ライフサイエンスコーパス: brain disease

1 ques have become commonplace in the study of brain disease.

2 untington's disease is an autosomal dominant brain disease.

3 s therefore critical to our understanding of brain disease.

4 ural brain involvement, including Muscle Eye Brain disease.

5 rkers for, and contributors to, small-vessel brain disease.

6 clinical expression in carriers of genes for brain disease.

7 y may augment metabolic cascades relevant to brain disease.

8 he host cell receptor prevents severe murine brain disease.

9 n of the contribution of viral infections to brain disease.

10 ication of both neoplastic and nonneoplastic brain disease.

11 or elucidating certain manifestations of the brain disease.

12 utic potential of MSRA in ischemic heart and brain disease.

13 rams for healthy individuals and people with brain disease.

14 th multiple sclerosis and 4 subjects without brain disease.

15 the Walker-Warburg syndrome, and muscle-eye-brain disease.

16 age and sex effects in cognitive ability and brain disease.

17 byrinth signal intensity or enhancement, and brain disease.

18 a new approach for abnormality detection of brain disease.

19 uscle, brain and eye, such as the muscle-eye-brain disease.

20 specific XFI to study the role of taurine in brain disease.

21 with the concept of a developmental pathway brain disease.

22 a specific molecular mechanism in a complex brain disease.

23 ), to Walker-Warburg Syndrome and Muscle-Eye-Brain disease.

24 biguous causal relationship of serum AB with brain disease.

25 ) and ocular abnormalities termed muscle-eye-brain disease.

26 other anomalies had a coexisting congenital brain disease.

27 ying other antibodies that may contribute to brain disease.

28 tations disrupting their function cause >130 brain diseases.

29 hundreds of gene mutations causing over 100 brain diseases.

30 quired for effective and timely treatment of brain diseases.

31 reveal the role of endogenous GDNF in human brain diseases.

32 forms of psychopathology and in degenerative brain diseases.

33 in lipid biology contribute to degenerative brain diseases.

34 ld provide a therapeutic target for treating brain diseases.

35 nd isoforms could provide insight into human brain diseases.

36 ons, which are common early features of many brain diseases.

37 es vascular permeability in many retinal and brain diseases.

38 iRNA for therapy of drug addiction and other brain diseases.

39 se biology and provide useful information on brain diseases.

40 n is found in a variety of neurodegenerative brain diseases.

41 ribute to the development of immune-mediated brain diseases.

42 roinflammation in patients with AD and other brain diseases.

43 pecially for restoring neuronal functions in brain diseases.

44 tegrity and the BBB breakdown in HIV-related brain diseases.

45 the pathology, and may play a role in other brain diseases.

46 ssue is used for the study of many different brain diseases.

47 e neuroinflammation in vivo in patients with brain diseases.

48 at can monitor the metabolic changes in most brain diseases.

49 g a formidable hurdle to drug development in brain diseases.

50 may not be unique to these rare degenerative brain diseases.

51 nd might improve diagnosis and management of brain diseases.

52 s the blood-brain barrier (BBB) for treating brain diseases.

53 could have important implications for common brain diseases.

54 ting gene expression changes taking place in brain diseases.

55 velopment of aging-related neurodegenerative brain diseases.

56 cells of the brain and contribute to common brain diseases.

57 tic interpretations of genetic liability for brain diseases.

58 iable strategy for influencing the course of brain diseases.

59 o understand the roles of microglia in human brain diseases.

60 therapeutic scope against hypoxia-associated brain diseases.

61 CXCL10 production by activated microglia in brain diseases.

62 obably applicable also to other small-vessel brain diseases.

63 tructure are highly consistent correlates of brain diseases.

64 es affecting brain connectivity and risk for brain diseases.

65 e useful in terms of therapeutic options for brain diseases.

66 tely associated with the etiology of several brain diseases.

67 ual HDAC proteins during the pathogenesis of brain diseases.

68 acy of cell-based treatments of inflammatory brain diseases.

69 el of one of these CMDs, known as muscle-eye-brain disease, a disorder that is caused by loss of an e

70 As with many other brain diseases, addiction has embedded behavioral and so

71 explain the incomplete relationship between brain disease and cognitive status in people with neurol

72 t a search for frontal and anterior temporal brain disease and for dementing disorders.

73 e demonstrated that patients with muscle-eye-brain disease and Fukuyama congenital muscular dystrophy

74 rome (AGS) presents as a severe neurological brain disease and is a genetic mimic of the sequelae of

75 mpaired, leading to a lack of concurrence of brain disease and tissue injury in other organs.

76 Fukuyama CMD, muscle-eye-brain disease and Walker-Warburg syndrome, each associat

77 observed in the human conditions muscle-eye-brain disease and Walker-Warburg syndrome.

78 Further progress in understanding brain diseases and behavior demands fuller collaboration

79 Mutations causing brain diseases and cancer in humans and mice have been a

80 Synaptic function is affected in many brain diseases and disorders.

81 edical and clinical investigation of various brain diseases and disorders.

