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図書
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Rita Moretti, Paola Torre, Rodolofo M. Antonello, editors
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論文
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Nisikawa, Yuichi ; Watanabe, Kohei ; Holobar, Aleš ; Maeda , Noriaki ; Maruyama, Hirofumi ; Tanaka, Shinobu ; 西川, 裕一
概要:
金沢大学理工研究域フロンティア工学系<br />Patients with Parkinson's disease (PD) have greater laterality of muscle contraction properties
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than other people with parkinsonism diseases. However, few studies have reported the laterality of MU activation properties of the lower extremity muscles in patients with PD. The aim of the present study was to identify the laterality of MU behavior in PD patients using high-density surface electromyography (HD-SEMG). Eleven female patients with PD (age, 69.2 ± 6.2 years, disease duration, 2.7 ± 0.9 years, Unified Parkinson's disease Rating Scale score, 13 (9–16)), and 9 control female subjects (age, 66.8 ± 3.5 years) were enrolled in the present study. All subjects performed a sustained isometric knee extension in a 30% maximal voluntary contraction (MVC) task for 20 s. HD-SEMG signals were used to record and extract single MU firing behavior in the vastus lateralis muscle during submaximal isometric knee extensor contractions with 64 electrodes and decomposed with the convolution kernel compensation technique to extract individuals MUs. Compared to the control subjects, the patients with PD exhibited laterality of the MU firing rate and an absence of a relationship between the mean MU firing rate and MU threshold. Patients with PD exhibit laterality of MU behavior and experience MU behavioral abnormalities even with mild symptoms such as Hoehn & Yahr stage ≤ 3 and disease duration = 2.7 ± 0.9. These findings suggest the importance of considering the detection of abnormal muscle properties in PD patients beginning in the early phase of the disease. © 2020 Federation of European Neuroscience Societies and John Wiley & Sons Ltd<br />Embargo Period 12 months<br />We gratefully thank Dr. Tadashi Toyama and Dr. Sakae Miyagi, who helped perform the statistical analyses. This study was supported by research grants from JSPS KAKENHI for Young Scientists (17K17908 and 20K19448 to YN). This study was also partially supported by Bilateral Joint Research Projects of JSPS (1082626 to KW and AH) and the Slovenian Research Agency (Projects J2‐1731 and L7‐9421 and Program funding P2‐0041 to AH).
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論文
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Sakai, Kenji ; Ono, Kenjiro ; Harada, Hiromi ; Shima, Keisuke ; Notoya, Masako ; Yamada, Masahito
概要:
Patients with Parkinson's disease (PD) may develop progressive dementia late in their clinical course. Dementia in PD is
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mostly related to neuropathological findings of extensive Lewy bodies (LBs), with or without the coexistence of Alzheimer's disease (AD) pathology. Aphasia has been reported in patients with LB diseases with AD pathology; however, there have been no reports of typical PD patients developing progressive aphasia during their clinical course. We describe a female PD patient who later developed progressive conduction aphasia characterized by phonemic paraphasia and disturbance in repetition of short sentences without disturbance in writing or auditory comprehension. No episodes of fluctuations of attention, memory complaints, or planning errors were observed. She experienced episodes of visual hallucination. Her low scores on the Mini-Mental State Examination suggested impairment of orientation and attention, and her scores on Raven's Coloured Progressive Matrices test indicated impaired visuospatial functions. However, her cognitive deficits were not sufficiently severe to impair her daily life. Brain magnetic resonance images revealed atrophy of the left superior temporal gyrus and widening of the left sylvian fissure. [ 18F]-fluorodeoxyglucose positron emission tomography revealed glucose hypometabolism in the left cerebral hemisphere. These findings may be related to conduction aphasia. During the progression of PD lesions, the brainstem LB is assumed to take an upward course, extend to the limbic system, and then extend to the neocortex. Conduction aphasia observed in our patient may be associated with an unusual progression of the LB pathology from the brainstem to the left temporoparietal lobe. © Springer-Verlag 2012.
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論文
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大川, 浩子 ; 谷本, 明日香 ; 旭, 満里子 ; 成橋, 和正 ; 松下, 良 ; 坂尻, 顕一 ; 宮本, 謙一
概要:
The control of drug use for Parkinson's disease is very important for both the QOL and ADL of patients. Nowadays, patients with Parkinson's disease are treated with the concomitant use with L-dopa, dopamine receptor agonists and
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norepinephrine receptor agonists. However, these drugs elicit some adverse effects. Therefore, we tried to search for the effects and adverse effects, based on patient histories. As a result of our investigations, most patients broke out with tremors and were administered anticholinergic drugs, while a few patients were treated with L-dopa as the first drug of choice. Avoid the administration of L-dopa at first seemed to help prevent the onset of Wearing-off or On-off phenomenon. Gastric mucosal cytoprotective drugs appeared to be effective for preventing of gastric symptoms due to drugs for Parkinson's disease. Moreover, we found that mental symptoms only rarely occurred after the readministration of anticholinergic drugs. We must be careful to treat patients with brain infarction after the onset of mental symptoms. These results are valuable for helping to improve the treatment of Parkinson's disease, and may also help in performing further studies on the use of new drugs.
