ライフサイエンスコーパス: brain disease

1 biguous causal relationship of serum AB with brain disease.

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

3 other anomalies had a coexisting congenital brain disease.

4 ying other antibodies that may contribute to brain disease.

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

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

7 s therefore critical to our understanding of brain disease.

8 ural brain involvement, including Muscle Eye Brain disease.

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

10 clinical expression in carriers of genes for brain disease.

11 y may augment metabolic cascades relevant to brain disease.

12 he host cell receptor prevents severe murine brain disease.

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

14 ication of both neoplastic and nonneoplastic brain disease.

15 or elucidating certain manifestations of the brain disease.

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

17 th multiple sclerosis and 4 subjects without brain disease.

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

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

20 byrinth signal intensity or enhancement, and brain disease.

21 neration, are emerging as primary drivers of brain disease.

22 clinical trials, or their interactions with brain disease.

23 diagnosis and management of this devastating brain disease.

24 o the pathophysiology and treatment of human brain disease.

25 , hitherto not linked to human developmental brain disease.

26 icity of diagnoses of prodromal degenerative brain disease.

27 mponent of chromatin remodeling machinery in brain disease.

28 a new approach for abnormality detection of brain disease.

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

30 rams for healthy individuals and people with brain disease.

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

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

33 with the concept of a developmental pathway brain disease.

34 a specific molecular mechanism in a complex brain disease.

35 nity of pathogenic hallmarks of AD and other brain diseases.

36 therapeutic scope against hypoxia-associated brain diseases.

37 CXCL10 production by activated microglia in brain diseases.

38 S-CoV-2 infection could trigger and/or worse brain diseases.

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

40 tructure are highly consistent correlates of brain diseases.

41 es affecting brain connectivity and risk for brain diseases.

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

43 tely associated with the etiology of several brain diseases.

44 ual HDAC proteins during the pathogenesis of brain diseases.

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

46 hundreds of gene mutations causing over 100 brain diseases.

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

48 forms of psychopathology and in degenerative brain diseases.

49 in lipid biology contribute to degenerative brain diseases.

50 ld provide a therapeutic target for treating brain diseases.

51 nd isoforms could provide insight into human brain diseases.

52 es vascular permeability in many retinal and brain diseases.

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

54 se biology and provide useful information on brain diseases.

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

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

57 roinflammation in patients with AD and other brain diseases.

58 pecially for restoring neuronal functions in brain diseases.

59 3 (TDP-43) proteinopathy is seen in multiple brain diseases.

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

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

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

63 etic contributions to the pathophysiology of brain diseases.

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

65 neuropathological processes associated with brain diseases.

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

67 y diseases, including cancers and kidney and brain diseases.

68 in the initiation and progression of various brain diseases.

69 ecture and function lies at the root of many brain diseases.

70 non-invasive neural modulation tool to treat brain diseases.

71 currently the greatest challenge in treating brain diseases.

72 ular and developmental mechanisms underlying brain diseases.

73 rovide disease-relevant information for some brain diseases.

74 ism, have been implicated in a wide range of brain diseases.

75 be implicated in the pathogenesis of several brain diseases.

76 ng-term depression (LTD) in animal models of brain diseases.

77 scovery of potential therapeutic targets for brain diseases.

78 mits our understanding of the role of HEA in brain diseases.

79 activity, as well as its altered dynamics in brain diseases.

80 egion of action for risk genes implicated in brain diseases.

81 y role in learning and is altered in several brain diseases.

82 on to spatial, therapeutic windows to target brain diseases.

83 implications for the study and treatment of brain diseases.

84 apeutic lesions were used as a treatment for brain diseases.

85 ysregulated ISR and circadian dysfunction in brain diseases.

86 RNA interference therapy of other tumors or brain diseases.

87 ovides a window into the cellular origins of brain diseases.

88 ers that may aid in the diagnosis of certain brain diseases.

89 tations disrupting their function cause >130 brain diseases.

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

91 quired for effective and timely treatment of brain diseases.

92 king in the field of brain bioenergetics and brain diseases.

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

94 e neuroinflammation in vivo in patients with brain diseases.

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

96 shown promise as a nanocarrier for treating brain diseases.

97 nd might improve diagnosis and management of brain diseases.

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

99 could have important implications for common brain diseases.

100 ting gene expression changes taking place in brain diseases.

101 velopment of aging-related neurodegenerative brain diseases.

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

103 tic interpretations of genetic liability for brain diseases.

104 iable strategy for influencing the course of brain diseases.

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

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

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

108 Q transgenic mice exhibited aggravated HSV-1 brain disease and elevated CNS viral loads.

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

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

111 al measures can improve our understanding of brain disease and help identify novel interventions.

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

113 ts utility in developing novel NHP models of brain disease and suggest its potential for querying cir

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

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

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

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

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

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

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

121 or, but this limits functional recovery from brain diseases and dysfunctions in later life.

122 es/neurites, have not been clearly linked to brain diseases and have been largely non-toxic in experi

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

124 compared monitoring performance across these brain diseases and none has applied a multiple lesion mo

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

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

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

128 ght into the pathophysiology of small vessel brain disease, and its relationship with brain health an

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

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

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

132 Thus, CM is one of the most prevalent lethal brain diseases, and one for which we have no effective t

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

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

135 ecline, or whether patients with preclinical brain disease are more likely to develop delirium.

