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1 pendence has traditionally been considered a brain disorder.
2 n LIS1 causes lissencephaly, a developmental brain disorder.
3 RNA binding protein associated with a human brain disorder.
4 ause in some patients CFS is thought to be a brain disorder.
5 comparing other mouse strains and models of brain disorder.
6 ut instead leads to a discrete developmental brain disorder.
7 myelination, is implicated in many forms of brain disorder.
8 ques to quantitative studies of this complex brain disorder.
9 life and were more directly related to their brain disorder.
10 se elimination in health and a developmental brain disorder.
11 iants in the molecular genetic dissection of brain disorders.
12 ay be sites of deregulation in developmental brain disorders.
13 ey matter architecture plays in a variety of brain disorders.
14 athophysiological mechanisms in a variety of brain disorders.
15 ssion in the brain has been observed in many brain disorders.
16 potential as therapeutic agents for multiple brain disorders.
17 sy is one of the most common and intractable brain disorders.
18 a common pathologic process in developmental brain disorders.
19 tractive approach for modeling aging-related brain disorders.
20 ially facilitating diagnosis and therapy for brain disorders.
21 evelopmental processes common among distinct brain disorders.
22 is known about I/E ratio dynamics in complex brain disorders.
23 provide novel therapeutic targets for adult brain disorders.
24 deficient in individuals with SCZ and other brain disorders.
25 lopment of precision medicine strategies for brain disorders.
26 their dysfunction is implicated in multiple brain disorders.
27 ove cognitive function and behavior in these brain disorders.
28 o assist in the innovation of treatments for brain disorders.
29 roles in neuronal development, survival, and brain disorders.
30 on is central to the pathogenesis of several brain disorders.
31 ew small-molecule drugs for the treatment of brain disorders.
32 n more than 20 000 subjects and 26 different brain disorders.
33 their dysfunction may contribute to various brain disorders.
34 abnormal than non-hubs in many (if not all) brain disorders.
35 n mature neural circuits and are involved in brain disorders.
36 lop cell type-targeted therapeutics to treat brain disorders.
37 ted studies have been performed using PRP in brain disorders.
38 e involved in the pathophysiology of certain brain disorders.
39 lopment, cognition and synaptic pathology of brain disorders.
40 ble successful genetic analyses of polygenic brain disorders.
41 thophysiology, and treatment of degenerative brain disorders.
42 al processes of multiple sclerosis and other brain disorders.
43 e for a cohort of patients with these common brain disorders.
44 ience and the persistent needs of those with brain disorders.
45 irections and implications for understanding brain disorders.
46 me an essential tool for treating a range of brain disorders.
47 ng of common nonfamilial "sporadic" forms of brain disorders.
48 omising targets for the treatment of various brain disorders.
49 ies of neuroanatomy in mouse models of human brain disorders.
50 ination as a pathophysiological mechanism in brain disorders.
51 f clinical interventions to treat DA-related brain disorders.
52 ic and epigenetic risk maps of developmental brain disorders.
53 degeneration, Parkinson's disease, and other brain disorders.
54 anding how neural plasticity is expressed in brain disorders.
55 munity as a comparative instrument to assess brain disorders.
56 ial progenitors for the treatment of various brain disorders.
57 as a model in the study of this and relevant brain disorders.
58 ed our understanding of mechanisms mediating brain disorders.
59 expression regulation with implications for brain disorders.
60 the applicability of mouse models for human brain disorders.
61 bances in self-awareness observed in various brain disorders.
62 axis response to stress and related chronic brain disorders.
63 ntral nervous system (CNS) and of associated brain disorders.
64 expression can be used in the study of human brain disorders.
65 as a major obstacle to the treatment of most brain disorders.
66 ic drugs for the treatment of striatal-based brain disorders.
67 and neurogenesis in a wide variety of human brain disorders.
68 ent of future therapies for stroke and other brain disorders.
69 to treatment for these common, debilitating brain disorders.
70 plications for reparative cell therapies for brain disorders.
71 FSCN1 as a candidate gene for developmental brain disorders.
72 is now utilized for an increasing number of brain disorders.
73 euronal apoptosis in neurodegenerative human brain disorders.
