ライフサイエンスコーパス: cognitive disorder

1 rain, providing a basis for the seizures and cognitive disorder.

2 ural networks is a key mechanism of vascular cognitive disorder.

3 lopment and their dysfunction leads to human cognitive disorders.

4 triatum and cortex that results in motor and cognitive disorders.

5 mphasis on the development of treatments for cognitive disorders.

6 resents a promising therapeutic strategy for cognitive disorders.

7 ns in SV recycling have been associated with cognitive disorders.

8 e sleepiness (EDS) as well as other sleep or cognitive disorders.

9 test the disconnection mechanism directly in cognitive disorders.

10 rranean diet score with the incident risk of cognitive disorders.

11 e possible involvement of Notch signaling in cognitive disorders.

12 ment of schizophrenia, and potentially other cognitive disorders.

13 rbations in Rho GTPase signaling may lead to cognitive disorders.

14 tors such as dopamine have a central role in cognitive disorders.

15 ined by its association with common and rare cognitive disorders.

16 alleviate symptoms associated with numerous cognitive disorders.

17 te for further evaluation as a treatment for cognitive disorders.

18 neration, demyelinating and aging-associated cognitive disorders.

19 the pathophysiology of a variety of mood and cognitive disorders.

20 ntributes to multiple neurodevelopmental and cognitive disorders.

21 erns of Mediterranean diet score on incident cognitive disorders.

22 neurobiological predisposition to later-life cognitive disorders.

23 tegory was not significantly associated with cognitive disorders.

24 tertiary research clinic that specialized in cognitive disorders.

25 systems and potential avenues for correcting cognitive disorders.

26 neurodevelopment and may underlie postnatal cognitive disorders.

27 restore learning and memory in a variety of cognitive disorders.

28 elated complications, diabetes mellitus, and cognitive disorders.

29 t strategies for improving working memory in cognitive disorders.

30 outcomes for the fetus, including postnatal cognitive disorders.

31 nd reduce neuropathology in rodent models of cognitive disorders.

32 tween orchiectomy and GnRHa for diabetes and cognitive disorders.

33 host of neurodegenerative and developmental cognitive disorders.

34 tribute to the pathogenesis of developmental cognitive disorders.

35 ay be of therapeutic benefit in AD and other cognitive disorders.

36 ic plasticity and are implicated in multiple cognitive disorders.

37 a novel therapeutic target for treatment of cognitive disorders.

38 loss may hold promise for new treatments for cognitive disorders.

39 g pathology in many symptomatically distinct cognitive disorders.

40 f value in the treatment of mGluR-LTD-linked cognitive disorders.

41 ribute to our understanding and treatment of cognitive disorders.

42 and with it, the prevalence of postoperative cognitive disorders.

43 e for GRASP1 in the pathophysiology of human cognitive disorders.

44 several human intellectual disabilities and cognitive disorders.

45 s of BAF complexes in human intellectual and cognitive disorders.

46 roach for the treatment of schizophrenia and cognitive disorders.

47 rain development and pathogenesis of diverse cognitive disorders.

48 s to treat infectious diseases, cancers, and cognitive disorders.

49 f fibrinogen in infection, inflammation, and cognitive disorders.

50 linical candidate for potential treatment of cognitive disorders.

51 y are especially dosage-sensitive targets of cognitive disorders.

52 tanding of the epigenetic changes underlying cognitive disorders.

53 compounds for the treatment of affective and cognitive disorders.

54 vulnerability or resilience to emotional and cognitive disorders.

55 increases the risk for anxiety, immune, and cognitive disorders.

56 ies can induce mood, anxiety, psychotic, and cognitive disorders.

57 icity have been linked to drug addiction and cognitive disorders.

58 lation may inform therapeutic strategies for cognitive disorders.

59 uting genetic factor in Chr22qter-associated cognitive disorders.

60 ty, sleep apnea, cardiovascular disease, and cognitive disorders, a broad spectrum of collateral oral

61 lexia is one of the most prevalent childhood cognitive disorders, affecting approximately 5% of schoo

62 For example, one of the best known cognitive disorders, Alzheimer's disease (AD), is treate

63 iscuss the prevalence and characteristics of cognitive disorders and dementia in patients with CKD, b

64 ages of CKD have a higher risk of developing cognitive disorders and dementia.

65 responsible for the involvement of Shrm4 in cognitive disorders and epilepsy.

66 to the National Institute of Neurologic and Cognitive Disorders and Stroke (NINCDS) compared with 14

67 ion might help to identify people at risk of cognitive disorders and to facilitate the development of

68 lay a crucial role in cancer, infectious and cognitive disorders, and cardiovascular diseases.

69 of tCS for major depression, schizophrenia, cognitive disorders, and substance use disorders.

70 inversely associated with the developing of cognitive disorders, and the pooled RR (95% CI) was 0.79

71 biquitin ligase that is mutated in the human cognitive disorder Angelman syndrome and duplicated in s

72 A variety of cognitive disorders are worsened by stress exposure and

73 d promising diagnostic accuracy for vascular cognitive disorder (area under the curve, 0.82 [95% conf

74 B-cell proliferative disorders, depression, cognitive disorders, arthritis and Sjogren's syndrome).

75 cognitive impairment refers to all forms of cognitive disorder associated with cerebrovascular disea

76 llnesses such as autism, mental retardation, cognitive disorders associated with Alzheimer and Parkin

77 n and circadian disruption underlie mood and cognitive disorders associated with irregular light sche

78 implications for understanding the origin of cognitive disorders associated with Reelin deficiency.

