ライフサイエンスコーパス: cerebral

1 cordings of firing rate of DRN 5-HT neurons, cerebral 5-HT depletion, and optogenetic activation and

2 In NCI, proNGF correlated with cerebral Abeta and tau deposition and to cognitive perfo

3 ker that is specific for AD, correlates with cerebral Abeta and tau pathology, and predicts future co

4 uopathies is the misfolding, aggregation and cerebral accumulation of tau deposits.

5 onally, controls were able to modulate their cerebral activity based on task difficulty.

6 llness, time to disease onset, morphology of cerebral alpha-synuclein deposits and the conformational

7 Cerebral amyloid angiopathy (CAA) and beta-amyloid (Abet

8 farcts and leukoencephalopathy (CADASIL) and cerebral amyloid angiopathy (CAA) are two distinct vascu

9 Cerebral amyloid angiopathy (CAA), where beta-amyloid (A

10 ain vasculature lead to a condition known as cerebral amyloid angiopathy (CAA), which impairs blood-b

11 Hereditary cerebral amyloid angiopathy (HCAA) is a rare familial fo

12 Fourteen autopsy cases with cerebral amyloid angiopathy (mean age at death 73 years,

13 Although chronic hypertension and cerebral amyloid angiopathy are the underlying cerebral

14 s to be the result of predominantly advanced cerebral amyloid angiopathy of the leptomeningeal vessel

15 des excellent contrast for Abeta plaques and cerebral amyloid angiopathy.

16 ablished haemorrhagic neuroimaging marker of cerebral amyloid angiopathy.

17 Although cerebral amyloid-beta deposition occurs on a continuum,

18 monitoring allows the in vivo evaluation of cerebral and cardiovascular haemodynamic responses to di

19 exaggerated the vasoconstrictor responses of cerebral and mesenteric resistance arteries.

20 characterize involvement of uremic toxins in cerebral and neurobehavioral abnormalities in three rat

21 mpared with those without, displayed greater cerebral and regional volume and greater regional surfac

22 eometric feature has been applied to predict cerebral aneurysm rupture, but not examined as predictor

23 ding various intravascular methods, treating cerebral aneurysms can be still a therapeutic challenge.

24 wever, which neurons control the dynamics of cerebral arteries is not well understood.

25 We present a case of focal cerebral arteriopathy and ischemic stroke in a pediatric

26 had poorly reactive pupils with asymptomatic cerebral arteriopathy resembling her daughters.

27 fined by location (at proximal/distal middle cerebral artery (MCA), within/beyond diffusion-weighted

28 Cerebral blood velocity in the middle cerebral artery (MCAv) was obtained by transcranial Dopp

29 interval [CI]: 1.1, 2.8; P = .02) and middle cerebral artery location (OR, 1.9; 95% CI: 1.2, 3.0; P =

30 mboembolic events were female sex and middle cerebral artery location.

31 Using the mouse middle cerebral artery occlusion (MCAO) stroke model, we have e

32 We induced transient middle cerebral artery occlusion (tMCAO) in T2D/obese mice (aft

33 rct volumes 3 and 7 d after transient middle cerebral artery occlusion (tMCAo), independent of changi

34 We used a transient middle cerebral artery occlusion model to induce stroke and exa

35 fecal transplant gavage 3 days after middle cerebral artery occlusion using young donor biome (2-3 m

36 rious microvascular settings, such as middle cerebral artery occlusion, femoral artery clipping, and

37 80 male rats underwent 90-min middle cerebral artery occlusion.

38 t strokes are caused by occlusion of a major cerebral artery, and substantial advances have been made

39 r individuals and found associations between cerebral atherosclerosis and reduced synaptic signaling

40 sistently, single-cell RNA sequencing showed cerebral atherosclerosis associated with higher oligoden

41 imaging findings of vascular brain injury or cerebral atrophy in adult American Indians.

42 acterized by amyloid plaques and progressive cerebral atrophy.

43 Dynamic cerebral autoregulation (CA) is manifested by changes in

44 Dynamic cerebral autoregulation (CA) is often expressed by the m

45 lacement is associated with worsening global cerebral autoregulation and cerebral autoregulation asym

46 erebral autoregulation, and interhemispheric cerebral autoregulation asymmetry were assessed using mi

47 worsening global cerebral autoregulation and cerebral autoregulation asymmetry, and poor long-term cl

48 s between lateral brain displacement, global cerebral autoregulation, and interhemispheric cerebral a

49 multimodal monitoring, was used to evaluate cerebral autoregulation.

