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Article ; Online: Neurometabolic causes of dystonia: Sepiapterin reductase-deficient dopamine- and serotonin-responsive dystonia-plus syndrome.

Furukawa, Yoshiaki / Tomizawa, Yuji / Nakahara, Toshiki

2021 Volume 425, Page(s) 117468

MeSH term(s)	Alcohol Oxidoreductases ; Dopamine ; Dystonia/complications ; Dystonia/genetics ; Humans ; Serotonin
Chemical Substances	Serotonin (333DO1RDJY) ; Alcohol Oxidoreductases (EC 1.1.-) ; sepiapterin reductase (EC 1.1.1.153) ; Dopamine (VTD58H1Z2X)
Language	English
Publishing date	2021-04-21
Publishing country	Netherlands
Document type	Letter ; Comment
ZDB-ID	80160-4
ISSN	1878-5883 ; 0022-510X ; 0374-8642
ISSN (online)	1878-5883
ISSN	0022-510X ; 0374-8642
DOI	10.1016/j.jns.2021.117468
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Zs.A 308: Show issues

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Article ; Online: Abdominal Epilepsy Associated With Alzheimer's Disease.

Hayashida, Arisa / Tomizawa, Yuji / Nakahara, Toshiki / Furukawa, Yoshiaki

Journal of the American Geriatrics Society

2016 Volume 64, Issue 5, Page(s) 1146–1147

MeSH term(s)	Aged ; Alzheimer Disease/complications ; Alzheimer Disease/diagnosis ; Electroencephalography ; Epilepsies, Partial/diagnosis ; Epilepsies, Partial/etiology ; Female ; Humans ; Tomography, Emission-Computed, Single-Photon
Language	English
Publishing date	2016
Publishing country	United States
Document type	Case Reports ; Letter
ZDB-ID	80363-7
ISSN	1532-5415 ; 0002-8614
ISSN (online)	1532-5415
ISSN	0002-8614
DOI	10.1111/jgs.14125
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Ud II Zs.168: Show issues

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Article ; Online: Ophthalmic nerve hypertrophy in chronic inflammatory demyelinating polyradiculoneuropathy.

Okuzumi, Ayami / Hatano, Taku / Nakahara, Toshiki / Yokoyama, Kazumasa / Hattori, Nobutaka

Neurology

2014 Volume 82, Issue 17, Page(s) 1566–1567

MeSH term(s)	Cranial Nerve Diseases/diagnosis ; Cranial Nerve Diseases/etiology ; Female ; Humans ; Hypertrophy/etiology ; Hypertrophy/pathology ; Imaging, Three-Dimensional ; Magnetic Resonance Imaging ; Middle Aged ; Ophthalmic Nerve/pathology ; Polyradiculoneuropathy, Chronic Inflammatory Demyelinating/complications ; Polyradiculoneuropathy, Chronic Inflammatory Demyelinating/diagnosis
Language	English
Publishing date	2014-04-29
Publishing country	United States
Document type	Case Reports ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	207147-2
ISSN	1526-632X ; 0028-3878
ISSN (online)	1526-632X
ISSN	0028-3878
DOI	10.1212/WNL.0000000000000362
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Ui II Zs.153: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Zs.MG 18: Show issues
Zs.MO 374: Show issues

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Article ; Online: Pilot study of H₂ therapy in Parkinson's disease: a randomized double-blind placebo-controlled trial.

Yoritaka, Asako / Takanashi, Masashi / Hirayama, Masaaki / Nakahara, Toshiki / Ohta, Shigeo / Hattori, Nobutaka

Movement disorders : official journal of the Movement Disorder Society

2013 Volume 28, Issue 6, Page(s) 836–839

Abstract: Background: Oxidative stress is involved in the progression of Parkinson's disease (PD). Recent studies have confirmed that molecular hydrogen (H₂) functions as a highly effective antioxidant in cultured cells and animal models. Drinking H₂-dissolved ... ...

