ライフサイエンスコーパス: cortical thinning

1 sful epilepsy surgery interrupts progressive cortical thinning.

2 osure group showed significant and bilateral cortical thinning.

3 of reduced anterior cingulate activation and cortical thinning.

4 sive enlargement of the medullary cavity and cortical thinning.

5 Children with ADHD had the slowest rate of cortical thinning.

6 ith and contribute additively to hippocampal cortical thinning.

7 es were associated with discrete patterns of cortical thinning.

8 up times, and its primary impact was through cortical thinning.

9 ain development, including hydrocephalus and cortical thinning.

10 stains, and 2) were correlated with apparent cortical thinning.

11 n the context of seizure severity and global cortical thinning.

12 o adulthood, and how these changes relate to cortical thinning.

13 n of tau pathology with cognitive decline or cortical thinning.

14 on pattern suggests a role for complement in cortical thinning.

15 eal OCs seen in these mice and reduced their cortical thinning.

16 n changes might precede diffuse atrophy with cortical thinning.

17 e hydrolase or FAAH) were more vulnerable to cortical thinning.

18 of known protective factors for age-related cortical thinning.

19 p = 0.024) were associated with more severe cortical thinning.

20 extrapolated to further adult aging-related cortical thinning.

21 an be characterised by a specific pattern of cortical thinning.

22 5%) and glial (61%) density with substantial cortical thinning (30%) were observed.

23 oking is associated with diffuse accelerated cortical thinning, a biomarker of cognitive decline in a

24 models to estimate the rates of accelerated cortical thinning across 68 regions from the Desikan-Kil

25 ifferences in cortical thickness and rate of cortical thinning across childhood relative to their non

26 nces in cortical thickness and trajectory of cortical thinning across childhood.

27 s, increased CAC scores were associated with cortical thinning across several brain regions, which ge

28 obar CMBs were independently associated with cortical thinning across the entire cortical regions whi

29 low-risk groups, detecting large expanses of cortical thinning across the lateral surface of the righ

30 isk families also revealed large expanses of cortical thinning across the lateral surface of the righ

31 Regions in this network undergo cortical thinning and breakdown in structural and functi

32 erum NfL was predictive for both the rate of cortical thinning and cognitive changes assessed by the

33 apeutic effect on knee OA pain by preventing cortical thinning and decreases in functional connectivi

34 Conclusion Motor and extramotor cortical thinning and diffusion-tensor MR imaging altera

35 d hydronephrosis and hydroureter with marked cortical thinning and multiple bilateral PET-avid pulmon

36 ubcortical regions lagging behind prefrontal cortical thinning and myelination and greater cortical s

37 a metabolically expensive process linked to cortical thinning and myelination, whereas paralimbic ar

38 Significant cortical thinning and neural resource allocation changes

39 thy is associated with a distinct pattern of cortical thinning and reduced functional connectivity.

40 methodology allows for a distinction between cortical thinning and reduction in cortical area and rev

41 e relationship between the rates of regional cortical thinning and severity of symptoms of hyperactiv

42 We compared regional percentage change of cortical thinning and subcortical atrophy over 18 months

43 r clinical progression, exhibited pronounced cortical thinning and subcortical atrophy over time.

44 Longitudinally, cortical thinning and subcortical atrophy patterns showe

45 matter integrity contributed to significant cortical thinning and subsequently longitudinal cognitiv

46 C9orf72 mutation carriers have faster cortical thinning and surface loss throughout adulthood

47 lear factor (NF)-kB activation, restored the cortical thinning and synaptic maturation defects in the

48 sults showed that iRBD patients present with cortical thinning and tissue deformation, which correlat

49 , a significant association between regional cortical thinning and total functional capacity, current

50 well documented using MRI, revealing ongoing cortical thinning and volume loss.

51 uli in direct proportion to the magnitude of cortical thinning and white matter hypoplasia within the

52 Purpose To investigate the patterns of cortical thinning and white matter tract damage in patie

53 silience) converged through their effects on cortical thinning and worsening cognition and together e

54 lobally, sulcal widening was associated with cortical thinning and, for the frontal cortex, with loss

55 to accelerated structural maturation (i.e., cortical thinning) and higher MDD GRS were linked to del

56 gional change in macrostructure (atrophy and cortical thinning), and microstructure (diffusion metric

57 re children also showed frontal and parietal cortical thinning, and an inverse dose-response relation

58 urological problems, including microcephaly, cortical thinning, and blindness during early developmen

59 of associations among chronic hyperglycemia, cortical thinning, and depressive symptoms in T1D.

