ライフサイエンスコーパス: cerebral

1 response was spatially overlapping with high cerebral 5-HT1BR densities.

2 We hypothesized that cerebral A1AR availability after an extended wake period

3 We assessed cerebral Abeta on Pittsburgh Compound B (PiB) positron e

4 es, ten were positive for Zika virus and had cerebral abnormalities, 13 were positive for Zika infect

5 were positive for Zika infection but had no cerebral abnormalities, and 11 were negative for Zika vi

6 and 11 were negative for Zika virus but had cerebral abnormalities.

7 In multivariate logistic regression, cerebral abscess was associated with low oxygen saturati

8 ated to identify potential associations with cerebral abscess.

9 The cerebral adenosine A2A receptor is an attractive therape

10 Cerebral adrenoleukodystrophy is characterized by demyel

11 analysed data from 14 adult males with adult cerebral adrenoleukodystrophy treated with allogeneic ha

12 death, sex, cerebral neuritic plaque scores, cerebral alpha-synuclein scores, presence of cerebrovasc

13 of parenchymal amyloid-beta (Abeta) plaques, cerebral amyloid angiopathy (CAA) and neurofibrillary ta

14 oligomeric strain selectively induces acute cerebral amyloid angiopathy (CAA) in neonatally-injected

15 st AD patients have cerebrovascular amyloid (cerebral amyloid angiopathy (CAA), and cardiovascular ri

16 mited by poor clearance of a core AD lesion, cerebral amyloid angiopathy (CAA).

17 osis (CSS) are the characteristic markers of cerebral amyloid angiopathy (CAA).

18 Determining the presence and burden of cerebral amyloid angiopathy is particularly important wh

19 The term 'cerebral amyloid angiopathy' now encompasses not only a

20 sporadic AD and two pathways associated with cerebral amyloid angiopathy.

21 ermore, we report a significant reduction of cerebral amyloid burden and BACE1 accumulation in dystro

22 ous concentration gradients across the human cerebral and femoral circulation at rest and during exer

23 imaged, and may be a surrogate biomarker of cerebral and systemic vascular risk in patients with OSA

24 s an effective and safe treatment method for cerebral aneurysms, although it carries the risk of some

25 es of an effective endovascular treatment of cerebral aneurysms.

26 Amongst the cerebral areas identified using in vivo tractography, in

27 urodegeneration was also evident in specific cerebral areas in late disease.

28 In patch-clamp experiments using native cerebral arterial myocytes, membrane stretch-induced cat

29 orated patch clamp electrophysiology and rat cerebral arterial myocytes, we monitored STOCs in the pr

30 ximately 30-fold higher than AT1 Ra in whole cerebral arteries and approximately 45-fold higher in is

31 rents in smooth muscle cells and constricted cerebral arteries from both groups.

32 bral artery myocytes and vasoconstriction of cerebral arteries.

33 currents to induce myogenic constriction of cerebral arteries.

34 enchyma, hydrocephalus, and so-called middle cerebral artery (MCA) "pseudofeeders" were correlated wi

35 stroke induction by occlusion of the middle cerebral artery markedly reduced infarct size, and this

36 angiotensin II stimulates TRPM4 currents in cerebral artery myocytes and vasoconstriction of cerebra

37 he animals were subjected to a 2-hour middle cerebral artery occlusion (MCAO) and sacrificed at 24 ho

38 ere subjected to 60 min of reversible middle cerebral artery occlusion and evaluated for infarct volu

39 hemic stroke and in mice subjected to middle cerebral artery occlusion, natural killer (NK) cells dis

40 thrombotic cortical injury, transient middle cerebral artery occlusion, or neonatal hypoxic-ischemic

41 and approximately 45-fold higher in isolated cerebral artery smooth muscle cells.

42 on In this study, patients with acute middle cerebral artery stroke with absence of cortical vein opa

43 white matter tracts, and involved the middle cerebral artery territory for 112 patients (73%).

44 l internal carotid artery or proximal middle cerebral artery who had last been known to be well 6 to

45 abnormalities, abnormal cortical formation, cerebral atrophy, ventriculomegaly, hydrocephaly, and ce

46 individuals reveals delay in myelination and cerebral atrophy.