Abstract	Background: Oxidative stress is involved in the progression of Parkinson's disease (PD). Recent studies have confirmed that molecular hydrogen (H₂) functions as a highly effective antioxidant in cultured cells and animal models. Drinking H₂-dissolved water (H₂-water) reduced oxidative stress and improved Parkinson's features in model animals. Methods: In this a placebo-controlled, randomized, double-blind, parallel-group clinical pilot study, the authors assessed the efficacy of H₂ -water in Japanese patients with levodopa-medicated PD. Participants drank 1,000 mL/day of H₂-water or pseudo water for 48 weeks. Results: Total Unified Parkinson's Disease Rating Scale (UPDRS) scores in the H₂-water group (n=9) improved (median, -1.0; mean ± standard deviation, -5.7 ± 8.4), whereas UPDRS scores in the placebo group (n=8) worsened (median, 4.5; mean ± standard deviation, 4.1 ± 9.2). Despite the minimal number of patients and the short duration of the trial, the difference was significant (P<0.05). Conclusions: The results indicated that drinking H₂-water was safe and well tolerated, and a significant improvement in total UPDRS scores for patients in the H₂-water group was demonstrated.
MeSH term(s)	Aged ; Antiparkinson Agents/therapeutic use ; Double-Blind Method ; Female ; Humans ; Hydrogen/therapeutic use ; Japan ; Levodopa/therapeutic use ; Male ; Middle Aged ; Parkinson Disease/drug therapy ; Pilot Projects ; Severity of Illness Index ; Statistics, Nonparametric ; Water/administration & dosage
Chemical Substances	Antiparkinson Agents ; Water (059QF0KO0R) ; Levodopa (46627O600J) ; Hydrogen (7YNJ3PO35Z)
Language	English
Publishing date	2013-06
Publishing country	United States
Document type	Journal Article ; Randomized Controlled Trial
ZDB-ID	607633-6
ISSN	1531-8257 ; 0885-3185
ISSN (online)	1531-8257
ISSN	0885-3185
DOI	10.1002/mds.25375
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Zs.A 2555: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 238: Show issues

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Article ; Online: Randomized, double-blind, placebo-controlled pilot trial of reduced coenzyme Q10 for Parkinson's disease.

Yoritaka, Asako / Kawajiri, Sumihiro / Yamamoto, Yorihiro / Nakahara, Toshiki / Ando, Maya / Hashimoto, Kazuhiko / Nagase, Midori / Saito, Yufuko / Hattori, Nobutaka

Parkinsonism & related disorders

2015 Volume 21, Issue 8, Page(s) 911–916

Abstract: Introduction: Mitochondrial complex I deficiencies have been found in post-mortem brains of patients with Parkinson's disease (PD). Coenzyme Q10 (CoQ10) is the electron acceptor found in complexes I and II, and is a potent antioxidant. A recent trial of ...

Abstract	Introduction: Mitochondrial complex I deficiencies have been found in post-mortem brains of patients with Parkinson's disease (PD). Coenzyme Q10 (CoQ10) is the electron acceptor found in complexes I and II, and is a potent antioxidant. A recent trial of the oxidized form of CoQ10 for PD failed to show benefits; however, the reduced form of CoQ10 (ubiquinol-10) has shown better neuroprotective effects in animal models. Methods: Randomized, double-blind, placebo-controlled, parallel-group pilot trials were conducted to assess the efficacy of ubiquinol-10 in Japanese patients with PD. Participants were divided into two groups: PD experiencing wearing off (Group A), and early PD, without levodopa (with or without a dopamine agonist) (Group B). Participants took 300 mg of ubiquinol-10 or placebo per day for 48 weeks (Group A) or 96 weeks (Group B). Results: In Group A, total Unified Parkinson's Disease Rating Scale (UPDRS) scores decreased in the ubiquinol-10 group (n = 14; mean ± SD [-4.2 ± 8.2]), indicating improvement in symptoms. There was a statistically significant difference (p < 0.05) compared with the placebo group (n = 12; 2.9 ± 8.9). In Group B, UPDRS increased in the ubiquinol-10 group (n = 14; 3.9 ± 8.0), as well as in the placebo group (n = 8; 5.1 ± 10.3). Conclusions: This is the first report showing that ubiquinol-10 may significantly improve PD with wearing off, as judged by total UPDRS scores, and that ubiquinol-10 is safe and well tolerated.
MeSH term(s)	Aged ; Antioxidants/administration & dosage ; Antioxidants/pharmacology ; Double-Blind Method ; Female ; Humans ; Male ; Middle Aged ; Neuroprotective Agents/administration & dosage ; Neuroprotective Agents/pharmacology ; Parkinson Disease/drug therapy ; Pilot Projects ; Treatment Outcome ; Ubiquinone/administration & dosage ; Ubiquinone/analogs & derivatives ; Ubiquinone/pharmacology
Chemical Substances	Antioxidants ; Neuroprotective Agents ; Ubiquinone (1339-63-5) ; coenzyme Q10 (EJ27X76M46) ; ubiquinol (M9NL0C577Y)
Language	English
Publishing date	2015-08
Publishing country	England
Document type	Journal Article ; Randomized Controlled Trial
ZDB-ID	1311489-x
ISSN	1873-5126 ; 1353-8020
ISSN (online)	1873-5126
ISSN	1353-8020
DOI	10.1016/j.parkreldis.2015.05.022
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Zs.A 4553: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 420: Show issues