60 or to cortical volume reductions in aging is cortical thinning, and that magnitude of change varies w

61 for Alzheimer's disease was associated with cortical thinning as a function of time since injury.

62 causes selective elimination of neurons and cortical thinning as observed in some forms of mental re

63 how a similar but less pronounced pattern of cortical thinning as patients with a psychotic disorder,

64 he symptomatic stage and was associated with cortical thinning assessed by magnetic resonance imaging

65 Cortical thinning associated with THI in the left SFC an

66 ple, a 75-year-old with abnormal amyloid and cortical thinning biomarkers has about a 20% chance of c

67 I study on BD, we did not detect accelerated cortical thinning but noted faster ventricular enlargeme

68 These reductions were mainly driven by cortical thinning, but there were also cortical area red

69 l increase, which yields to equally vigorous cortical thinning by early adolescence.

70 Our cortical thinning classifier included nine microRNAs, p=

71 have significantly more extensive and severe cortical thinning compared to females, despite similar a

72 CHR-NC also exhibited accelerated cortical thinning compared to HC in several of these are

73 nitive impairment showed more severe frontal cortical thinning compared to healthy controls.

74 extensive atrophy and greater percentage of cortical thinning compared to Parkinson's disease with n

75 irst study indicating that prefrontotemporal cortical thinning constitutes a relevant cortical pathom

76 sability and impaired cognitive performance; cortical thinning correlated with increased thalamic TSP

77 aralleled at postmortem by striatal atrophy, cortical thinning, degeneration of medium spiny neurons,

78 est possible time interval in which rates of cortical thinning differ between CHR-C, CHR non-converte

79 Cortical thinning distribution correlated with the neuro

80 han the P102L group and this correlated with cortical thinning distribution.

81 Slower cortical thinning during adolescence characterizes the p

82 ural brain networks that undergo coordinated cortical thinning during adolescence, which is in part g

83 ally, they examined whether a slower rate of cortical thinning during late childhood and adolescence,

84 ranscriptomic correlates of this accelerated cortical thinning, emphasizing the need for future longi

85 particular, the association of exercise with cortical thinning had regional specificity in the bilate

86 nalysis of the fetal brain, diffuse cerebral cortical thinning, high ZIKV RNA loads, and viral partic

87 The mice also exhibited cortical thinning, impaired neurogenesis and loss of neu

88 Whether MRI measurements of cortical thinning improve the differentiation between Al

89 at 25 gestational weeks was associated with cortical thinning in 19% of the whole cortex and 24% of

90 eukocytes associated with annualized rate of cortical thinning in a subsample of the NAPLS cohort (N=

91 mpal activity was negatively correlated with cortical thinning in a subset of regions, including the

92 al atrophy in Abeta- individuals and by mean cortical thinning in Abeta+ individuals.

93 es have found reduced gray matter volume and cortical thinning in acutely underweight patients to nor

94 Cortical thinning in AD patients with depressive symptom

95 udinal hippocampal atrophy, and longitudinal cortical thinning in AD signature regions.

96 that widespread tau was associated with mean cortical thinning in AD signature regions.

97 eased hippocampal activation correlated with cortical thinning in AD-signature regions.

98 n conclusion, the characteristic patterns of cortical thinning in Alzheimer's disease and FTD suggest

99 through cortical thickness, suggesting that cortical thinning in Alzheimer's disease-vulnerable brai

100 ar neuron depletion and progressive cerebral cortical thinning in an animal model of Canavan disease.

101 orms of childhood abuse were associated with cortical thinning in areas critical to the perception an

102 ively normal adults, CAC was associated with cortical thinning in areas related to cognitive function

103 ood and discrepantly accelerated age-related cortical thinning in autism spectrum disorders suggest t

104 thicker cortex at ~3 years of age and faster cortical thinning in autistic females.

105 seline related to faster subsequent rates of cortical thinning in both AD signature regions (~0.15%/y

106 The pattern of cortical thinning in children exposed to prenatal matern

107 Significant (p < .01) cortical thinning in children primarily in the right fro

108 sing magnetic resonance imaging, we detected cortical thinning in frontal and parietal lobes in group

109 ognitive impairment demonstrated more severe cortical thinning in frontal and temporo-parietal cortic

110 Compared to ageing-related cortical thinning in healthy subjects, we found progress

111 evidence linking the complement system with cortical thinning in humans, a process potentially invol

112 We found a global pattern of accelerated cortical thinning in individuals with schizophrenia comp

113 th antisocial personality disorder exhibited cortical thinning in inferior mesial frontal cortices.