136 In addition, their roles in a number of brain diseases are being recognized.

137 Over 130 brain diseases are caused by mutations that disrupt gene

138 its brain biodistribution; and second, many brain diseases are intricately linked to microcirculatio

139 Lissencephaly ('smooth brain') is a severe brain disease associated with numerous symptoms, includi

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

141 foci in patients and facilitate the study of brain diseases associated with epilepsy.

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

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

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

145 ze proof of concept applications focusing on brain disease-associated genes, and discuss the promisin

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

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

148 s with intellectual disability, degenerative brain disease, brain injury, psychiatric disorders, func

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

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

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

152 nervous system and are widely implicated in brain diseases, but the molecular mechanisms by which as

153 d in aged individuals and accompany numerous brain diseases, but their functional importance is not u

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

155 Brain diseases can be compared and aggregated based on t

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

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

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

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

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

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

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

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

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

165 n called CSPa contributes to the progressive brain disease CLN4.

166 nstruct more accurate classifiers of several brain diseases, compared to directly training classifier

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

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

169 fits as a drug delivery vehicle for treating brain diseases due to their endogenous and innate attrib

170 Genes associated with risk for brain disease exhibit characteristic expression patterns

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

172 te that CA may contribute in some autoimmune brain diseases, exporting brain substances that interact

173 ontribute to cognitive impairment in chronic brain disease featuring elevated IFN-gamma levels, blood

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

175 dementia, intellectual disability, and other brain diseases from 1977 through 2016 (n = 1 248 252).

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

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

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

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

180 ted protein 1 (AJAP1) has been implicated in brain diseases; however, a pathogenic mechanism has not

181 Analysis of 40 common human brain diseases identifies 5 major transcriptional patter

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

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

184 owing use of myeloid cell therapies to treat brain disease in humans.

185 phalopathy (PML), an oft-fatal demyelinating brain disease in individuals receiving immunomodulatory

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

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

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

189 the presence and progression of subclinical brain disease in the general population.

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

191 in, and they present a robust model to study brain disease in vitro.

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

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

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

195 ween healthy and injured mice with different brain diseases in vivo.

196 ttern of biomarkers can be observed in other brain diseases in which Alzheimer's disease pathology is

197 n and has been implicated in a wide range of brain diseases including brain tumors, multiple sclerosi

198 In the setting of brain disease, including autism, brain tumors, and neuro

199 001 may have benefit in the treatment of TSC brain disease, including infantile spasms.

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

201 erebrospinal fluid (CSF) are associated with brain diseases, including Alzheimer's disease (AD), Park

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

203 ning cognitive function and enhanced risk of brain diseases, including cancer and neurodegenerative d

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

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

206 ativity observed in individuals with certain brain diseases, including paradoxical creativity increas

207 Imaging signatures of various brain diseases, including schizophrenia and Alzheimer's

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

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

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

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

212 Heterogeneity of brain diseases is a challenge for precision diagnosis/pr

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

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

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

216 isis provides a contemporary example of how "brain disease" is not moderated by the environmental con

217 o inhibition (E/I ratio) imbalances in human brain diseases, is a highly relevant functional measurem

218 ificant improvements in our understanding of brain diseases, many barriers remain.

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

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

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

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

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

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

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

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

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

228 rtunity for a fundamental rethink about the "brain disease model" of addiction that dominates researc

229 consequences of the risk variants linked to brain disease must be resolved.

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

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

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

233 Schizophrenia is a serious brain disease of uncertain etiology.

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

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

236 tion may contribute to common lung, eye, and brain diseases of prematurity classically associated wit

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

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

239 tem (CNS) phenotypes; however, the effect of brain disease on these inferences is unclear.

240 ary concepts relevant to understanding human brain diseases, on the genetic, subcellular, cellular, c

241 ctional alterations rather than degenerative brain disease or another structural lesion.

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

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

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

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

246 study human cortical development and explore brain disease pathology but also provide potential prosp

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

248 Brain diseases refer to any pathological conditions that

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

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

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

252 We conclude that small vessel brain disease seems to affect chronic aphasia severity t

253 neuropsychiatric or neurodegenerative human brain diseases.SIGNIFICANCE STATEMENT The common marmose

254 onal fate and function and are implicated in brain disease states.

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

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

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

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

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

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

261 refrontal dysfunction is a common feature of brain diseases such as schizophrenia and contributes to

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

263 lobal life expectancy increases, age-related brain diseases such as stroke and dementia have become l

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

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

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

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

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

269 A number of loci colocalized with brain diseases, such as glioma and stroke.

270 In addition, several brain diseases, such as neurological diseases and mood d

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

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

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

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

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

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

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

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

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

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

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

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

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

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

285 whereas there was no distinct enrichment of brain disease variants on the human lineage compared to

286 ly, conserved features were more enriched in brain disease variants, whereas there was no distinct en

287 oing so provide a contemporary update of the brain disease view of addiction.

288 Brain disease was observed, with the greatest involvemen

289 and common genetic variation associated with brain diseases, we defined noncoding regulatory regions

290 results with genetic risk factors for human brain diseases, we identified the cortical cell types an

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

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

293 esults obtained between studies of different brain diseases where P2Y(1) targeting has been proposed

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

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

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

297 is work has potential implications for other brain diseases with exaggerated neuronal synchronization

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

299 lized diagnosis of the molecular profiles of brain diseases with the potential to translate to the cl

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