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Article: Ischemic tolerance in chemical preconditioning: possible role of astrocytic glutamine synthetase buffering glutamate-mediated neurotoxicity.

Hoshi, Akihiko / Nakahara, Toshiki / Kayama, Hisae / Yamamoto, Teiji

Journal of neuroscience research

2006 Volume 84, Issue 1, Page(s) 130–141

Abstract: Glutamine synthetase (GS), localized to astrocyte is a key enzyme in the glutamate-glutamine pathway in the brain. 3-Nitropropionic acid (3-NPA) is an irreversible inhibitor of succinate dehydrogenase in the tricarboxylic-acid cycle, and provides ... ...

Abstract	Glutamine synthetase (GS), localized to astrocyte is a key enzyme in the glutamate-glutamine pathway in the brain. 3-Nitropropionic acid (3-NPA) is an irreversible inhibitor of succinate dehydrogenase in the tricarboxylic-acid cycle, and provides ischemic tolerance to the brain. So far, there have been no reports on the relationship of astrocytic GS and ischemic tolerance by chemical preconditioning. In order to test the hypothesis that astrocytes serve a pivotal role in 3-NPA-induced chemical preconditioning, we have investigated the temporal profile of GS expression in astrocyte parallel with those of glial fibrillary acidic protein and heat-shock protein 70 (HSP70). In our rat model of permanent focal ischemia, preconditioning with 3-NPA singnificantly reduced the subsequent neurological deficits and infarct volume within 24-72 hours after treatment. Immunohistochemically, protoplasmic astrocytes in the cortex and striatum were activated in terms of upregulation of GS and more abundant protoplasmic processes with 3-NPA preconditioning, however, HSP70 expression could not be induced. Thus, the activation of astrocytes and upregulation of GS play an important role in 3-NPA-induced preconditioning but HSP70 does not. In view of glutamate being imposed on the cerebral ischemic damage, the astrocytic GS may contribute to 3-NPA-induced ischemic tolerance.
MeSH term(s)	Animals ; Astrocytes/drug effects ; Astrocytes/enzymology ; Behavior, Animal/drug effects ; Brain/drug effects ; Brain/pathology ; Brain Infarction/etiology ; Brain Infarction/pathology ; Convulsants/administration & dosage ; Gene Expression Regulation/drug effects ; Gene Expression Regulation/physiology ; Glutamate-Ammonia Ligase/physiology ; Immunohistochemistry/methods ; Infarction, Middle Cerebral Artery/metabolism ; Infarction, Middle Cerebral Artery/physiopathology ; Ischemic Preconditioning/methods ; Male ; Nerve Tissue Proteins/metabolism ; Nitro Compounds/administration & dosage ; Propionates/administration & dosage ; Rats ; Rats, Sprague-Dawley ; Time Factors
Chemical Substances	Convulsants ; Nerve Tissue Proteins ; Nitro Compounds ; Propionates ; Glutamate-Ammonia Ligase (EC 6.3.1.2) ; 3-nitropropionic acid (QY4L0FOX0D)
Language	English
Publishing date	2006-07
Publishing country	United States
Document type	Comparative Study ; Journal Article
ZDB-ID	195324-2
ISSN	1097-4547 ; 0360-4012
ISSN (online)	1097-4547
ISSN	0360-4012
DOI	10.1002/jnr.20869
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Zs.A 1232: Show issues