79 sticity in the hippocampus may contribute to cognitive disorders associated with TBI (traumatic brain

80 veral neurodevelopmental disorders including cognitive disorders, autism, juvenile-onset schizophreni

81 imals but cannot be used in the treatment of cognitive disorders because of anxiogenic and convulsant

82 ry importance in the design of therapies for cognitive disorders, because this type of memory is impa

83 We show that Phf6, a gene mutated in the cognitive disorder Borjeson-Forssman-Lehmann syndrome, i

84 ked with schizophrenia, a neurodevelopmental cognitive disorder characterized by imbalances in glutam

85 serves as a new target for the treatment of cognitive disorders characterized by aberrant neuronal m

86 in 111 patients who presented to the Oxford Cognitive Disorders Clinic, Oxford, UK, including 29 amn

87 7 MCI subjects drawn from a university-based cognitive disorders clinic.

88 ry early after infection, yet HIV-associated cognitive disorders do not typically manifest until the

89 romising lead compounds for the treatment of cognitive disorders, e.g., Alzheimer's disease.

90 ors are potential compounds for treatment of cognitive disorders, e.g., Alzheimer's disease.

91 bjects met diagnostic criteria for syndromic cognitive disorders (five MCMD and one HAD).

92 rovide an explanation for lifelong disabling cognitive disorder, guide prognosis, and highlight medic

93 neuropathic pain, and neurodegenerative and cognitive disorders has been exhibited clinically for se

94 connect them to behavioral endophenotypes in cognitive disorders has proven to be an effective approa

95 Episodic memory deficit is a common cognitive disorder in human temporal lobe epilepsy (TLE)

96 te to the sensorimotor gating deficiency and cognitive disorders in aging mice.

97 tential preventative target of Abeta-related cognitive disorders in HIV-affected patients.

98 To treat cognitive disorders in humans, new effective therapies t

99 ial implications to the basis of age-related cognitive disorders in humans.

100 s in IL1RAPL1-regulated pathways can lead to cognitive disorders in humans.

101 s in IL1RAPL1-regulated pathways can lead to cognitive disorders in humans.SIGNIFICANCE STATEMENT Abn

102 celerated cognitive impairment or even frank cognitive disorders in later life.

103 re of the changes resulting in the motor and cognitive disorders in the chronic stage is unknown.

104 The high rate of psychiatric and cognitive disorders in the patients with degenerative ce

105 f VCI has evolved to describe a continuum of cognitive disorders in which vascular brain injury plays

106 Postoperative cognitive disorders including delirium and postoperative

107 herapeutic approaches toward psychiatric and cognitive disorders, including cognitive impairment asso

108 art cerebrovascular disease plays in several cognitive disorders, including the hereditary vascular d

109 The high incidence of involvement in cognitive disorders is also found in mouse mutants and i

110 e neuronal damage seen in AIDS patients with cognitive disorders is caused indirectly via viral and c

111 volvement of organophosphate insecticides in cognitive disorders is supported by epidemiologic and bi

112 s involvement in pathologies associated with cognitive disorders is unknown.

113 ndent kinase 5 (Cdk5) has been implicated in cognitive disorders, its role in learning has been obscu

114 g disability (RD), or dyslexia, is a complex cognitive disorder manifested by difficulties in learnin

115 Cognitive disorders may also be associated with drugs of

116 When aberrations in this process occur, cognitive disorders may result.

117 with no sequalae (n = 5), to moderate, with cognitive disorders (n = 4).

118 Our results support the hypothesis that cognitive disorders observed in vine workers may be asso

119 sophila model system for study of hereditary cognitive disorders of humans.

120 idence linking PPI deficits with some of the cognitive disorders of schizophrenia.

121 dysregulated translational control to treat cognitive disorders of synaptic dysfunction.

122 n axon tracts, which could contribute to the cognitive disorders of these patients, has not been expl

123 herapeutic agent for preventing and treating cognitive disorders of various origins, preferably in pa

124 ease subjects met DSM-IV criteria for either cognitive disorder or dementia.

125 range of pathological conditions, including cognitive disorders, Parkinson's disease, and neuropathi

126 pendent kinase 5 signalling in cognition and cognitive disorders remains unclear.

127 ehavior and also suggest a strategy to treat cognitive disorders resulting from synapse loss.

128 perspective on the association of TCF4 with cognitive disorders.SIGNIFICANCE STATEMENT The importanc

129 ve function, and its possible involvement in cognitive disorders such as Alzheimer's disease.

130 cular basis for a cerebellar contribution to cognitive disorders such as autism.

131 mechanisms underlying memory impairments in cognitive disorders, such as Alzheimer's disease (AD), a

132 berrant epigenetic modifications may lead to cognitive disorders that affect learning and memory, and

133 dissecting the molecular pathways underlying cognitive disorders that disrupt speech, language, and v

134 en the cortex and hippocampus, especially in cognitive disorders that involve both structures, such a

135 schizophrenia, Parkinson's disease, autism, cognitive disorders) that are linked with abnormalities

136 Despite being one of the most common cognitive disorders, the clinical diagnosis of ADHD is b

137 AR) hypofunction as an underlying factor for cognitive disorders, the precise roles of various NMDAR

138 t of Mediterranean diet in the occurrence of cognitive disorders; therefore, we performed an updated

139 he importance of specific HAT modulators for cognitive disorder treatment.

140 Cognitive disorders, vacuolar myelopathy, and sensory ne

141 ination antiretroviral therapy (ART) for HIV cognitive disorders vary substantially between individua

142 .1%], classified as having probable vascular cognitive disorder) were older than nonimpaired patients

143 Auts2, a gene linked to human evolution and cognitive disorders, which displays strong clustering of

144 gene expression program are mutated in human cognitive disorders, which suggest that this program is