ライフサイエンスコーパス: nonmotor

1 itary and acquired conditions-both motor and nonmotor.

2 vermal cortex to visual motion perception is nonmotor and involves a cerebellar influence on informat

3 d spectrum of brain systems involved in both nonmotor and motor function.

4 approaches and may be a result of undetected nonmotor and motor symptoms, but confirmation will be re

5 he output of the cerebellum targets multiple nonmotor areas in the prefrontal and posterior parietal

6 the access to conceptual knowledge stored in nonmotor areas is strongly debated.

7 Our results indicate that multiple motor and nonmotor areas of the cerebral cortex contain output neu

8 nect the cerebellum with the motor areas and nonmotor areas of the neocortex, and with the hypothalam

9 involved in the functional regulation of the nonmotor areas of the neocortex, including the prefronta

10 been hypothesized that spread of current to nonmotor areas of the subthalamic nucleus may be respons

11 on access to conceptual knowledge stored in nonmotor areas.

12 ty of skeletal muscles being reinnervated by nonmotor axons remains largely unknown.

13 Does the cerebellum influence nonmotor behavior?

14 unction have faced additional scrutiny since nonmotor behaviors may also be controlled by the cerebel

15 metabolism, and age-dependent alterations in nonmotor behaviors without inclusions.

16 predictive modeling is thought to extend to nonmotor behaviors.

17 lum also maintains abundant connections with nonmotor brain regions throughout postnatal life.

18 ys, that kinesin-5 homotetramers require the nonmotor C terminus for crosslinking and relative slidin

19 of the cerebellum to both motor control and nonmotor cognitive functions.

20 ether distraction was tested during motor or nonmotor cognitive tasks.

21 leep disturbances are recognized as a common nonmotor complaint in Parkinson disease but their etiolo

22 role of SERT in the development of motor and nonmotor complications in patients with PD, and we perfo

23 al participation of cerebellar structures in nonmotor cortical networks remains poorly understood and

24 ortical neurons project to diverse motor and nonmotor cortical regions, are organized topographically

25 input from deep layers of diverse motor and nonmotor cortical regions, some of which form reciprocal

26 e we examined how the abundance of motor and nonmotor cross-linkers affects the speed of cytokinetic

27 model predicted that intermediate levels of nonmotor cross-linkers are ideal for contractility; in v

28 romoted by moderate levels of both motor and nonmotor cross-linkers but attenuated by an over-abundan

29 as cytoskeletal cross-linking by myosins and nonmotor cross-linkers, are thought to promote contracti

30 attenuated by an over-abundance of motor and nonmotor cross-linkers.

31 Recognition of nonmotor disability is essential not only for ascertaini

32 e to onset of motor complications, change in nonmotor disability, and quality-of-life measures.

33 p to 40 weeks included measures of motor and nonmotor disability.

34 However, there are numerous other motor and nonmotor disease manifestations.

35 or and motor learning but also for acquiring nonmotor dispositions and tendencies that depend on new

36 rectional kinesin-5s share a long N-terminal nonmotor domain (NTnmd), absent in exclusively plus-end-

37 However, it is not known how the nonmotor domain contributes to motor activity, or how a

38 The nonmotor domain is unusual and is rich in Asn, Gln, and

39 Here, we have introduced mutations in the nonmotor domain of UNC-104 and examined whether these mu

40 its many signs similar to PD, notably in the nonmotor domain, exhibits abnormal noradrenergic markers

41 revalence by symptom description within each nonmotor domain.

42 ct to the pre-SMA are located in a ventral, "nonmotor" domain of the nucleus, whereas dentate neurons

43 2)) with both the N terminus of Spc7 and the nonmotor domains of the Klp5-Klp6 (kinesin-8) complex is

44 Mutant Myo5 proteins with deletions in nonmotor domains were expressed in myo3Delta myo5Delta c

45 a unifying cerebellar function in motor and nonmotor domains.

46 dispose striatal circuitry to both motor and nonmotor dysfunction later in life.

47 tor (eg, tremor, rigidity, bradykinesia) and nonmotor (eg, constipation, cognition, mood, sleep) sign

48 elations, and studies of cognitive and other nonmotor elements of PD.

49 the Unified Parkinson's Disease Rating Scale Nonmotor Experiences of Daily Living, the original Unifi

50 Nonmotor factors may reasonably be included in the selec

51 ng of the etiopathogenesis of this important nonmotor feature.