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Article: [Distigmine bromide induced Parkinsonism. A case report].

Sato, Shoichiro / Nakamura, Koichiro / Nakahara, Toshiki / Yamamoto, Teiji

Rinsho shinkeigaku = Clinical neurology

2005 Volume 45, Issue 8, Page(s) 600–602

Abstract: A 74-year-old man became unable to walk two days following the initiation of administration of oral distigmine bromide, 10 mg per day, for his constipation. Neurological examination revealed bradykinesia, rigidity and fine postural tremor without ... ...

Abstract	A 74-year-old man became unable to walk two days following the initiation of administration of oral distigmine bromide, 10 mg per day, for his constipation. Neurological examination revealed bradykinesia, rigidity and fine postural tremor without laterality. T2 weighted MRI showed mild front-temporal atrophy and multiple hyperintensities in both deep white matters. His symptoms fully improved one week after discontinuance of distigmine bromide. This is the first case report of distigmine bromide induced Parkinsonism.
MeSH term(s)	Aged ; Constipation/drug therapy ; Humans ; Male ; Parkinson Disease, Secondary/chemically induced ; Pyridinium Compounds/adverse effects
Chemical Substances	Pyridinium Compounds ; distigmine (T940307O7B)
Language	Japanese
Publishing date	2005-08
Publishing country	Japan
Document type	Case Reports ; English Abstract ; Journal Article
ZDB-ID	604200-4
ISSN	1882-0654 ; 0009-918X
ISSN (online)	1882-0654
ISSN	0009-918X
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Zs.B 1455: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Zs.MO 223: Show issues

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Article: The critical threshold of 3-nitropropionic acid-induced ischemic tolerance in the rat.

Hoshi, Akihiko / Nakahara, Toshiki / Ogata, Masahiro / Yamamoto, Teiji

Brain research

2005 Volume 1050, Issue 1-2, Page(s) 33–39

Abstract: 3-Nitropropionic acid (3-NPA) is a suicide inactivator of succinate dehydrogenase (SDH), commonly used as a pharmacological model of Huntington's disease in rodents. Several studies have shown that a single administration of 3-NPA given systemically ... ...

Abstract	3-Nitropropionic acid (3-NPA) is a suicide inactivator of succinate dehydrogenase (SDH), commonly used as a pharmacological model of Huntington's disease in rodents. Several studies have shown that a single administration of 3-NPA given systemically provides subsequent ischemic tolerance. The present study has tested the hypothesis that 3-NPA is capable of inducing tolerance in a model of permanent focal cerebral ischemia and whether 3-NPA can be truly applicable as a tolerance-inducer to ischemia. Rats given 3-NPA intraperitoneally revealed that the mortality of 3-NPA of 15, 20, and 25 mg/kg groups was 20.5, 38.8, and 83.3%, respectively. All rats survived without behavioral sequelae at smaller doses. Three days after 3-NPA preconditioning, the rats showing no behavioral changes underwent the permanent middle cerebral artery occlusion. The groups treated with 10 and 15 mg/kg of 3-NPA showed significantly reduced neurological deficits and infarction volumes in comparison with the control group, whereas the groups treated with 5 and 20 mg/kg of 3-NPA revealed no tolerance effects. When the regional SDH activity (% of control) was photometrically semi-quantified, it was observed that the activity was reduced to 90.8, 76.1, 67.8, and 64.3% in the outer layers of the cerebral cortex, and to 79.4, 67.5, 63.2, and 62.9% in the striatum 1 h after 3-NPA application (5, 10, 15, 20 mg/kg), respectively. In conclusion, although the preconditioning with 3-NPA is clearly shown in the setting of permanent ischemia, the preconditioning with this mitochondrial toxin demonstrated a rather narrow safety margin (critical threshold).
MeSH term(s)	Animals ; Brain Ischemia/drug therapy ; Brain Ischemia/mortality ; Brain Ischemia/pathology ; Convulsants/pharmacology ; Dose-Response Relationship, Drug ; Injections, Intraperitoneal ; Ischemic Preconditioning/methods ; Male ; Nitro Compounds ; Propionates/pharmacology ; Rats ; Rats, Sprague-Dawley ; Succinate Dehydrogenase/antagonists & inhibitors
Chemical Substances	Convulsants ; Nitro Compounds ; Propionates ; Succinate Dehydrogenase (EC 1.3.99.1) ; 3-nitropropionic acid (QY4L0FOX0D)
Language	English
Publishing date	2005-07-19
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	1200-2
ISSN	1872-6240 ; 0006-8993
ISSN (online)	1872-6240
ISSN	0006-8993
DOI	10.1016/j.brainres.2005.05.028
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Zs.A 161: Show issues