50 Cerebral autosomal dominant arteriopathy with subcortica

51 The small-vessel disorder cerebral autosomal dominant arteriopathy with subcortica

52 highly sensitive in the characterization of cerebral AVMs measuring less than 3cm, of those located

53 euronal death in a transgenic mouse model of cerebral beta-amyloidosis.

54 mal studies indicate that insulin influences cerebral bioenergetics, enhances synaptic viability and

55 nknown Core cooling by 1.0 degrees C reduced cerebral blood flow (CBF) by 20-30% and cerebral oxygen

56 heimer's disease, attenuates the increase in cerebral blood flow (CBF) evoked by neural activity (fun

57 (ASL) MRI, nonresponders exhibited increased cerebral blood flow (CBF) in bilateral anterior hippocam

58 ed by the mean arterial blood pressure (MAP)-cerebral blood flow (CBF) relationship, with little atte

59 l collateral vessels play a critical role in cerebral blood flow (CBF) restoration following ischemic

60 Aerobic exercise elicits increases in cerebral blood flow (CBF), as well as core body temperat

61 ystem that conducts continuous monitoring of cerebral blood flow (CBF).

62 ffusivity), white matter lesions (WMLs), and cerebral blood flow (CBF).

63 degrees C); however, such exercise increases cerebral blood flow (CBF; +10-20%) mediated via small el

64 is a neuroimaging technique used to measure cerebral blood flow (CBF; perfusion) to understand brain

65 The influence of reproductive hormones on cerebral blood flow and sex differences in the ability o

66 Here, we reveal a mechanism for cerebral blood flow control, a precapillary sphincter at

67 sham procedure with continuous monitoring of cerebral blood flow using laser Doppler, NIRS and ICP.

68 appropriately matched increases in regional cerebral blood flow) is preserved during both exercise a

69 CKD is associated with abnormalities in cerebral blood flow, cerebral neurochemical concentratio

70 matter tracts and a colocalized increase in cerebral blood flow.

71 ion of blood pressure, body temperature, and cerebral blood flow.

72 pivotal role in coupling neural activity and cerebral blood flow.

73 Cerebral blood velocity in the middle cerebral artery (M

74 roduct of metabolism, has a strong impact on cerebral blood vessels, a phenomenon known as cerebrovas

75 , where beta-amyloid (Abeta) deposits around cerebral blood vessels, is a major contributor of vascul

76 mount of glucose transporter type 1-positive cerebral blood vessels, reverted cerebral vasoreactivity

77 nd REM sleep, mice showed large increases in cerebral blood volume ([HbT]) and arteriole diameter rel

78 rmality volume, Gaussian-normalized relative cerebral blood volume (nrCBV), Gaussian-normalized relat

79 high glutamate/glutamine and elevated focal cerebral blood volume on functional magnetic resonance i

80 n emerging technique that detects changes of cerebral blood volume triggered by brain activation.

81 pathologies of hippocampal dysfunction-focal cerebral blood volume, focal atrophy, and evidence of el

82 n (PFBC), a genetic disease characterized by cerebral calcium-phosphate deposition and associated wit

83 for the molecular and cellular mechanisms of cerebral cavernous malformation pathologies.

84 GCK-1 (germinal center kinase-1) and CCM-3 (cerebral cavernous malformations-3), participate in a ne

85 ither platelets or T cells displayed reduced cerebral CD4(+) T-cell infiltration and thrombotic activ

86 healthy controls to characterize preclinical cerebral changes leading to symptoms.

87 ed endocannabinoid dysregulation focusing on cerebral changes that are temporally proximal to stresso

88 Cerebral choline metabolism is crucial for normal brain

89 reatment and improvement or normalization of cerebral circulation time CTT).

90 mportant role in the control of systemic and cerebral circulation.

91 st types of interneurons to migrate into the cerebral cortex and become incorporated into functional

92 The cerebral cortex and cerebellum both play important roles

93 cographic (ECoG) activity across the lateral cerebral cortex as people heard and then mentally rehear

94 Neurons in the cerebral cortex connect through descending pathways to h

95 The mouse cerebral cortex contains neurons that express choline ac

96 rns that yield important insights into human cerebral cortex development.

97 des evidence of common mechanisms across the cerebral cortex for generating global percepts from sepa

98 However, gadolinium retention in the cerebral cortex has not been systematically investigated

99 that result from abnormal development of the cerebral cortex in utero.