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論文
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Ono, Kenjiro ; Ikeda, Tokuhei ; Takasaki, Jun-ichi ; Yamada, Masahito
概要:
Lewy bodies composed of aggregates of α-Synuclein (αS) in the brain are the main histopathological features of Lewy body
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diseases (LBD) such as Parkinson's disease and dementia with Lewy bodies. Mutations such as E46K, A30P and A53T in the αS gene cause autosomal dominant LBD in a number of kindreds. Although these mutations accelerate fibril formation, their precise effects at early stages of the αS aggregation process remain unknown. To answer this question, we examined the aggregation including monomer conformational dynamics and oligomerization of the E46K, A30P, A53T and A30P/A53T mutations and wild type (WT) using thioflavin S assay, circular dichroism spectroscopy, photo-induced cross-linking of unmodified proteins, electron microscopy, and atomic force microscopy. Relative to WT αS, E46K αS accelerated the kinetics of the secondary structure change and oligomerization, whereas A30P αS decelerated them. These effects were reflected in changes in average oligomer size. The mutant oligomers of E46K αS functioned as fibril seeds significantly more efficiently than those of WT αS, whereas the mutant oligomers of A30P αS were less efficient. Our results that mutations of familial LBD had opposite effects at early stages of αS assembly may provide new insight into the molecular mechanisms of LBD. © 2011 Elsevier Inc.
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論文
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Sakai, Kenji ; Ono, Kenjiro ; Harada, Hiromi ; Shima, Keisuke ; Notoya, Masako ; Yamada, Masahito
概要:
Patients with Parkinson's disease (PD) may develop progressive dementia late in their clinical course. Dementia in PD is
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mostly related to neuropathological findings of extensive Lewy bodies (LBs), with or without the coexistence of Alzheimer's disease (AD) pathology. Aphasia has been reported in patients with LB diseases with AD pathology; however, there have been no reports of typical PD patients developing progressive aphasia during their clinical course. We describe a female PD patient who later developed progressive conduction aphasia characterized by phonemic paraphasia and disturbance in repetition of short sentences without disturbance in writing or auditory comprehension. No episodes of fluctuations of attention, memory complaints, or planning errors were observed. She experienced episodes of visual hallucination. Her low scores on the Mini-Mental State Examination suggested impairment of orientation and attention, and her scores on Raven's Coloured Progressive Matrices test indicated impaired visuospatial functions. However, her cognitive deficits were not sufficiently severe to impair her daily life. Brain magnetic resonance images revealed atrophy of the left superior temporal gyrus and widening of the left sylvian fissure. [18F]-fluorodeoxyglucose positron emission tomography revealed glucose hypometabolism in the left cerebral hemisphere. These findings may be related to conduction aphasia. During the progression of PD lesions, the brainstem LB is assumed to take an upward course, extend to the limbic system, and then extend to the neocortex. Conduction aphasia observed in our patient may be associated with an unusual progression of the LB pathology from the brainstem to the left temporoparietal lobe. © 2011 Springer-Verlag.
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論文
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Nishikawa, Yuichi ; Watanabe, Kohei ; Takahashi, Tetsuya ; Maeda , Noriaki ; Maruyama, Hirofumi ; Tanaka, Shinobu ; Hyngstrom, Allison ; 西川, 裕一 ; 田中, 志信
概要:
金沢大学理工研究域フロンティア工学系<br />The aim of this study was to quantify the laterality of motor unit (MU) activation properties in
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people with Parkinson’s disease (PD) during force production (low- to high-intensity contraction) using high-density surface electromyography (HD-SEMG). Sixteen females with PD (age = 69.9 ± 7.6 years, disease duration = 4.9 ± 5.1 years) and 14 healthy female subjects (age = 68.6 ± 3.6 years) were enrolled in the study and performed submaximal ramp-up contractions during isometric knee extension. HD-SEMG signals were recorded from both vastus lateralis muscles. We calculated the level of heterogeneity in the spatial distribution patterns of the HD-SEMG signals and determined the modified entropy, coefficient of variation of the root mean square (RMS), and correlation coefficient to evaluate MU activation properties. Pearson’s correlation coefficients were calculated to examine the relationships between disease severity and the RMS and EMG variables. The RMS value and heterogeneity were significantly higher and lower on the more-affected side in people with PD than on the other side in people with PD or either side in control subjects (p < 0.05). People with PD exhibited the temporal changes of spatial MUs activation properties showed significant laterality when compared to healthy control subjects not only in the low-intensity contractions but also in high-intensity contraction. Moderate-to-strong correlations were observed between disease severity and RMS and EMG variables in people with PD (r > 0.6, p < 0.001). We compared the laterality of MU activation properties between the people with PD and the control subjects. These findings suggest that people with PD have asymmetrical MU activation properties, regardless of the magnitude of force production.