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Article ; Online: Motor and non-motor symptoms of 1453 patients with Parkinson's disease: prevalence and risks.

Yoritaka, Asako / Shimo, Yasushi / Takanashi, Masashi / Fukae, Jiro / Hatano, Taku / Nakahara, Toshiki / Miyamato, Nobukazu / Urabe, Takao / Mori, Hideo / Hattori, Nobutaka

Parkinsonism & related disorders

2013 Volume 19, Issue 8, Page(s) 725–731

Abstract: Purpose: We examined the prevalence and risk of clinical symptoms in a large number of Japanese patients with Parkinson's disease (PD) (n = 1453; 650 males).: Methods: Events were analyzed using Kaplan-Meier survival curves, logistic regression, and ... ...

Abstract	Purpose: We examined the prevalence and risk of clinical symptoms in a large number of Japanese patients with Parkinson's disease (PD) (n = 1453; 650 males). Methods: Events were analyzed using Kaplan-Meier survival curves, logistic regression, and Cox proportional-hazards models. Results: The mean age (SD) was 67.7 (10.0), age of onset was 58.0 (11.5), and disease duration was 9.7 (6.6) years. The mean modified Hoehn and Yahr stage was 2.8 (1.2). Most patients (88.9%) received levodopa (547.7 (257.6) mg/day). A large proportion (81.3%) received dopamine agonists (136.2 (140.7) mg/day). About 23.4% received pain treatment 6.9 (5.1) years after the onset; females (p < 0.05) and patients with late-onset PD (≥60 years, p < 0.001) were more likely to be affected. About 44.7% of patients had wearing-off 7.5 (4.7) years after the onset, and it was more common in females (p < 0.001) and patients with early-onset PD (p < 0.001). Camptocormia was found in 9.5% of patients 8.1 (6.2) years after the onset, and it was more common in females (p < 0.05) and patients with late-onset PD (p < 0.05). About 28.6% of patients developed psychosis 9.0 (5.4) years after the onset, and it was more likely to occur in patients with late-onset PD (p < 0.001). Late-onset PD and cerebrovascular disease were also associated with increased risk of pneumonia. Conclusions: Considering that very few studies have assessed numerous clinical symptoms in the same report, these data provide a useful reference for the clinical course of PD.
MeSH term(s)	Aged ; Cohort Studies ; Female ; Follow-Up Studies ; Humans ; Male ; Middle Aged ; Motor Skills Disorders/diagnosis ; Motor Skills Disorders/epidemiology ; Motor Skills Disorders/physiopathology ; Parkinson Disease/diagnosis ; Parkinson Disease/epidemiology ; Parkinson Disease/physiopathology ; Prevalence ; Retrospective Studies ; Risk Factors
Language	English
Publishing date	2013-08
Publishing country	England
Document type	Journal Article
ZDB-ID	1311489-x
ISSN	1873-5126 ; 1353-8020
ISSN (online)	1873-5126
ISSN	1353-8020
DOI	10.1016/j.parkreldis.2013.04.001
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Zs.A 4553: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 420: Show issues

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Article ; Online: Effects of Pioglitazone for Secondary Stroke Prevention in Patients with Impaired Glucose Tolerance and Newly Diagnosed Diabetes: The J-SPIRIT Study.