100 The cerebral cortex is the main striatal afferent, and progr

101 niscent of processes in the developing human cerebral cortex necessary for generating expanded neuron

102 axonal regeneration of mechanically injured cerebral cortex neurons from mice.

103 Here, we derive organoids resembling the cerebral cortex or the hindbrain/spinal cord and assembl

104 regates (neurofibrillary tangles) across the cerebral cortex parallels symptom severity(2,3).

105 o many experimental observations, neurons in cerebral cortex tend to operate in an asynchronous regim

106 of amygdala functional connectivity with the cerebral cortex that related to individual differences i

107 Here, we use the male and female mouse cerebral cortex to show that a higher percentage of micr

108 that model features of the developing human cerebral cortex(1,2).

109 pical surface of the ventricular zone of the cerebral cortex(5-8).

110 we quantify the neuronal composition of the cerebral cortex, cerebellum and remaining brain structur

111 tathione, glutamate, and/or glutamine in the cerebral cortex, consistent with a post-inflammatory res

112 ndantly expressed in cells of the developing cerebral cortex, including neural progenitor cells and d

113 n on neuronal function, in particular in the cerebral cortex, remain little studied.

114 citatory inputs of interneurons in the mouse cerebral cortex, respectively.

115 In the cerebral cortex, single-cell RNA sequencing (scRNA-seq)

116 pread extensive connectivity with the entire cerebral cortex, suggesting a prominent role in 'higher

117 critical circuits for movement control: the cerebral cortex, the cerebellum, and the basal ganglia.

118 CB1) in the formation of sensory maps in the cerebral cortex, the topographic representation of the w

119 alog the vast diversity of cell types in the cerebral cortex.

120 ocused on the role of regions located within cerebral cortex.

121 their functional relations with areas in the cerebral cortex.

122 mpaired, resulting in disorganization of the cerebral cortex.

123 ions are a prominent activity pattern in the cerebral cortex.

124 cortex is much more tightly folded than the cerebral cortex.

125 neuron identity demarcates each layer of the cerebral cortex.

126 ons that were synchronized across the BG and cerebral cortex.

127 nced spatiotemporal dynamics observed in the cerebral cortex; however, evidence of a causal relations

128 Cerebral cortical architecture at birth encodes regional

129 Cerebral cortical development in mammals involves a high

130 DES+) revision to the original TBM model for cerebral cortical expansion and folding.

131 biallelic FLVCR2 mutations exhibited reduced cerebral cortical layers, enlargement of the cerebral ve

132 We then assembled these organoids with cerebral cortical organoids in three-dimensional culture

133 ferentiated them into three-dimensional (3D) cerebral cortical organoids.

134 allest shrew in our dataset, have diminutive cerebral cortices, which makes the cerebellum appear rel

135 astrocytes activation as well as suppressing cerebral cytokines levels.

136 dence of epilepsy surgery preventing further cerebral damage and provide incentives for offering earl

137 cal hallmarks of Alzheimer's disease (AD) is cerebral deposition of amyloid plaques composed of amylo

138 To study its cerebral distribution and association with plasma concen

139 e elucidation of the relationship between Li cerebral distribution and its therapeutic response, nota

140 Cerebral dopamine neurotrophic factor (CDNF) is expresse

141 Cerebral dopamine neurotrophic factor (CDNF) protects do

142 isplay severe neurotoxicity, including fatal cerebral edema associated with T cell infiltration into

143 sions in foetuses like haemorrhages, diffuse cerebral edema, necrotizing encephalitis and decreased b

144 emia-induced CCC phosphorylation, attenuates cerebral edema, protects against brain damage, and impro

145 , and RNA-seq was performed on microglia and cerebral endothelial cells (CECs).

146 We hypothesized that overall cerebral energy supply remains constant, regardless of o

147 .001), in-hospital major adverse cardiac and cerebral events (odds ratio, 0.41 [95% CI, 0.27-0.62]; P

148 uroimaging investigations failed to identify cerebral features associated with fatality in Asian adul

149 Cerebral functional connectivity at rest is lower in ADH

150 cuneus, a structure of central importance to cerebral functional organization, may be particularly vu

151 Methods: Forty-three patients with cerebral gliomas (9 low-grade, 34 high-grade; 9 primary

152 Net cerebral glucose/lactate exchange, and biomarkers of oxi

153 ith a 3T magnetic resonance machine to study cerebral glymphatics and meningeal lymphatics in patient

154 al cry, hypotonia, epilepsy, polyneuropathy, cerebral gray matter atrophy), visual impairment, testic

155 ebrovascular risk is associated with reduced cerebral grey matter and white matter integrity within a

156 edominately male, thus limiting knowledge of cerebral growth in females with ASD.