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論文
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北尾, 康子 ; Kitao, Yasuko
概要:
パーキンソン病(PD)は黒質ドーパミン神経の選択的変性により、進行性の運動障害をきたす原因不明の神経変性疾患である。本研究において我々は、小胞体ストレス蛋白の一つORP150、若年性遺伝性パーキンソン病の原因遺伝子の一つであり、ユビキチン架
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橋酵素であるParkin、Parkinの基質として同定され、小胞体ストレスを誘起することが判明している蛋白質Pael受容体(Parkinassociated endothelin like receptor: PaelR)、更に、やはり小胞体を誘起することが判明している分泌系蛋白質Megsinを用いて、パーキンソニズムにおける小胞体ストレスの役割をより明らかにする事を目指した。アデノウイルスを用いて、PaelRをマウス線条体から逆行性に黒質緻密層(SNpc)に発現させた所、SNpc特異的に小胞体ストレス由来の神経細胞死が起こり、それらはGRP78やParkin等の小胞体関連蛋白の強制発現で改善されたが、HSP70など細胞質局在のストレス蛋白の強制発現では改善されなかった。また、小胞体ストレスモデル動物であるメグシン過剰発現ラット(Tg Meg rat)の海馬及びSNpcでは、神経細胞内凝集体の存在、小胞体ストレスの上昇に加えて、神経変性(神経細胞死)が観察された。このことから、SNpcの神経細胞が特に小胞体ストレスに対して脆弱であることが明らかになった。本研究を通じて、小胞体ストレスとパーキンソニズム発症の関連がより明らかになり、今後、小胞体ストレス制御による新しい神経保護法の開発が可能になると期待される。<br />Selective loss of dopaminergic neurons is the final common pathway in Parkinson's disease, the second most common neurodegenerative disorder. Selective neuronal expression of Pael-R(Parkin associated endothelin-like receptor)in mouse brain was achieved by injecting adenoviral vectors carrying a modified neuron-specific promoter and Cre-recombinase into the striatum. Upregulation of Pael-Receptor in the substantia nigra pars compacts (SNpc) of mice by retrograde infection induced endoplasmic reticulum(ER) stress lead to decreased levels of tyrosine hydroxylase and death of dopaminergic neurons. Neuronal cell death was not observed in the other areas of the brain projecting to/from the SNpc. The role of ER stress in dopaminergic neuronal vulnerability was highlighted by their decreased survival in mice deficient in the ubiquitin-protein ligase Parkin and the ER chaperone ORP150(150 kDa oxygen regulated protein), compared with their robust survival consequent to overexpression of either P arkin or an ER chaperone, 78 kDa glucose regulated protein (GRP78). Dopamine-related toxicity was also a key factor, as a dopamine synthetase inhibitor blocked neuronal death in parkin null mice. These data suggest a model in which ER- and dopamine-related slam are major contributors to decreased viability of dopaminergic neurons in a setting relevant to Parkinson's disease.FENIB (familial encephalopathy with neuroserpin inclusion bodies)is caused by intracellular accumulation/polymerization of mutant neuroserpins. Transgenic rats overexpressing megsin (Tg meg), a newly identified serine protease inhibitor (serpin), demonstrated intraneuronal periodic-acid Schiff (PAS)-positive inclusions distributed throughout deeper layers of cerebral cortex, CA1 of the hippocampus, and substantia nigra. Hippocampal extracts from Tg meg rats showed increased expression of ER stress proteins, and activation of caspases-12 & -3, associated with decreased neuronal density. Enhanced ER stress was also observed in dopaminergic neurons in the substantia nigra, in parallel with decreased neuronal viability and motor coordination. In each case, PAS-positive inclusions were also positive for megsin. These data suggest that overexpression of megsin results in ER stress, eventuating in the formation of PAS-positive inclusions. Tg meg rats provide a novel model relevant to FENIB in which accumulation of serpins in the ER induces selective dysfunction/loss of specific neuronal populations.<br />研究課題/領域番号:17500226, 研究期間(年度):2005-2007<br />出典：「小胞体ストレスとパーキンソニズム発症の関連に関する研究」研究成果報告書 課題番号17500226 (KAKEN：科学研究費助成事業データベース（国立情報学研究所）) 本文データは著者版報告書より作成
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