47 Cerebral autoregulation (CA) is a protective mechanism t

48 nship between dynamic (dCA) and steady-state cerebral autoregulation (sCA).

49 ration >15%) and explored the lower limit of cerebral autoregulation at patient and population levels

50 autoregulation reactivity index was the only cerebral autoregulation index that predicted patient out

51 Cerebral autosomal-dominant arteriopathy with subcortica

52 cale and school performance in children with cerebral AVF and the American Spinal Injury Association

53 responses in rat barrel cortex, measured by cerebral blood flow (CBF) and neurophysiological recordi

54 Resting-state regional cerebral blood flow (CBF) can be measured noninvasively

55 Cessation of cerebral blood flow (CBF) leads to cell death in the inf

56 Following this training period, hippocampal cerebral blood flow (CBF) was measured by functional mag

57 indicators: (1) global and regional resting cerebral blood flow (CBF), (2) oxygen extraction fractio

58 were used to study structural connectivity, cerebral blood flow (CBF), and corticospinal excitabilit

59 erstitial brain tissue (Pbto2), and regional cerebral blood flow (CBF).

60 effect of age and diagnosis on glutamate and cerebral blood flow (rCBF) in adults with SZ and healthy

61 We measured regional cerebral blood flow (rCBF) using pseudo-continuous arter

62 g the previously validated measure (relative cerebral blood flow [rCBF], <30%), thrombectomy patients

63 Hence, cerebral blood flow and cerebral oxygenation are importa

64 Moreover, we observed higher cerebral blood flow and lower oxygen saturation in femal

65 ted cancer survivors had significantly lower cerebral blood flow and metabolic activity in key brain

66 entration, oxygen saturation, and indices of cerebral blood flow and metabolism.

67 lities are combined with long periods of low cerebral blood flow and/or circulatory arrest.

68 CA) is a protective mechanism that maintains cerebral blood flow at a relatively constant level despi

69 technology that provides a direct measure of cerebral blood flow in response to cognitive activity.

70 ntional individuals showed increased resting cerebral blood flow in the ventral striatum and ventrome

71 Cerebral blood flow in these brain regions correlated wi

72 hanisms must be playing hand in hand, namely cerebral blood flow increase and microvascular flow homo

73 Impaired oxygen delivery due to reduced cerebral blood flow is the hallmark of delayed cerebral

74 BDG patients had significantly higher cerebral blood flow than did Fontan patients.

75 oride application followed by measurement of cerebral blood flow using a combination of laser Doppler

76 the acetazolamide-induced change in regional cerebral blood flow using SPECT with (99m)Tc-labeled hex

77 In addition, (15)O-H2O scans to measure cerebral blood flow were acquired before each (11)C-erlo

78 termined by transcranial Doppler ultrasound (cerebral blood flow) and constant infusion thermodilutio

79 l reconstruction and their relationship with cerebral blood flow, oxygen delivery, and carbon dioxide

80 lature in response to changes in pressure or cerebral blood flow.

81 ratio of mean arterial pressure to regional cerebral blood flow.

82 Simultaneously, we measured changes in cerebral blood volume (CBV) as a proxy of drug effects o

83 etic stimulation of TH(VTA) neurons enhanced cerebral blood volume signals in striatal target regions

84 Cerebral calcifications, when associated with white matt

85 to the development of the vascular disorder Cerebral Cavernous Malformation (CCM).

86 Cerebral cavernous malformations (CCMs) are a cause of s

87 d to in utero inflammation via an endogenous cerebral cholinergic anti-inflammatory pathway.

88 remained unaffected in the celiac artery and cerebral circulation.

89 es PPK in plasma and PKal inhibition reduces cerebral complications associated with tPA-mediated thro

90 Malformations of the cerebral cortex (MCCs) are devastating developmental dis

91 Notably, gene sets pertaining to the cerebral cortex (which did not differ in volume between

92 ing an ectopic neuronal layer that resembles cerebral cortex abnormalities in humans.