114 ty in RLPFC could be partly accounted for by cortical thinning in IPL.

115 ), baseline WMH volumes were associated with cortical thinning in medial temporal and frontal/parieta

116 reduced higher visual function at baseline, cortical thinning in parietal, occipital and frontal cor

117 an unbiased estimate of the distribution of cortical thinning in patients (relative to controls) by

118 The appearance of cortical thinning in patients with HCHWA-D indicates tha

119 objectives were to test the hypothesis that cortical thinning in patients with schizophrenia (relati

120 g reductions in brain volume and progressive cortical thinning in patients with schizophrenia who are

121 rnalizing behavior (p < .05) was mediated by cortical thinning in prefrontal areas of the right hemis

122 Children with ADHD show relative cortical thinning in regions important for attentional c

123 better clinical outcome, is associated with cortical thinning in regions important in attentional co

124 ontrast, emotional abuse was associated with cortical thinning in regions relevant to self-awareness

125 enes whose expression is related to abnormal cortical thinning in schizophrenia have been identified.

126 omplement pathway may contribute to aberrant cortical thinning in schizophrenia prodromes and reduced

127 relation between regional amyloid burden and cortical thinning in specific brain regions.

128 symptoms in AD patients are associated with cortical thinning in temporal and parietal regions.

129 elative to controls, patients showed greater cortical thinning in temporal-prefrontal ROIs than in co

130 ke value ratio at baseline related to faster cortical thinning in the AD signature Mayo region, but t

131 More pronounced cortical thinning in the anterior insula and a greater i

132 eference shift was statistically mediated by cortical thinning in the dorsomedial prefrontal cortex.

133 was specifically associated with pronounced cortical thinning in the genital representation field of

134 y developing cohort without ADHD showed that cortical thinning in the group not taking psychostimulan

135 The group difference was due to more rapid cortical thinning in the group not taking psychostimulan

136 ood disorders is associated with progressive cortical thinning in the left inferior frontal and prece

137 peduncle, and smaller grey matter volume and cortical thinning in the leg area of the primary motor a

138 rly inattentive symptoms, so did the rate of cortical thinning in the medial and dorsolateral prefron

139 Reduced cortical glucose metabolism and cortical thinning in the medial and lateral parietal lob

140 Violence was associated with cortical thinning in the medial inferior frontal and lat

141 The analysis revealed accelerated cortical thinning in the post-COVID brain, which was mor

142 ically, total WMH volume was associated with cortical thinning in the right caudal middle frontal cor

143 These findings suggest that cortical thinning in the right hemisphere produces distu

144 The magnitude of cortical thinning in the temporal pole was found to corr

145 In particular, an extension of cortical thinning in the temporo-parietal regions in add

146 Cortical thinning in these areas was reduced after surgi

147 ere to detect the characteristic patterns of cortical thinning in these two types of dementia, to tes

148 ntrast with previous findings of age-related cortical thinning in this same autism spectrum disorders

149 se of one symptom of adult ADHD, the rate of cortical thinning increased by .0018 mm (SE = .0004, t =

150 seline cortical thickness and slower rate of cortical thinning independent of tau.

151 Age-related cortical thinning is driven by deep layers and accompani

152 Age-appropriate cortical thinning is more rapid in younger adolescent dr

153 Our findings show schizophrenia-related cortical thinning is spatially associated with functiona

154 ated with cortical thinning, suggesting that cortical thinning is spatially associated with white mat

155 reduction in cortical area and reveals that cortical thinning is the most important factor in volume

156 These differences were explained by faster cortical thinning linearly throughout adulthood in a sim

157 Mechanisms underlying cortical thinning may provide novel treatment targets pr

158 lso examined whether hippocampal atrophy and cortical thinning mediate tau effects on future memory d

159 there was a decrease in the rate of regional cortical thinning of 0.0054 mm/year (SE=0.0019 mm/year).

160 the group not taking psychostimulants (mean cortical thinning of 0.16 mm/year [SD=0.17], compared wi

161 nges in bone composition, and trabecular and cortical thinning of bone accompanied by increased bone

162 Patients showed abnormal cortical thinning of temporal cortices and thickness inc

163 The preference shift was associated with cortical thinning of the dorsomedial prefrontal cortex a

164 s who improved were more likely to have less cortical thinning of the left medial frontal cortex and

165 Cortical thinning of the left mPFC was associated with a

166 myoclonic epilepsy (JME) is associated with cortical thinning of the motor areas.