74 target for drug development in a variety of brain disorders.
75 ch are important in the pathogenesis of many brain disorders.
76 and abnormal patterns of gene expression in brain disorders.
77 ive enhancement and the treatment of diverse brain disorders.
78 prevention, diagnostics, and therapeutics of brain disorders.
79 al brain function and in the pathogenesis of brain disorders.
80 l nervous system and implications in various brain disorders.
81 tions, when applied to the analysis of human brain disorders.
82 e neuronal death associated with a number of brain disorders.
83 e applied to analyze the anatomical basis of brain disorders.
84 ic variations observed in complex congenital brain disorders.
85 rain function and to better understanding of brain disorders.
86 g stress, trauma, infection, and in specific brain disorders.
87 t could be used for imaging amyloid or other brain disorders.
88 ective compounds for use in the treatment of brain disorders.
89 mental processes and the complex pathways of brain disorders.
90 netics efficiently into new therapeutics for brain disorders.
91 tanding of the role of the receptor in human brain disorders.
92 t can counteract deficits underlying various brain disorders.
93 ge cohorts of individuals with developmental brain disorders.
94 luN2B antagonists with therapeutic value for brain disorders.
95 CKD is linked with various brain disorders.
96 l and genetic heterogeneity of developmental brain disorders.
97 rable neurons for in vitro investigations of brain disorders.
98 y of this approach for epigenomic studies of brain disorders.
99 hat transcriptionally mimic autism and other brain disorders.
100 on is implicated in the etiology of numerous brain disorders.
101 barrier, could be a precious tool to tackle brain disorders.
102 he pathophysiological role of neuroligins in brain disorders.
103 roRNA profiles have been implicated in human brain disorders.
104 nt novel therapeutic targets in HD and other brain disorders.
105 of candidate genes related to developmental brain disorders.
106 ndividuals with any one of six developmental brain disorders.
107 bition and might contribute to developmental brain disorders.
108 sex-specific susceptibility and severity of brain disorders.
109 y and prevention of delayed complications in brain disorders.
110 n of the resting brain and how it changes in brain disorders.
111 has been increasingly implicated in numerous brain disorders.
112 dysregulation is also implicated in numerous brain disorders.
113 ierarchies in the brain and their defects in brain disorders.
114 r challenge to treatment of a broad range of brain disorders.
115 herapeutic implications for neuropsychiatric brain disorders.
116 ognitive processes and their dysfunctions in brain disorders.
117 ltiple neural circuit alterations underlying brain disorders.
118 ion patterns may enable treatment of various brain disorders.
119 applications for amblyopia and other visual brain disorders.
120 terations in processes such as aging [4] and brain disorders [5], highlighting the importance of rest
122 ding of how changes in inhibition in complex brain disorders affect I/E dynamics, leading to region-s
124 attern of expression, which occur in several brain disorders, alter synaptic maturation and function
125 ses--'not organic', a physical disability, a brain disorder and a psychiatric problem--as well as con
127 d that this mutation underlies the carrier's brain disorder and sought to explore its functional cons
128 ively controls progression of Abeta-mediated brain disorder and that it may have the potential to be
129 to underlie CNS pathophysiology in heritable brain disorders and age-related neurodegenerative and co
130 Neuroinflammation is involved in several brain disorders and can be monitored through expression
133 understanding the pathological mechanisms of brain disorders and for developing new approaches to eff
134 ns in homeostatic mechanisms associated with brain disorders and implications for identifying new tre
136 ongly up-regulated in various forms of acute brain disorders and injuries including epilepsy, stroke
137 -brain barrier dysfunction is common in most brain disorders and is associated with disease course an
140 on (DBS) has been used to treat a variety of brain disorders and shows promise in alleviating cogniti
141 g of the neurobiological and mental basis of brain disorders and that such insights will be key to pr
143 y during adulthood may exacerbate underlying brain disorders and/or worsen recovery from brain stress
144 Cigarette smoking is a chronic relapsing brain disorder, and remains a premier cause of morbidity
145 neuronal injury associated with a number of brain disorders, and Ca(2+)-permeable AMPA receptors (CP
146 ial embryonic lethality, growth retardation, brain disorders, and maternal effect lethality, phenotyp
147 nked to increased risk of neurodevelopmental brain disorders, and recent evidence implicates altered
148 erstanding of developmental and degenerative brain disorders, and we discuss how they could influence
149 DRB6, associated with both immunological and brain disorders, and ZFP57, a trans-acting regulator of
153 roteins encoded by genes involved in complex brain disorders are distributed through spatiotemporal p
155 leading theory holds that neurodevelopmental brain disorders arise from imbalances in excitatory and
156 l lobe epilepsy (TLE), a common, intractable brain disorder, arises in children with febrile status e
157 linked to the pathogenesis of a spectrum of brain disorders, as well as cancer and several periphera
158 understanding, preventing, and treating some brain disorders associated with alcohol abuse and alcoho
159 a potential therapeutic target for treating brain disorders associated with dysregulated Dscam expre
162 otential of zebrafish tests to model complex brain disorders associated with monoamine dysregulation.