93 sive connections with various regions of the cerebral cortex and by hypotheses surrounding its possib

94 s, which may receive synaptic input from the cerebral cortex and other brain regions beyond the core

95 The cerebral cortex contains "immature" neurons, which are g

96 s with Huntington disease whose striatum and cerebral cortex develop inclusions associated with exten

97 acroscopic anatomical characteristics of the cerebral cortex have been identified in individuals affe

98 an important role in the development of the cerebral cortex in humans and mice.

99 of reproducible folding in the gyrencephalic cerebral cortex is a topic of great interest to neurosci

100 usion anisotropy within the developing fetal cerebral cortex is longitudinally characterized in the r

101 contrast, the number of inputs per neuron in cerebral cortex is more uniform and large.

102 The cerebral cortex is organized into specialized sensory ar

103 teristics similar to a phenotype seen in the cerebral cortex of Vldlr(null) mice.

104 SCs were topically applied to the surface of cerebral cortex within 1 hour of experimental TBI.

105 nvestigators have paid much attention to the cerebral cortex, few studies have detailed the basal gan

106 , i.e. the distance of each contact from the cerebral cortex, in order to discriminate between white

107 c and hypoxia-induced lactate release in the cerebral cortex, which was normalized by OP treatment.

108 listic microvascular networks from the mouse cerebral cortex.

109 expression of anti-oxidative enzymes in the cerebral cortex.

110 pses, about 1 per microm(3) in the mammalian cerebral cortex.

111 en excitatory and inhibitory synapses in the cerebral cortex.

112 s (the striatum and cerebellum), but not the cerebral cortex.

113 al swollen morphology in the hippocampus and cerebral cortex.

114 Memories of experiences are stored in the cerebral cortex.

115 the hippocampus and 22.1 +/- 4.9 muM in the cerebral cortex.

116 represents the folding characteristic of the cerebral cortex.

117 with the notion of lateralized functions in cerebral cortex.

118 mpaired neuronal migration in the developing cerebral cortex.

119 a nigra pars compacta (SNpc) and, later, the cerebral cortex.

120 man and mouse cerebellar astrocytes than did cerebral cortical astrocytes, suggesting that IFNAR sign

121 were distinct from the patterns observed for cerebral cortical surface area expansion.

122 e correlations between cerebellar volume and cerebral cortical thickness in frontotemporal regions (i

123 by increasing O-GlcNAcylation, to reduce the cerebral damage and improve the clinical outcome of isch

124 All presented with cerebral demyelinating lesions and gadolinium enhancemen

125 Qualitative assessment demonstrated cerebral diaschisis in 16 of 17 (94%) cases with THGr(Ce

126 d or no neurological deficit) or 2 (moderate cerebral disability) was considered a good functional ou

127 e outcomes of boys with cALD and early-stage cerebral disease who were treated with an allogeneic HSC

128 for further validation in gliomas and other cerebral diseases.

129 were significantly associated with improved cerebral edema and clinical outcome.

130 Hyponatremic encephalopathy, symptomatic cerebral edema due to a low osmolar state, is a medical

131 c symptoms to life-threatening high-altitude cerebral edema in less than 1% of patients.

132 luggish CBF compared to CMS patients without cerebral edema; but what triggers this complication is u

133 ent (TAVR) may be reduced with transcatheter cerebral embolic protection (TCEP).

134 etermine the efficacy and adverse effects of cerebral embolic protection devices in reducing ischemic

135 ts in haemorrhagic stroke, and management of cerebral emergencies other than stroke.

136 nvolved an increased type 1 inflammation and cerebral endotheliopathy, characterized by elevated NF-k

137 Complex alterations in cerebral energetic metabolism arise after traumatic brai

138 In-hospital major adverse cardiac and cerebral events occurred in 2.0% in fTRA and 2.9% in TFA

139 been associated with fetal abnormalities and cerebral folate deficiency-related developmental disorde

140 , 25 men; mean age +/- SD, 48 +/- 14 y) with cerebral gliomas (World Health Organization [WHO] grade

141 de additional information on tumor extent of cerebral gliomas compared with anatomic imaging; however

142 ents with MMF exhibited a spatial pattern of cerebral glucose hypometabolism (P < 0.001) involving th

143 ural circuitry (measured with PET imaging of cerebral glucose metabolism at baseline and at 6 and 12

144 We detected significant changes in cerebral glucose metabolism in key anorexia nervosa-rela

145 Intensive Blood Pressure Reduction in Acute Cerebral Haemorrhage Trials (INTERACT 1 and 2).

146 Hereditary cerebral haemorrhage with amyloidosis-Dutch type (HCHWA-

147 induced by controlled cortical impact on one cerebral hemisphere.