Tanaka, Ryota / Yamashiro, Kazuo / Okuma, Yasuyuki / Shimura, Hideki / Nakamura, Shinichiro / Ueno, Yuji / Tanaka, Yasutaka / Miyamoto, Nobukazu / Tomizawa, Yuji / Nakahara, Toshiki / Furukawa, Yoshiaki / Watada, Hirotaka / Kawamori, Ryuzo / Hattori, Nobutaka / Urabe, Takao

Journal of atherosclerosis and thrombosis

2015 Volume 22, Issue 12, Page(s) 1305–1316

Abstract: Aim: Prediabetes is an independent risk factor for future stroke. However, no effective treatment has yet been established for the recurrence of stroke in patients with prediabetes. Here we investigated the effects of pioglitazone, a potent peroxisome ... ...

Abstract	Aim: Prediabetes is an independent risk factor for future stroke. However, no effective treatment has yet been established for the recurrence of stroke in patients with prediabetes. Here we investigated the effects of pioglitazone, a potent peroxisome proliferator-activated receptor-gamma agonist, for the reduction of recurrent stroke in patients with prediabetes. Methods: Participants were patients who had a symptomatic ischemic stroke or transient ischemic attack (TIA) without a history of type 2 diabetes mellitus and who were diagnosed to have IGT or newly diagnosed diabetes by a 75-g oral glucose tolerance test. These patients were randomized to either receive or not receive pioglitazone. The primary endpoint was a recurrence of ischemic stroke. Results: A total of 120 patients were enrolled in the study. Sixty-three patients received pioglitazone and 57 were enrolled in the control group that did not receive pioglitazone. The majority of patients (68.3%) were prescribed 15 mg of pioglitazone, while the remaining patients (31.7%) were treated with 30 mg of pioglitazone. Over a median follow-up period of 2.8 years, treatment with pioglitazone was found to be associated with a lower rate of the primary endpoint (recurrence of stroke) than that observed in the control group [event rate=4.8% pioglitazone vs 10.5% control, hazard ratio=0.62, 95% confidence interval 0.13-2.35, p=0.49]. However, differences were not statistically significant. Conclusions: While this study was too underpowered to determine the effect of pioglitazone, the result failed to show beneficial effects in patients of ischemic stroke or TIA with impaired glucose tolerance and newly diagnosed diabetes.
MeSH term(s)	Adult ; Aged ; Aged, 80 and over ; Brain Ischemia/pathology ; Diabetes Mellitus, Type 2/complications ; Diabetes Mellitus, Type 2/drug therapy ; Female ; Glucose Intolerance/complications ; Glucose Intolerance/diagnosis ; Glucose Tolerance Test ; Humans ; Insulin Resistance ; Male ; Middle Aged ; PPAR gamma/agonists ; Prediabetic State/complications ; Prediabetic State/diagnosis ; Prospective Studies ; Recurrence ; Risk Factors ; Secondary Prevention/methods ; Stroke/pathology ; Stroke/prevention & control ; Thiazolidinediones/therapeutic use ; Treatment Outcome
Chemical Substances	PPAR gamma ; Thiazolidinediones ; pioglitazone (X4OV71U42S)
Language	English
Publishing date	2015
Publishing country	Japan
Document type	Journal Article ; Multicenter Study ; Randomized Controlled Trial ; Research Support, Non-U.S. Gov't
ZDB-ID	2011474-6
ISSN	1880-3873 ; 1340-3478
ISSN (online)	1880-3873
ISSN	1340-3478
DOI	10.5551/jat.30007
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Zs.A 5192: Show issues

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