157 IFICANCE STATEMENT Focal damage to the right cerebral hemisphere may result in a variety of deficits,

158 atory fronto-temporal projection in the left cerebral hemisphere.

159 tions by co-opting the capacities of the two cerebral hemispheres.

160 NIRS was used to measure cerebral hemoglobin and oxygen saturation.

161 trial flutter, indirect hyperbilirubinaemia, cerebral hemorrhage, and mental status change (in two [1

162 Chronic cerebral hypoperfusion is associated with vascular demen

163 Regional cerebral hypoperfusion is characteristic of Alzheimer's

164 Cerebral hypoperfusion may initiate complex molecular an

165 ontributes to the pathophysiology of chronic cerebral hypoperfusion-induced brain injury and may ther

166 , a lower chance of modified Thrombolysis in Cerebral Infarction (mTICI) grade 2b to 3 reperfusion (a

167 We report the first case of coinciding cerebral infarction and venous sinus thrombosis unveilin

168 in recanalization (modified Thrombolysis-In-Cerebral-Infarction 2b-3), good clinical outcome (modifi

169 Progression of WMLs and cerebral infarctions in FD is mainly related to age, sex

170 ned in vivo approaches showed that increased cerebral infiltration of ACE10 as compared to wild-type

171 dence that deregulated insulin activities or cerebral insulin resistance contributes to neuroinflamma

172 mice developed Alzheimer's like pathologies, cerebral insulin resistance, and cognitive impairments.

173 These distinct cerebellar-cerebral interactions respond differently to physiologic

174 pping in MRI and PET indicated that elevated cerebral iron load was related to lower cognitive perfor

175 onist MK801-in mouse and rat models of focal cerebral ischaemia.

176 he outcomes of interest were occurrence of a cerebral ischaemic event (either stroke or transient isc

177 There were 70 cerebral ischaemic events (AER 2.93 per 100 patient-year

178 favorable performance for predicting delayed cerebral ischemia (DCI) (area under curve (AUC) > 0.750)

179 SR was defined as modified thrombolysis in cerebral ischemia 2b to 3.

180 )methanimine oxide (17) is a novel agent for cerebral ischemia therapy as it is able to scavenge diff

181 tion (viral and fungal), multiple sclerosis, cerebral ischemia, and cerebral malaria.

182 NPCs and mitochondrial fate determination in cerebral ischemia, and in improving neurological deficit

183 osis and autophagy following transient focal cerebral ischemia.

184 rebrain and determine its roles after global cerebral ischemia.

185 l molecule CGRP receptor antagonists, worsen cerebral ischemia.

186 y blockers might thus aggravate coincidental cerebral ischemic events.

187 Cerebral lateralisation of function is common characteri

188 Background Detection of cerebral lesions at MRI may benefit from a chemically st

189 Cerebral malaria (CM) is the most common form of severe

190 organ-specific fatal pathologies, including cerebral malaria (CM), driven by a high parasite load, l

191 attenuated and the incidence of experimental cerebral malaria is significantly decreased in Pbyop1Del

192 ddress, of which 272 (5%) were classified as cerebral malaria while 1001 (10%) were severe malaria an

193 t pathogenic patterns in pediatric and adult cerebral malaria with a stronger cytotoxic component in

194 months to 12 years old with severe malaria (cerebral malaria, n = 253 or severe malarial anemia, n =

195 Three parasitic infections - cerebral malaria, Taenia solium cysticercosis and onchoc

196 rospective cohorts of Malawian children with cerebral malaria.

197 , multiple sclerosis, cerebral ischemia, and cerebral malaria.

198 All three individuals have cerebral malformations, seizures, global developmental d

199 e noninvasive absolute quantification of the cerebral metabolic rate for glucose (CMRGlc) in a clinic

200 nhalation enabled dynamic measurement of the cerebral metabolic rate of oxygen (CMRO(2)) consumption.

201 This study demonstrated that the cerebral metabolic rate was increased by ~20% with passi

202 the brain, but it does markedly increase the cerebral metabolic rate, independently of PaCO2 .

