, Sarah / Iwamuro, Hirokazu / Lefaucheur, Jean Pascal / Thiriez, Claire / Fenelon, Gilles / Lucas, Cherry / Brugières, Pierre / Gabriel, Inanna / Abhay, Kou / Drouot, Xavier / Tani, Naoki / Kas, Aurelie / Ghaleh, Bijan / Le Corvoisier, Philippe / Dolphin, Patrice / Breen, David P / Mason, Sarah / Guzman, Natalie Valle / Mazarakis, Nicholas D / Radcliffe, Pippa A / Harrop, Richard / Kingsman, Susan M / Rascol, Olivier / Naylor, Stuart / Barker, Roger A / Hantraye, Philippe / Remy, Philippe / Cesaro, Pierre / Mitrophanous, Kyriacos A. ·AP-HP, Groupe Hospitalier Henri-Mondor, DHU PePsy, UF Neurochirurgie Fonctionnelle, Neurologie, Neurophysiologie, Anesthésie, Centre d'Investigation Clinique 006, Plateforme de Ressources Biologiques, Créteil, France; Université Paris 12, Faculté de Médecine, Créteil, France. Electronic address: stephane.palfi@hmn.aphp.fr. · AP-HP, Groupe Hospitalier Henri-Mondor, DHU PePsy, UF Neurochirurgie Fonctionnelle, Neurologie, Neurophysiologie, Anesthésie, Centre d'Investigation Clinique 006, Plateforme de Ressources Biologiques, Créteil, France; Université Paris 12, Faculté de Médecine, Créteil, France. · Oxford BioMedica, Oxford, UK. · CEA, DSV I(2)BM, MIRCen and CNRS URA2210, Fontenay-aux-Roses, France. · John van Geest Centre for Brain Repair and Addenbrooke's Hospital, Cambridge, UK. · AP-HP, Groupe Hospitalier Henri-Mondor, DHU PePsy, UF Neurochirurgie Fonctionnelle, Neurologie, Neurophysiologie, Anesthésie, Centre d'Investigation Clinique 006, Plateforme de Ressources Biologiques, Créteil, France; Université Paris 12, Faculté de Médecine, Créteil, France; INSERM U955, E01, Institut de Recherche Biomédicale, Créteil, France. · Gene Therapy, Centre of Neuroinflammation and Neurodegeneration, Division of Brain Sciences, Faculty of Medicine, Hammersmith Hospital Campus, London, UK. · CIC9302 and UMR 825, INSERM and Department of Pharmacology and Neurosciences, University Hospital and University of Toulouse III, Toulouse, France. · AP-HP, Groupe Hospitalier Henri-Mondor, DHU PePsy, UF Neurochirurgie Fonctionnelle, Neurologie, Neurophysiologie, Anesthésie, Centre d'Investigation Clinique 006, Plateforme de Ressources Biologiques, Créteil, France; Université Paris 12, Faculté de Médecine, Créteil, France; CEA, DSV I(2)BM, MIRCen and CNRS URA2210, Fontenay-aux-Roses, France. ·Lancet · Pubmed #24412048.

ABSTRACT: BACKGROUND: Parkinson's disease is typically treated with oral dopamine replacement therapies; however, long-term treatment leads to motor complications and, occasionally, impulse control disorders caused by intermittent stimulation of dopamine receptors and off-target effects, respectively. We aimed to assess the safety, tolerability, and efficacy of bilateral, intrastriatal delivery of ProSavin, a lentiviral vector-based gene therapy aimed at restoring local and continuous dopamine production in patients with advanced Parkinson's disease. METHODS: We undertook a phase 1/2 open-label trial with 12-month follow-up at two study sites (France and UK) to assess the safety and efficacy of ProSavin after bilateral injection into the putamen of patients with Parkinson's disease. All patients were then enrolled in a separate open-label follow-up study of long-term safety. Three doses were assessed in separate cohorts: low dose (1·9×10(7) transducing units [TU]); mid dose (4·0×10(7) TU); and high dose (1×10(8) TU). Inclusion criteria were age 48-65 years, disease duration 5 years or longer, motor fluctuations, and 50% or higher motor response to oral dopaminergic therapy. The primary endpoints of the phase 1/2 study were the number and severity of adverse events associated with ProSavin and motor responses as assessed with Unified Parkinson's Disease Rating Scale (UPDRS) part III (off medication) scores, at 6 months after vector administration. Both trials are registered at ClinicalTrials.gov, NCT00627588 and NCT01856439. FINDINGS: 15 patients received ProSavin and were followed up (three at low dose, six mid dose, six high dose). During the first 12 months of follow-up, 54 drug-related adverse events were reported (51 mild, three moderate). Most common were increased on-medication dyskinesias (20 events, 11 patients) and on-off phenomena (12 events, nine patients). No serious adverse events related to the study drug or surgical procedure were reported. A significant improvement in mean UPDRS part III motor scores off medication was recorded in all patients at 6 months (mean score 38 [SD 9] vs 26 [8], n=15, p=0·0001) and 12 months (38 vs 27 [8]; n=15, p=0·0001) compared with baseline. INTERPRETATION: ProSavin was safe and well tolerated in patients with advanced Parkinson's disease. Improvement in motor behaviour was observed in all patients. FUNDING: Oxford BioMedica.

3 Article [Pathophysiology of Parkinson's disease from the viewpoint of deep brain stimulation]. 2012

Iwamuro, Hirokazu. ·Neuroscience Division, Center for Applied Medical Research, University of Navarra, Pamplona, Spain. ·Rinsho Shinkeigaku · Pubmed #23196563.

ABSTRACT: Remarkable effectiveness of deep brain stimulation (DBS) for Parkinson's disease (PD) has occupied the interest of many scientists and their efforts for elucidating its mechanism have given us a lot of clues for understanding of pathophysiology of PD. The early idea that DBS inhibits neuronal activity of the stimulated nucleus was based on the observation that it shows similar effects as lesions, standing behind the so-called firing rate model of PD pathophysiology. However, it has been also revealed that DBS induces changes indicative of activation of outputs from the stimulated structure, which is inconsistent with the firing rate model. On the other hand, recent studies have demonstrated abnormal discharge pattern in the subthalamic nucleus and the globus pallidus of parkinsonian state, such as burst and oscillation, and its suppression by DBS. These support an idea that the pathological discharge interrupts normal information flow in the basal ganglia. Taken together, changes of firing pattern in the basal ganglia may be crucial for the PD pathophysiology, not a simple increase or decrease in firing rates. Besides, since DBS seems to affect the entire system of the basal ganglia and more, it is necessary to approach its mechanism with a systems-wide view.