52 A comprehensive spectrum of motor and nonmotor features (motor severity, motor complications,

53 the disease course, studies demonstrate that nonmotor features are not solely a late manifestation.

54 These nonmotor features identify a diffuse/malignant subgroup

55 requency, pathophysiology, and importance of nonmotor features in Parkinson's disease as well as the

56 w highlights recent advances in premotor and nonmotor features in Parkinson's disease, focusing on th

57 nce supporting other therapies for motor and nonmotor features is less well established.

58 contribute differentially to both motor and nonmotor features of behavior.

59 Many of these nonmotor features reflect disturbances in nondopaminergi

60 These include various nonmotor features that predate the motor manifestations

61 Associations with early nonmotor features, including hypotension (OR, 6.84; 95%

62 ellar pathology could play a role in certain nonmotor functional deficits, thereby calling for a broa

63 in the basal ganglia for different motor and nonmotor functions and opening new questions on the arch

64 This study provides new evidence for LCN in nonmotor functions and sex-dependent differences in beha

65 increasingly recognized for its influence on nonmotor functions and structures.

66 Although a cerebellar contribution to nonmotor functions has been supported by recent studies

67 uli, suggesting that the cerebellum supports nonmotor functions in cognitive and emotional domains.

68 llar catecholamines in modulating cerebellar nonmotor functions is unknown.

69 erebellum is also consistently implicated in nonmotor functions such as language and working memory.

70 ssed in brain regions that are involved with nonmotor functions, including the neocortex and hippocam

71 impact of the murine and human cerebellum on nonmotor functions.

72 eural circuit activity for diverse motor and nonmotor functions.

73 nerative disorder characterized by motor and nonmotor impairments, including constipation.

74 In addition, a number of nonmotor manifestations can precede the onset of motor s

75 ep and alertness are some of the most common nonmotor manifestations of Parkinson disease (PD) and cu

76 y is one of the most common and debilitating nonmotor manifestations of Parkinson's disease (PD) and

77 The cause of nonmotor manifestations of PD is multifactorial, but to

78 Nonmotor manifestations of PD play a significant role in

79 ght serve as complementary therapies for the nonmotor manifestations of PD.

80 and a generally severe phenotype, including nonmotor manifestations.

81 , motor signs, cognitive function, and other nonmotor manifestations.

82 the midzonal, antiparallel MT-cross-linking nonmotor MAP, Feo, to this "slide-and-flux-or-elongate"

83 endence of microtubule interaction for three nonmotor MAPs (NuMA, PRC1, and EB1) required for cell di

84 Our findings reveal how nonmotor MAPs can generate frictional resistance in dyna

85 d conventional motor variables compared with nonmotor measures explained most of the variance of decl

86 centrioles and thus prevents triploidy by a nonmotor mechanism.

87 c mouse models of LRRK2 to explore potential nonmotor mechanisms of PD.

88 erebellum has been implicated in a number of nonmotor mental disorders such as autism spectrum disord

89 -terminal motor domain, kinesin-5 also has a nonmotor microtubule binding site in its C terminus [6].

90 tilizes a combination of four motor and four nonmotor microtubule binding sites for its microtubule o

91 Rather, kinesin-5 utilizes nonmotor microtubule binding sites to tune its microtubu

92 CENP-F is a nonmotor microtubule-binding protein that participates i

93 ingle microtubules depends on its N-terminal nonmotor microtubule-binding tail, as KlpA without the t

94 Second, Kif15 harbors a nonmotor MT-binding site, enabling dimeric Kif15 to cros

95 However, the extent to which nonmotor networks contribute to this activity is unclear

96 erebellum may guide the maturation of remote nonmotor neural circuitry and influence cognitive develo

97 n, underscores the importance of considering nonmotor neurons as therapeutic targets.

98 deficits, underscores the critical role that nonmotor neurons play in disease progression and highlig

99 ), and the previous cases were attributed to nonmotor off symptoms.

100 recent evidence shows that it is involved in nonmotor operations as well, an important question is wh

101 h more male than female participants) with a nonmotor outcome follow-up period ranging from 30 days t

102 natural history, and factors associated with nonmotor outcomes across multiple domains are unclear.