82 attention for the diagnosis and treatment of brain diseases and neurological disorders.

83 mplexan parasite that can cause eye disease, brain disease, and death, especially in congenitally inf

84 sting new links between splicing regulation, brain disease, and development.

85 include Walker-Warburg syndrome, muscle-eye-brain disease, and Fukuyama-type congenital muscular dys

86 f brain-behavior relationships, the study of brain disease, and, ultimately, clinical applications of

87 whether their illness is primary, due to SLE brain disease, and/or due to treatments for SLE.

88 ron-specific enolase-producing tumors, acute brain diseases, and hemolysis.

89 s have emerged as important factors for many brain diseases, and the discovery of epigenetic processe

90 n establishing the causal role of viruses in brain disease are explored here.

91 s emerged as a critical pathogenic factor in brain diseases associated with activation of N-methyl-D-

92 In contrast, GWAS meta-analyses of two other brain diseases associated with hippocampal pathology (Al

93 COX-2 is likely to play a role also in other brain diseases associated with inflammation.

94 about when and where in the developing human brain disease-associated genes converge.

95 oup B, asymptomatic or minimally symptomatic brain disease at presentation; and group C, development

96 on of this network can withstand more severe brain disease before exhibiting cognition similar to pat

97 Cocaine addiction is a chronically relapsing brain disease, but its neural basis is not yet well unde

98 has long been implicated in pathogenesis of brain disease, but its role in the spinal cord is unclea

99 m is involved in the pathogenesis of several brain diseases, but its physiological functions remain u

100 pt arose from the discovery that devastating brain diseases called spongiform encephalopathies are tr

101 ronal circuit are fundamentally altered in a brain disease caused by a known molecular defect and tha

102 ltifocal leukoencephalopathy (PML) is a rare brain disease caused by reactivation of the JC virus.

103 cephalopathy (PML) is a rare but often fatal brain disease caused by reactivation of the polyomavirus

104 Prion diseases represent the archetype of brain diseases caused by protein misfolding, the most co

105 Prion diseases represent the archetype of brain diseases caused by protein misfolding, with the mo

106 MGnT1) knockout mouse, a model of muscle-eye-brain disease, caused by breaches in the pial basement m

107 Future studies might elucidate how brain diseases change this modular architecture within b

108 ions in the human LIS1 gene cause the smooth brain disease classical lissencephaly.

109 ith genetic and proteome data provides a new brain disease classification system based on molecular e

110 The spectrum of inflammatory brain disease continues to expand with the recognition o

111 his paradigm suggests that antibody-mediated brain disease does not depend on immune complex formatio

112 with brain malformations, such as muscle-eye-brain disease, exhibit neural ectopias caused by overmig

113 nfectious agents that cause invariably fatal brain diseases following silent incubation periods that

114 ncluding Walker-Warburg syndrome, muscle-eye-brain disease, Fukuyama congenital muscular dystrophy, a

115 nce of genes related to synaptic function in brain disease has been implied in studies describing de

116 A number of human brain diseases have been associated with disturbances in

117 is known about how these processes result in brain disease, how SVD lesions contribute to neurologica

118 as independently associated with subclinical brain disease in a community-based cohort without overt

119 elationship of LVEF and GLS with subclinical brain disease in a community-based cohort.

120 s the most common cause of neurodegenerative brain disease in preadulthood.

121 of magnetic resonance spectroscopy to study brain disease in preclinical models.

122 ailure, but its association with subclinical brain disease in the general population is unknown.

123 They show an inflammatory component of brain disease in the two MPS, as is known for many neuro

124 Chronic pain should thus be considered a brain disease in which alterations in neural networks af

125 Addiction is a chronic brain disease in which individuals cannot control their

126 ence is indirect and comes from analogies to brain diseases in adults, and from models of brain damag

127 001 may have benefit in the treatment of TSC brain disease, including infantile spasms.

128 ducing damage to brain in distinct models of brain disease, including ischemia.

129 may play a pathophysiological role in human brain diseases, including autism spectrum disorder, anxi

130 (mTOR) pathway are found in a wide range of brain diseases, including FMCDs.

131 despite continuing neuronal loss in several brain diseases, including multiple sclerosis (MS).

132 arrangements of SV40 RR are not required for brain disease induction in immunosuppressed monkeys.