164 ors (mGluRs) are potential novel targets for brain disorders associated with the dysfunction of prefr
166 may provide an entry point for understanding brain disorders at a causal mechanistic level, and that
168 stitutes of Health, McKnight Neuroscience of Brain Disorders award, the Fondo de Investigaciones Sani
169 utes of Health, the McKnight Neuroscience of Brain Disorders award, The Fondo de Investigaciones Sani
170 is increasingly applied for the treatment of brain disorders, but its mechanism of action remains unk
171 2 (NPY2) receptors are implicated in diverse brain disorders, but no suitable PET radiotracers are cu
172 ing is implicated in cognitive processes and brain disorders, but the effect of DRD2 variants remains
173 ry targeting ciliopathy genes known to cause brain disorders, but whose roles in brain development ar
175 e now being developed for treatment of human brain disorders by direct delivery inside the blood brai
176 ol to people after stroke or other traumatic brain disorders by helping to guide activity-dependent b
177 pilepsies are one of the most common serious brain disorders, can occur at all ages, and have many po
178 reutzfeldt-Jakob disease (CJD), an incurable brain disorder caused by alterations in prion protein st
179 nant progressive and fatal neurodegenerative brain disorder caused by an expanded CAG/polyglutamine r
181 sical lissencephaly is a human developmental brain disorder characterized by a paucity of cortical gy
182 Hemimegalencephaly (HMG) is a developmental brain disorder characterized by an enlarged, malformed c
183 Joubert syndrome (JS) is a developmental brain disorder characterized by cerebellar vermis hypopl
184 ecognizing addiction as a chronic, relapsing brain disorder characterized by compulsive drug seeking
185 nal ceroid lipofuscinosis, which is a severe brain disorder characterized by progressive loss of brai
187 proach not only for AD, but also for various brain disorders characterized by alterations in immediat
188 ene contributes to the cognitive deficits in brain disorders characterized by fewer dendritic spines.
189 g from studies addressing these illnesses as brain disorders, developmental disorders, and complex ge
190 nce our understanding of the human brain and brain disorders, discuss bioethical considerations, and
198 Herein, the authors present a summary of brain disorders in which MR spectroscopy has an impact o
199 enes with brain aging and, by extension, for brain disorders in which their expression is decreased.
201 ay also contribute to the pathophysiology of brain disorders including schizophrenia and fragile X sy
202 nicotinic acetylcholine receptor (nAChR) and brain disorders including schizophrenia, Alzheimer's dis
203 xic stresses involved in the pathogenesis of brain disorders including stroke, and Alzheimer's and Pa
204 rs (nAChR's) have been implicated in several brain disorders, including addiction, Parkinson's diseas
205 as a novel therapeutic approach to multiple brain disorders, including Alzheimer and Huntington dise
207 potential of zebrafish for modeling complex brain disorders, including attention-deficit/hyperactivi
208 developmental, neurological, and psychiatric brain disorders, including autism spectrum disorders, Pa
210 in the L1 gene are linked with a spectrum of brain disorders, including loss of the corticospinal tra
211 with many human cancers, as well as various brain disorders, including macrocephaly, seizures, Lherm
212 obstacle to the development of therapies for brain disorders, including Parkinson's disease (PD).
