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Parkinson Disease: HELP
Articles by Takashi Kudo
Based on 3 articles published since 2010
(Why 3 articles?)

Between 2010 and 2020, Takashi Kudo wrote the following 3 articles about Parkinson Disease.
+ Citations + Abstracts
1 Review Circadian dysfunction may be a key component of the non-motor symptoms of Parkinson's disease: insights from a transgenic mouse model. 2013

Willison, L David / Kudo, Takashi / Loh, Dawn H / Kuljis, Dika / Colwell, Christopher S. ·Division of Child and Adolescent Psychiatry, Laboratory of Circadian and Sleep Medicine, University of California, Los Angeles, David Geffen School of Medicine, Los Angeles, CA, USA. ·Exp Neurol · Pubmed #23353924.

ABSTRACT: Sleep disorders are nearly ubiquitous among patients with Parkinson's disease (PD), and they manifest early in the disease process. While there are a number of possible mechanisms underlying these sleep disturbances, a primary dysfunction of the circadian system should be considered as a contributing factor. Our laboratory's behavioral phenotyping of a well-validated transgenic mouse model of PD reveals that the electrical activity of neurons within the master pacemaker of the circadian system, the suprachiasmatic nuclei (SCN), is already disrupted at the onset of motor symptoms, although the core features of the intrinsic molecular oscillations in the SCN remain functional. Our observations suggest that the fundamental circadian deficit in these mice lies in the signaling output from the SCN, which may be caused by known mechanisms in PD etiology: oxidative stress and mitochondrial disruption. Disruption of the circadian system is expected to have pervasive effects throughout the body and may itself lead to neurological and cardiovascular disorders. In fact, there is much overlap in the non-motor symptoms experienced by PD patients and in the consequences of circadian disruption. This raises the possibility that the sleep and circadian dysfunction experienced by PD patients may not merely be a subsidiary of the motor symptoms, but an integral part of the disease. Furthermore, we speculate that circadian dysfunction can even accelerate the pathology underlying PD. If these hypotheses are correct, more aggressive treatment of the circadian misalignment and sleep disruptions in PD patients early in the pathogenesis of the disease may be powerful positive modulators of disease progression and patient quality of life.

2 Clinical Trial Evaluation of striatal oxidative stress in patients with Parkinson's disease using [62Cu]ATSM PET. 2011

Ikawa, Masamichi / Okazawa, Hidehiko / Kudo, Takashi / Kuriyama, Masaru / Fujibayashi, Yasuhisa / Yoneda, Makoto. ·Second Department of Internal Medicine (Neurology), Faculty of Medical Sciences, University of Fukui, Eiheiji-cho, Fukui 910-1193, Japan. ·Nucl Med Biol · Pubmed #21982566.

ABSTRACT: INTRODUCTION: To clarify the role of oxidative stress and mitochondrial dysfunction in the pathogenesis of Parkinson's disease (PD) in living patients, positron emission tomography (PET) with [(62)Cu]diacetyl-bis(N(4)-methylthiosemicarbazone) ([(62)Cu]ATSM) was applied to functional imaging of oxidative stress mainly due to mitochondrial dysfunction in the striata of patients with PD. METHODS: Fifteen PD patients who presented with lateral dominant symptoms at onset and six healthy controls underwent [(62)Cu]ATSM PET. Dynamic PET data acquisition was performed, and standardized uptake values (SUVs) were obtained from the delayed phase of dynamic data by means of region of interest analysis. The striatum-to-cerebellum SUV ratio (S/C ratio) was calculated from the SUV in all subjects of the striatum and the cerebellar cortex. RESULTS: The mean S/C ratio of the bilateral striata of the patients (1.15±0.10) was significantly increased compared with that of the controls (1.08±0.02) (P<.05). In the patients, the S/C ratio of the bilateral striata showed a positive correlation with the Unified Parkinson's Disease Rating Scale (UPDRS) rating (r=0.52, P<.05), and the S/C ratio of the striatum contralateral to the initially affected body side showed a strong positive correlation with the UPDRS rating (r=0.62, P<.05). CONCLUSIONS: [(62)Cu]ATSM PET imaging demonstrated that striatal oxidative stress was enhanced in PD patients compared with the controls and increased with the progression of disease severity, particularly in the contralateral striatum. These findings indicated that oxidative stress associates with striatal neurodegeneration in PD.

3 Article Circadian dysfunction in a mouse model of Parkinson's disease. 2011

Kudo, Takashi / Loh, Dawn H / Truong, Danny / Wu, Yingfei / Colwell, Christopher S. ·Department of Psychiatry & Biobehavioral Sciences, University of California-Los Angeles, Los Angeles, CA 90024, USA. ·Exp Neurol · Pubmed #21864527.

ABSTRACT: Many Parkinson's disease (PD) patients exhibit sleep disorders as part of their symptoms with evidence suggesting that REM sleep disorders may be intimately associated with this disease. Possible dysfunction in the circadian system in PD has received less attention, yet problems in circadian timing are common in neurodegenerative diseases. In the present study, we examined the expression of daily and circadian rhythms in the alpha-synuclein overexpressing (ASO) transgenic line. We found selective deficits in the expression of circadian rhythms of locomotor activity, including lower night-time activity and greater fragmentation in the wheel-running activity in this PD model. These alterations were prominent in young adult (3-4 mo) ASO mice and worsened progressively with age, consistent with prior reports of age-related loss of motor skills. The temporal distribution of sleep was also altered in the ASO mice compared to littermate controls. In the ASO mice, the peak/trough expression of the clock gene PERIOD2 was normal in the master pacemaker of the circadian system: the suprachiasmatic nucleus (SCN); however, the daytime firing rate of SCN neurons was reduced in the mutant mice. Together, this data raises the possibility that a weakening of circadian output is a core feature of PD. The reduction in magnitude of circadian output would be expected to have functional consequences throughout the body.