103 The evidence on nonmotor outcomes after acute ischemic stroke and intrac

104 The most prevalent adverse nonmotor outcomes by pooled prevalence were sleep distur

105 Pooled prevalence of nonmotor outcomes was estimated using random-effects mod

106 Patient-reported nonmotor outcomes were common after stroke.

107 The common factors associated with adverse nonmotor outcomes were female sex, studies with mixed st

108 o significant improvement over time for most nonmotor outcomes, except pain (coefficient = -11.0%; P

109 natural history and factors associated with nonmotor outcomes.

110 eat levodopa-related motor complications and nonmotor Parkinson's disease-related symptoms.

111 Organized assemblies of multiple motor/nonmotor particles are also illustrated toward optimal c

112 ons involving multiple motor/motor and motor/nonmotor particles, display controlled coordinated self-

113 elected to minimize the spread of current to nonmotor portions of the subthalamic nucleus using Cicer

114 terized by progressively worsening motor and nonmotor problems including cognitive and neuropsychiatr

115 , in that motor commands are tangled up with nonmotor processes such as attention and feedback proces

116 tal cortex, implicating a cerebellar role in nonmotor processes.

117 velopmentally closely related populations of nonmotor projection neurons [e.g., other subcerebral pro

118 The study of its nonmotor properties could shed light on the cognitive an

119 Kinesin-14 containing catalytic Kar3 and the nonmotor protein Vik1.

120 karyogamy, reportedly interacts with Cik1, a nonmotor protein, via its central, predicted coiled coil

121 a their kinetochores, and multiple motor and nonmotor proteins cooperate to regulate their behavior.

122 eds light on an emergent phenomenon in which nonmotor proteins work collectively via mechanochemical

123 s in oculomotor structures, but also suggest nonmotor recruitment of oculomotor machinery in decision

124 The highly helical Kar3/Cik1 nonmotor region and visible stalk indicate that dimeriza

125 circular dichroism (CD) spectroscopy of the nonmotor region shows characteristics of helical structu

126 Remarkably, the Kar3/Cik1 nonmotor region shows greater helicity by CD analysis an

127 ence of multisensory mirroring mechanisms in nonmotor regions [16-19].

128 g why and how susceptible cells in motor and nonmotor regions of the brain die in PD is the first ste

129 parameters that minimize current spread into nonmotor regions of the subthalamic nucleus.

130 in-1 activation posits that cargo binding to nonmotor regions relieves autoinhibition.

131 caused by a folded conformation that enables nonmotor regions to directly contact and inhibit the enz

132 njunction with activation of both motor- and nonmotor-related neurons.

133 , the level of activation of both motor- and nonmotor-related striatal neurons may play a critical ro

134 ding on dose and behavioral pattern, whereas nonmotor-related units are inhibited.

135 analyses, we identify that CSMN and related nonmotor SCPN specifically and progressively degenerate

136 s underwent epileptogenesis that resulted in nonmotor seizures and exhibited increased anxiety-like b

137 nd neurological data implicate cerebellum in nonmotor sensory, cognitive, vegetative, and affective f

138 cking PD from controls, even from the first, nonmotor signs and, very interestingly, also discriminat

139 cerebellar cortex and contribute to learning nonmotor skills.

140 ssociated proteins, among which is astrin, a nonmotor spindle protein.

141 complex containing two motor subunits and a nonmotor subunit known as kinesin-associated polypeptide

142 in the Chlamydomonas gene encoding KAP, the nonmotor subunit of Kinesin-2.

143 E STATEMENT Circadian disruption is a common nonmotor symptom of Huntington's disease (HD).

144 Depression, cognitive impairment, and other nonmotor symptoms (NMSs) are common early in Parkinson d

145 R], 8.7 [95% CI, 4.0-18.7]; P < .001), other nonmotor symptoms (OR, 10.0 [95% CI, 4.3-23.2]; P < .001

146 gy of PD, but it is now appreciated that the nonmotor symptoms affecting neuropsychiatric, sleep, aut

147 Diurnal fluctuations of motor and nonmotor symptoms and a high prevalence of sleep-wake di

148 ly more widespread impact, causing a host of nonmotor symptoms and associated pathology in multiple r

149 is safe and effective in improving motor and nonmotor symptoms and quality of life among Indian patie

150 VMAT2-deficient mice may display some of the nonmotor symptoms associated with PD.

151 on to motor deficits, there are a variety of nonmotor symptoms associated with PD.