213 signaling is suspected to underlie multiple brain disorders, including schizophrenia, Parkinson's di
215 Irritable bowel syndrome (IBS) is a gut-brain disorder involving alterations in intestinal sensi
218 of genetic causes among clinically distinct brain disorders is consistent with the concept of develo
220 that more than 40% of the societal burden of brain disorders is likely to be genetically mediated.
221 roaches to non-invasively treat a variety of brain disorders is transcranial magnetic stimulation (TM
223 ; consider the overarching effect of broader brain disorders on both epilepsy and neurobehavioural co
224 osure to infectious agents to development of brain disorders; others have identified autoantibodies i
225 y strategies to human personality traits and brain disorders, our data may be useful for developing f
226 e significant implications for understanding brain disorders presenting with cortical morphogenetic a
227 IK3R2 gene are associated with developmental brain disorders ranging from BPP with a normal head size
233 maceuticals are potential imaging agents for brain disorders, should these agents be enabled to under
234 el the pathogenesis of several developmental brain disorders.SIGNIFICANCE STATEMENT GABA is the major
235 tly identified complement gene mutations and brain disorders.SIGNIFICANCE STATEMENT The complement sy
239 (Dscam) is implicated in the pathogenesis of brain disorders such as Down syndrome (DS) and fragile X
240 ance in synaptic transmission underlies many brain disorders such as epilepsy, schizophrenia, and aut
241 on and aetiological understanding of complex brain disorders such as obsessive-compulsive disorder (O
242 normalities pertinent to dopamine-associated brain disorders such as schizophrenia and attention defi
246 al involvement of these molecules in certain brain disorders, such as addiction, Parkinson's disease,
248 AP1/Syngap1 commonly occurs in developmental brain disorders, such as intellectual disability, epilep
250 of these oscillations has been implicated in brain disorders, such as schizophrenia and Alzheimer's d
251 hibitory synapses is associated with complex brain disorders, such as schizophrenia and epilepsy.
254 ed genes, suggesting that the differences in brain disorder susceptibility between males and females
256 common, disabling, and undertreated episodic brain disorder that is more common in women than in men.
257 hrenia is a life-long, severe, and disabling brain disorder that requires chronic pharmacotherapy.
259 e brain's memory management system and human brain disorders that alter active forgetting mechanisms.
260 d as anesthetic agents and as drugs to treat brain disorders that are ameliorated by positive alloste
261 F14 gene in humans have been associated with brain disorders that are partially recapitulated in Fgf1
263 old promise for defining the pathogenesis of brain disorders that have resisted simple molecular desc
264 hyperactivity disorder (ADHD) are widespread brain disorders that involve disturbances of dopaminergi
265 gation of important underlying mechanisms of brain disorders that is not possible through neural reco
266 l application of B. caapi alkaloids to other brain disorders that may benefit from stimulation of end
269 channelopathies represent a growing class of brain disorders that usually result in paroxysmal disord
271 utes of Health, the McKnight Neuroscience of Brain Disorders, the Fondo de Investigaciones Sanitarias
272 nvestigations of neurobiological markers for brain disorders, the number of multi-site studies involv
273 ave been reported in the vascular-associated brain disorders, the roles of TLJN in AD brains are stil
274 type I lissencephaly, a severe developmental brain disorder thought to result from abnormal neuronal
275 ting psychiatric and medical formulations of brain disorders, thus fostering cross-fertilizing intera
277 to aid in determining the pathophysiology of brain disorders, to determine novel therapeutic strategi
279 zebrafish in modeling a wide range of human brain disorders, we also summarize recent applications a
280 imaging lesions that were common across all brain disorders were more likely to be located in hubs o
281 viance that was largely independent of their brain disorder, whereas late starters (onset at age 19 o
282 luminating the architecture of developmental brain disorders, which include structural malformations
288 lepsy and idiopathic hypersomnia are chronic brain disorders with an onset at a young age, whereas sl
289 data should inform treatment strategies for brain disorders with impaired motivation such as schizop
290 for myocardial ischemia, hypoxic tumors, and brain disorders with regionalized oxidative stress, such
291 rk of many neurodegenerative and psychiatric brain disorders, yet we know little about the mechanisms
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