148 d in the Antihypertensive Treatment of Acute Cerebral Hemorrhage II (ATACH-II) randomized clinical tr

149 with our predictions and with models of CR, cerebral hypometabolism was more severe in the group of

150 Cerebral hypoperfusion has previously been associated wi

151 Chronic cerebral hypoperfusion is a major cause of age-related v

152 Cerebral hypoperfusion is associated with accelerated co

153 We have previously shown that cerebral Hypoxia-ischemia (HI) results in activation of

154 Our understanding of events associated with cerebral hypoxia-ischemia during cardiopulmonary bypass

155 f MT, we exogenously administered MT-I after cerebral I/RI and found that it produced neuroprotection

156 age, n=6) demonstrated significantly smaller cerebral infarct volumes compared with wild-type mice.

157 racts (n = 4), deep vein thrombosis (n = 3), cerebral infarction (n = 2), headache (n = 2), and myelo

158 neck tumor survivors were hospitalized for a cerebral infarction (versus 0.06% expected).

159 CNS tumor survivors were hospitalized for a cerebral infarction (versus 0.1% expected), whereas at a

160 The excess risk of cerebral infarction among CNS tumor survivors increases

161 zation defined as a modified Thrombolysis in Cerebral Infarction score of 2b or 3 at the end of all e

162 atens oxygen delivery increasing the risk of cerebral infarction.

163 sexes that reproduces the spectrum of human cerebral injury and abnormal cortical growth.

164 that leads to abnormal brain development and cerebral injury through a poorly understood mechanism kn

165 ameliorated blood-brain barrier damage after cerebral ischaemia.

166 We examined the relationship between BP and cerebral ischemia (relative drop in cerebral saturation

167 Fifty-two patients at risk for delayed cerebral ischemia after aneurysmal subarachnoid hemorrha

168 more, we estimated intradialytic exposure to cerebral ischemia and hypotension for each patient, and

169 rebral blood flow is the hallmark of delayed cerebral ischemia following subarachnoid hemorrhage.

170 the effects of increased CD39 in an in vivo cerebral ischemia model, we developed a transgenic mouse

171 pilot study demonstrates that intradialytic cerebral ischemia occurs frequently, is not easily predi

172 substantial recanalization (Thrombolysis in Cerebral Ischemia scores 2B to 3; drip and ship, 84 [84.

173 loss and improved body weight recovery after cerebral ischemia, as well as muscle strength and motor

174 Following global cerebral ischemia, hippocampal CA1 pyramidal neurons are

175 his study reveals an important regulation of cerebral ischemia-reperfusion injury by O-GlcNAcylation

176 y of skeletal muscle mass and function after cerebral ischemia.

177 ragments were identified in the blood during cerebral ischemia.

178 all, 23.5% of hemodialysis sessions featured cerebral ischemia; 31.9% of these events were symptomati

179 es in the pathogenesis of cardiovascular and cerebral large-vessel disease compared with that of smal

180 Cerebral lateralization is expressed at both the structu

181 (ii) a module to determine the most probable cerebral location of the recorded activity, and (iii) a

182 Cerebral malaria (CM) is a severe complication of Plasmo

183 a major predictor of mortality in pediatric cerebral malaria (CM).

184 Cerebral malaria is a deadly outcome of infection by Pla

185 Here, using a mouse cerebral malaria model and small-molecule inhibitors, we

186 sunate remains the mainstay of treatment for cerebral malaria, but it is less effective in later stag

187 associated with increased risk of developing cerebral malaria.

188 crovasculature is the only one correlated to cerebral malaria.

189 ed as a neurological sequela in survivors of cerebral malaria.

190 l and clinically relevant imaging markers of cerebral maldevelopment, which offer new insights into t

191 2) oxygen extraction fraction (OEF), and (3) cerebral metabolic rate of oxygen (CMRO2).

