ライフサイエンスコーパス: nonmotor

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

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

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

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

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

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

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

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

9 on access to conceptual knowledge stored in nonmotor areas.

10 Does the cerebellum influence nonmotor behavior?

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

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

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

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

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

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

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

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

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

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

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

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

23 Recognition of nonmotor disability is essential not only for ascertaini

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

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

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

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

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

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

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

31 a unifying cerebellar function in motor and nonmotor domains.

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

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

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

35 Nonmotor factors may reasonably be included in the selec

36 ng of the etiopathogenesis of this important nonmotor feature.

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

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

39 These nonmotor features identify a diffuse/malignant subgroup

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

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

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

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

44 Many of these nonmotor features reflect disturbances in nondopaminergi

45 These include various nonmotor features that predate the motor manifestations

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

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

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

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

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

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

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

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

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

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

56 Nonmotor manifestations of PD play a significant role in

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

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

59 and a generally severe phenotype, including nonmotor manifestations.

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

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

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

63 centrioles and thus prevents triploidy by a nonmotor mechanism.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

104 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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

129 Nonmotor symptoms will affect quality of life more than

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

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

132 mergence of nonlevodopa responsive motor and nonmotor symptoms.

133 ormal functions, including certain motor and nonmotor symptoms.

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

135 t impair adult neurogenesis, contributing to nonmotor symptoms.

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

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

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

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

140 tochore-microtubule interactions mediated by nonmotor viscoelastic linkages.

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