167 Patients with ALS showed cortical thinning of the motor-related cortices and a di

168 The association of parietal WMH with cortical thinning of the right rostral middle frontal, r

169 ation of total and regional WMH volumes with cortical thinning over time was tested using general lin

170 at least one rim+ lesion was related to more cortical thinning (p = 0.03) in younger patients (< 45 y

171 spinal cord lesions, and global and regional cortical thinning) parameters were assessed in a trainin

172 ctions in cortical thickness and accelerated cortical thinning, particularly within the frontal and t

173 so in a manner partially mediated by rate of cortical thinning (point estimate=0.078 (95% CIs: 0.003,

174 unters to some extent the vulnerability that cortical thinning poses for developing familial depressi

175 sy and right-sided seizure focus with global cortical thinning, potentially due to greater brain-wide

176 Findings indicate that accelerated cortical thinning precedes psychosis onset and different

177 peractivity/impulsivity had a slower rate of cortical thinning, predominantly in prefrontal cortical

178 Albuminuria was also associated with cortical thinning, predominantly in the frontal and occi

179 nce of CSS was independently associated with cortical thinning primarily in the bilateral frontal reg

180 o)manic episodes were associated with faster cortical thinning, primarily in the prefrontal cortex.

181 exposed control subjects was associated with cortical thinning, primarily in the superior frontal and

182 001) and was associated with faster rates of cortical thinning (PTE x age interactions) in medial and

183 found that the computational model recreated cortical thinning (r = 0.51, P = 0.0007) and tissue defo

184 Our findings suggest that accelerated cortical thinning, rather than cortical thickness alone,

185 cognitive impairment demonstrated widespread cortical thinning relative to controls and atrophy of th

186 regions of thinner cortex as compared to HC, cortical thinning seems to better typify DSZ, being more

187 In mice, we have shown that the cortical thinning seen in the absence of Sfrp4 is associ

188 underlying white matter was correlated with cortical thinning, suggesting that cortical thinning is

189 l intensity differences were consistent with cortical thinning/sulcal widening and ventricular enlarg

190 (white matter microstructural integrity and cortical thinning), systemic vascular health preceding t

191 n had more protective effects on age-related cortical thinning than either parameter alone.

192 be epilepsy had a more consistent pattern of cortical thinning than patients with early-onset epileps

193 ening (from ages 8-14) and widespread linear cortical thinning that have dissociable relationships wi

194 d cortical tau deposition is associated with cortical thinning that may lead to more severe memory de

195 with chronic schizophrenia showed widespread cortical thinning that particularly affected the prefron

196 eritable disorder characterized by increased cortical thinning throughout the life span.

197 ntipsychotics was associated with prefrontal cortical thinning, treatment was also associated with be

198 tions (W-score, p < 0.05, FWE-corrected) and cortical thinning (W-score, p < 0.05, FDR-corrected) tha

199 Cortical thinning was accompanied by defective cortical

200 Cortical thinning was assessed by cortical mean thicknes

201 ental-outcome analyses suggested that faster cortical thinning was associated with more externalizing

202 prenatal depression coupled with subsequent cortical thinning was associated with presence of extern

203 erters and healthy controls, and the rate of cortical thinning was correlated with levels of proinfla

204 anatomical differences, significant regional cortical thinning was found in lithium-free euthymic pat

205 Significant cortical thinning was identified in the medicated patien

206 Cortical thinning was measured vertexwise by symmetrized

207 Whereas cortical thinning was most prominent in the depths of th

208 NAPLS3), this report investigated if steeper cortical thinning was observable prior to psychosis onse

209 Widespread further cortical thinning was observed in patients compared with

210 Cortical thinning was the primary determinant of the Exp

211 Cortical lesions and the annualized cortical thinning were also evaluated.

212 late childhood as well as the trajectory of cortical thinning were modeled using spatiotemporal line

213 st that central vision loss may give rise to cortical thinning, while in the same group of people, co

214 o modified the negative impact of tau-PET on cortical thinning, while older age was associated with h

215 The selective topographical associations of cortical thinning with clinical features of HD suggest t

216 Cortical thinning within AD signature regions may develo

217 l analyses further revealed that accelerated cortical thinning within nine networks was related to ir

218 pathological factors that influence rates of cortical thinning within these AD signature regions rema

219 Thus, area 46 exhibited marked cortical thinning without apparent neuronal degeneration

220 action: with increasing age, more pronounced cortical thinning would be observed in autism spectrum d