203 her respiratory alkalosis impacts the global cerebral metabolic response as well as the cerebral pro-

204 the relationship between local increases in cerebral metabolism and appropriately matched increases

205 Additionally, the increase in cerebral metabolism did not significantly impact the net

206 Conclusion: Reduced cerebral mGluR5 availability in alcohol-dependent patien

207 eighted magnetic resonance imaging to detect cerebral microbleeds (CMBs) as a marker of occult hemorr

208 nsities (WMH), enlarged perivascular spaces, cerebral microbleeds and lacunes.

209 ng evidence indicates an association between cerebral microhemorrhages (MHs) and amyloid beta accumul

210 ial of SSCE-MRI to provide insights into the cerebral microvasculature post-TBI.

211 smission of pulsatile energy to the delicate cerebral microvasculature.

212 and cognitive operations within large-scale cerebral networks generate subjective memory feelings.

213 d with abnormalities in cerebral blood flow, cerebral neurochemical concentrations, and white matter

214 upture were small aneurysm size and anterior cerebral or communicating artery location.

215 Here, we provide an overview of the cerebral organoid field and speculate how engineering st

216 hese genes in meningioma, we develop a human cerebral organoid model of meningioma and validate the h

217 address the underlying mechanism, we develop cerebral organoid models using induced pluripotent stem

218 ls from eight untreated and six METH-treated cerebral organoids and found that the organoids develope

219 In vitro, patient-derived cerebral organoids are smaller with a reduced number of

220 Cerebral organoids from AD patients carrying APOE epsilo

221 uidic platform to assemble and culture human cerebral organoids from human embryonic stem cells (hESC

222 processing, we employed cortical neurons and cerebral organoids generated from PITRM1-knockout human

223 2014) that can be used to reliably generate cerebral organoids of a telencephalic identity and maint

224 ible hPSCs with unmodified hPSCs to generate cerebral organoids, which expedited in situ myelination.

225 ing ex cranio brains, hemispherotomy, and in cerebral organoids.

226 In boys with ASD, cerebral overgrowth in the ASD with disproportionate meg

227 Cerebral oximetry index, derived from near-infrared spec

228 Cerebral oximetry showed fast rise in regional oxygen sa

229 uced cerebral blood flow (CBF) by 20-30% and cerebral oxygen delivery (CDO(2) ) by 12-19% at sea leve

230 extracorporeal resuscitation alone (regional cerebral oxygen saturation, 73% +/- 3% vs 52% +/- 8%; p

231 enrichment of damaging de novo mutations in cerebral palsy cases.

232 f 3.2% (95% CI, -3.3% to 9.6%; P = .47), and cerebral palsy occurred in 18/419 (4.3%) vs 25/443 (5.6%

233 velopmental impairment was defined as severe cerebral palsy or a composite motor or composite cogniti

234 mmonly manifesting with developmental delay, cerebral palsy or seizures.

235 Candidate cerebral palsy risk genes overlapped with neurodevelopme

236 rodevelopmental impairment (cognitive delay, cerebral palsy, or hearing or vision loss) at 22 to 26 m

237 In a clinical trial of cerebral palsy, the level of plasma interleukin-8 (IL-8)

238 regulation of early neuronal connectivity in cerebral palsy.

239 ith a working clinical diagnosis of dystonic cerebral palsy.

240 d substantively to the diagnosis of dystonic cerebral palsy.

241 tional TMS can probe two distinct cerebellar-cerebral pathways that likely contribute to independent

242 an increase in the dentate nucleus-to-middle cerebral peduncle signal intensity ratio at MRI.

243 more likely to have poor outcome (Pediatric Cerebral Performance Category score > 1, incidence rate

244 quantify the impact of hyperoxia upon global cerebral perfusion (gCBF), cognitive performance and cor

245 Manifesting in abnormal cerebral perfusion and cerebrospinal fluid convection, p

246 gation (SAHC) upon cardiovascular responses, cerebral perfusion and g-tolerance.

247 oxide treatment, whereas post-cardiac arrest cerebral perfusion differences were diminished.