152 nerative disorder characterized by motor and nonmotor symptoms due to the selective loss of midbrain

153 ntensively studied, molecular mechanisms for nonmotor symptoms in HD, such as psychiatric manifestati

154 f the circadian rhythm is one of most common nonmotor symptoms in Parkinson's disease (PD), but the m

155 drenergic neurons may underlie the disabling nonmotor symptoms in patients with Parkinson disease (PD

156 current evidence supporting the treatment of nonmotor symptoms in the advanced Parkinson's disease pa

157 nce indicates that PD is also accompanied by nonmotor symptoms including cognitive deficits, often ma

158 Evidence-based management of some nonmotor symptoms is limited by a paucity of high-qualit

159 isease as well as the recognition that these nonmotor symptoms occur in premotor, early, and later ph

160 Nonmotor symptoms of Parkinson disease (PD) often predat

161 ttime sleeping duration, is one of the early nonmotor symptoms of Parkinson disease.

162 , and age-dependent behaviors reminiscent of nonmotor symptoms of PD that were rescued by adrenergic

163 ne dysfunction may contribute to many of the nonmotor symptoms of PD, and interventions aimed at rest

164 ance our knowledge of the brain bases of the nonmotor symptoms of PD, including disrupted visual perc

165 NE) neurotransmission is associated with the nonmotor symptoms of PD, including sleep disturbances, e

166 ion reflect the field's growing focus on the nonmotor symptoms of PD, their brain bases, and the corr

167 -deficient mice may be a useful model of the nonmotor symptoms of PD.

168 ead to novel approaches for the treatment of nonmotor symptoms of PD.

169 K2 in the hippocampus that may contribute to nonmotor symptoms of PD.

170 and the limited treatment strategies for the nonmotor symptoms of the disease (ie, cognitive impairme

171 y new focus of research and treatment is the nonmotor symptoms of the disease, following from recent

172 mpaired in PD, which has been related to the nonmotor symptoms of the disease.

173 Nonmotor symptoms require nondopaminergic approaches (eg

174 Data was collected on SD using the Nonmotor Symptoms Scale (NMSS), Index of Erectile Functi

175 otor Parkinson's disease symptoms, and these nonmotor symptoms should be aggressively treated.

176 In addition, other nonmotor symptoms such as cognitive impairment are now r

177 disease patients experience a wide range of nonmotor symptoms throughout the disease course, studies

178 Nonmotor symptoms will affect quality of life more than

179 It appears that the combination of early PD nonmotor symptoms with imaging of the nigrostriatal dopa

180 exacerbate disease progression, particularly nonmotor symptoms, and contribute to the chronic neuroin

181 on is at odds with the observation that many nonmotor symptoms, including depression and cognitive in

182 d are associated with a variety of motor and nonmotor symptoms, including disturbances in mood, execu

183 nson disease) have prominent early motor and nonmotor symptoms, poor response to medication, and fast

184 kinson disease is characterized by motor and nonmotor symptoms, reduced striatal dopamine signaling,

185 tered approach to the treatment of motor and nonmotor symptoms.

186 t impair adult neurogenesis, contributing to nonmotor symptoms.

187 underlying neurobiology of earlier-appearing nonmotor symptoms.

188 tive disorder, is typified by both motor and nonmotor symptoms.

189 ected by PFBC present with diverse motor and nonmotor symptoms.

190 mergence of nonlevodopa responsive motor and nonmotor symptoms.

191 ormal functions, including certain motor and nonmotor symptoms.

192 cerebellum has an emerging relationship with nonmotor systems and may represent a powerful target for

193 ellar involvement in an increasing number of nonmotor tasks and systems has prompted an expansion of

194 n's disease (PD) patients report problems on nonmotor tasks that depend on visual or visuospatial abi

195 cleus (STN) has been implicated in motor and nonmotor tasks, and is an effective target of deep brain

196 tor signs and that extension of lesions into nonmotor territories may be deleterious.

197 ing Scale (MDS-UPDRS), together with several nonmotor tests, at baseline, 6 months, and 12 months and

198 lining daily physical activity compared with nonmotor variables.

199 tochore-microtubule interactions mediated by nonmotor viscoelastic linkages.

200 enital symptoms and restlessness, along with nonmotor wearing off and akathisia.