133 ich exercise training can reduce the risk of brain diseases, inform the optimization of exercise trai

134 other technologies previously used to study brain disease, iPSC modeling has the promise to influenc

135 ntries, the risk of environmentally mediated brain disease is augmented several fold by lack of infra

136 ibility of using genes as medicines to treat brain diseases is currently limited by the lack of safe

137 Pharmacologic remedy of many brain diseases is difficult because of the powerful drug

138 growing view that developing drugs to treat brain diseases is more difficult and often more time-con

139 Muscle eye brain disease (MEB) and Fukuyama congenital muscular dys

140 y demonstrated that patients with muscle-eye-brain disease (MEB) and Fukuyama congenital muscular dys

141 enital muscular dystrophy (FCMD), Muscle-Eye-Brain disease (MEB) and Walker-Warburg syndrome (WWS), w

142 Walker-Warburg Syndrome (WWS) and muscle-eye-brain disease (MEB) are caused by mutations in two genes

143 enital muscular dystrophy (FCMD), muscle-eye-brain disease (MEB), and Walker-Warburg syndrome are con

144 Muscle-eye-brain disease (MEB), is caused by mutations in the POMGn

145 ental study with a mouse model of muscle-eye-brain disease, mice deficient in O-mannose beta1,2-N-ace

146 ental study with a mouse model of muscle-eye-brain disease, mice deficient in O-mannose beta31,2-N-ac

147 onal Institute on Drug Abuse has advocated a brain disease model of addiction (BDMA).

148 Kleine-Levin syndrome (syndrome secondary to brain diseases; n = 4, atypical syndrome, n = 7; differe

149 ade alleviate neurodegeneration in different brain diseases, namely at early stages of another polygl

150 ciated diseases including ischemic heart and brain disease, neurodegeneration, or cancer.

151 Schizophrenia is a serious brain disease of uncertain etiology.

152 izophrenia is a common chronic and disabling brain disease of unknown etiology, pathogenesis, and mec

153 ase and death that resembles the wasting and brain diseases of HIV without the T cell immunodeficienc

154 tures created spontaneously by patients with brain disease often display impaired or diminished artis

155 ry knowledge) lessens the negative impact of brain disease on cognition, such that people with greate

156 lective disorders of reading, resulting from brain disease or injury, in previously literate adults.

157 Increasingly, research is showing how brain disease or poor physical health negatively impacts

158 utic potential for treatment of a variety of brain diseases or as pharmacological tools for studies o

159 otransmission are two early symptoms of most brain diseases, our work also provides a basis for under

160 ents with the frequently fatal demyelinating brain disease progressive multifocal leukoencephalopathy

161 rentiating the various types of inflammatory brain disease remains challenging and benefits from a sy

162 Autoimmune-mediated inflammatory brain diseases represent a rapidly evolving area of medi

163 The understanding of brain diseases requires the identification of the molecu

164 The increasing use of mouse models for human brain disease studies presents an emerging need for a ne

165 vel relationship could be more important for brain diseases study.

166 hey are also a core component of maladaptive brain diseases such as addiction.

167 y of using gene therapy for the treatment of brain diseases such as brain cancer, Alzheimer's and Par

168 rget for the treatment of cancer and several brain diseases such as depression and neurodegeneration.

169 derstand the pathophysiology of inflammatory brain diseases such as MS.

170 een made in recent years, drug discovery for brain diseases such as schizophrenia and mood disorders

171 mate receptors may play an important role in brain diseases such as stroke, brain or spinal cord trau

172 normal cerebral energy metabolism and during brain diseases such as stroke.

173 functioning and is thought to be involved in brain diseases, such as Alzheimer disease and depression

174 s traumatic brain injury and stroke, and for brain diseases, such as Alzheimer's and Parkinson's.

175 e of pathologies of interest in degenerative brain diseases, such as amyloid plaques and changes in c

176 nthesize these aldehydes die in degenerative brain diseases, such as Parkinson's and Alzheimer's.

177 potential therapeutic approaches to treating brain diseases, such as stroke, in which lactic acidosis

178 ppocampal sclerosis of ageing is a prevalent brain disease that afflicts older persons and has been l

179 Alzheimer's disease (AD) is a degenerative brain disease that destroys memory and other important m

180 Schizophrenia is a multifocal brain disease that involves abnormal brain connectivity.

181 osite: those pictures created in the face of brain disease that show enhanced or enduring artistry, a

182 T are primarily used to identify or rule out brain diseases that are associated with amyloid patholog

183 imaging signals and for the understanding of brain diseases that are associated with neurovascular dy

184 growth inhibitory factor is unique, and for brain diseases that have been related to oxidative or ni

185 e phosphorylation is usually associated with brain disease, these findings provide a powerful context

186 ions are infectious agents that cause lethal brain diseases; they arise from misfolding of a cell sur

187 contribute to the prevention of a series of brain diseases; this may be of special value given the a

188 odifies risk and/or severity of a variety of brain diseases through still elusive molecular mechanism

189 discuss obstacles and solutions for modeling brain disease using CPART.

190 Brain disease was observed, with the greatest involvemen

191 MS (age 27-77 years) and 6 subjects without brain disease were analyzed.

192 ency virus-infected rhesus monkeys with SV40 brain disease were analyzed.

193 y advances our understanding of degenerative brain disease with implications for both neuroscience an

194 evere Walker-Warburg syndrome and muscle-eye-brain disease with striking structural brain and eye def

195 uroscience identified addiction as a chronic brain disease with strong genetic, neurodevelopmental, a

196 The treatment of brain diseases with gene therapy requires the gene to be

197 ple sclerosis, the prototypical inflammatory brain disease, with ~0.4% of Purkinje cells being binucl