248 gen tension-brain oxygen tension gradient to cerebral perfusion pressure (p = 0.004) when comparing n

249 ocytes are acutely sensitive to decreases in cerebral perfusion pressure and may function as intracra

250 This appears necessary to establish a cerebral perfusion pressure on the order of 100 mm Hg at

251 ion, jugular venous bulb oxygen tension, and cerebral perfusion pressure were 29 mm Hg (SD, 9), 45 mm

252 brain oxygen tension, intracranial pressure, cerebral perfusion pressure, mean arterial pressure, and

253 Cerebral perfusion was compared vertex-wise according to

254 ain WM microstructural integrity and reduced cerebral perfusion, likely due to increased transmission

255 yed lower heart rates at different levels of cerebral perfusion, supporting the hypothesis of connexi

256 ncreased intracranial pressure and decreased cerebral perfusion.

257 radable end-product of oxidative stress; its cerebral presence reflects the cumulative amount of oxid

258 l cerebral metabolic response as well as the cerebral pro-oxidation and inflammatory response in pass

259 necrosis, osteoradionecrosis, vasculopathy, cerebral radionecrosis) and surgery (wound infections, f

260 However, the cerebral regional effects on metabolic information after

261 abolism did not significantly impact the net cerebral release of oxidative and inflammatory markers.

262 have already furthered our understanding of cerebral reorganization by estimating stroke-induced cha

263 f tenecteplase did not significantly improve cerebral reperfusion prior to endovascular thrombectomy.

264 visual speech comprehension and suggest that cerebral representations encoding word identities may be

265 Associations between cerebral small vessel disease (SVD) and inflammation hav

266 A study was undertaken to assess whether cerebral small vessel disease (SVD) computed tomographic

267 sis and development of vascular dementia and cerebral small vessel disease but not between atheroscle

268 on patterns in older adults with and without cerebral small vessel disease in vivo.

269 lar disease (i.e. atherosclerosis) and/or of cerebral small vessel disease or worse multiple sclerosi

270 structural changes, including MRI markers of cerebral small vessel disease, smaller brain tissue volu

271 ional and have an impact in diseases such as cerebral small vessel disease, the leading cause of vasc

272 old increase; P < 0.05) led to reductions in cerebral soluble amyloid-beta1-42, vascular and parenchy

273 plasma, synthetic urine (SU), and artificial cerebral spinal fluid (aCSF) using ethyl acetate as the

274 We tested 46 plasma samples and 36 cerebral spinal fluid (CSF) samples taken from patients

275 e coronavirus 2 from nasopharyngeal swab and cerebral spinal fluid.

276 echniques to determine whether reduced fetal cerebral substrate delivery impacts the brain globally,

277 metric reductions were associated with lower cerebral substrate delivery.

278 arteries (TGA), diagnoses with lowest fetal cerebral substrate delivery; "CHD-other," with other CHD

279 The diagnosis of cerebral SVD is largely based on brain magnetic resonanc

280 factors, and we discuss the evidence linking cerebral SVD with large vessel atheroma, atrial fibrilla

281 and near infrared spectroscopy (NIRS)-based cerebral tissue oxygen saturation (SctO2).

282 RAP footward towards the heart decreased the cerebral tissue saturation index, calf circumference and

283 Small cerebral vascular disease (SCeVD) demonstrated by white

284 Cavernous angiomas are cerebral vascular malformations that are usually congeni

285 automatically identifies key features of the cerebral vasculature such as branching of the internal i

286 ow and sex differences in the ability of the cerebral vasculature to increase its blood flow (cerebro

287 rch stiffening on transmitted pulsatility to cerebral vasculature, employing a computational approach

288 rebral amyloid angiopathy are the underlying cerebral vasculopathies accounting for the majority of I

289 patients with respiratory failure may cause cerebral vasoconstriction and compromise brain tissue pe

290 ngeal lymphatics in patients with reversible cerebral vasoconstriction syndrome (RCVS) with (n = 92)

291 1-positive cerebral blood vessels, reverted cerebral vasoreactivity, and HFD-induced effects in micr

292 Cerebral vasospasm (VSP) is a common phenomenon after an

293 cerebral cortical layers, enlargement of the cerebral ventricles, and microcephaly.

294 nifested by changes in the diameter of intra-cerebral vessels, which control cerebrovascular resistan

295 volume as well as proportion of GM to total cerebral volume were examined in a longitudinal sample c

296 Growth of total cerebral volume, gray matter (GM) volume, and white matt

297 rates of intellectual disability and larger cerebral volumes, may be underrepresented in studies of

298 whether these associations were modified by cerebral white matter hyperintensity (WMH) burden.

299 Cerebral white matter pathology is a common CNS manifest

300 atter were related to the lesion fraction in cerebral white matter.