192 s infarct risk in pediatric SCA by relieving cerebral metabolic stress at patient- and tissue-specifi

193 went positron emission tomography to measure cerebral metabolism in this cross-sectional study.

194 ential for in vivo non-invasive detection of cerebral metabolism post-TBI, providing a new tool to mo

195 Among the various techniques used to study cerebral metabolism, (13)C magnetic resonance spectrosco

196 Despite the fairly rare prevalence of cerebral metastases in NENs, a neurological work-up shou

197 he pancreas, it is associated with a risk of cerebral metastases lower than 2%.

198 crobleeds (OR, 1.18; 95% CI, 1.03-1.34), and cerebral (micro)infarctions (OR, 1.30; 95% CI, 1.21-1.39

199 Restricted lobar cerebral microbleeds (CMBs) and cortical superficial sid

200 erintensities (OR, 1.29; 95% CI, 1.19-1.39), cerebral microbleeds (OR, 1.18; 95% CI, 1.03-1.34), and

201 re and flow pulsatility transmitted into the cerebral microcirculation.

202 Cortical cerebral microinfarcts (CMIs), a novel MRI marker of cer

203 small vessel and large vessel disease, that cerebral microinfarcts are independently associated with

204 Cerebral microinfarcts are small lesions that are presum

205 Evidence from these advances suggests that cerebral microinfarcts can be manifestations of both sma

206 Criteria for the identification of cerebral microinfarcts with in-vivo MRI are provided to

207 ndividuals can have hundreds to thousands of cerebral microinfarcts, which cause measurable disruptio

208 ABSTRACT: The human cerebral microvascular endothelial cell line hCMEC/D3 wa

209 We investigated regional cerebral microvascular responses to acute (2 h) and prol

210 mouse BMECs after OGD as well as in isolated cerebral microvessels in mice after MCAO.

211 omical phenotypes described here reflect the cerebral morphology of a common ancestor of Pancrustacea

212 ing in vivo tractography, in addition to the cerebral motor cortex, major portions of CPC streamlines

213 he effects of acute physical exercise on the cerebral mu-opioid receptors (MOR) of 22 healthy recreat

214 Zika targets cerebral neural precursors, a cell population essential

215 ) in models that included age at death, sex, cerebral neuritic plaque scores, cerebral alpha-synuclei

216 tomography to test whether feeding triggers cerebral opioid release and whether this response is ass

217 Of 3096 acute cerebral or peripheral vascular events, 748 (24.2%) were

218 a cohort of children presenting at least one cerebral or spinal pial arteriovenous fistula (AVF), and

219 s of blood samples from Malian children with cerebral or uncomplicated malaria.

220 lts identify crucial functions for RB in the cerebral organoid model of human brain development.

221 Microfilament-engineered cerebral organoids (enCORs) display enhanced neuroectode

222 ogenesis and highlights the broad utility of cerebral organoids for modeling human neurodevelopmental

223 We created cerebral organoids from the isogenic iPSCs and found tha

224 Finally, we utilized the expanded cerebral organoids to show that infection with Zika viru

225 ll cultures, planarians, zebrafish and human cerebral organoids.

226 sted by HUWE1 immunofluorescence analysis of cerebral organoids.

227 ogy of disorders traditionally considered of cerebral origin.SIGNIFICANCE STATEMENT This study examin

228 ein (PPK) activation and the role of PKal on cerebral outcomes in a murine thrombotic stroke model tr

229 largely due to inadequate tools to quantify cerebral oxygen delivery and consumption non-invasively

230 Cerebral oxygen delivery was calculated using phase cont

231 determined whether transfusion could augment cerebral oxygen delivery, particularly in vulnerable bra

232 nd pre-ductal pulse oximetry, while regional cerebral oxygen saturation was estimated using near-infr

233 Hence, cerebral blood flow and cerebral oxygenation are important biomarkers of brain h

234 Dyskinetic cerebral palsy (DCP) is the second most common type of c

235 or system injury in children with unilateral cerebral palsy (USCP).

236 alsy (DCP) is the second most common type of cerebral palsy after spastic forms.

237 Incidence rates of cerebral palsy and hazard ratios (HRs) with 95% CIs, adj

238 pregnancy body mass index (BMI) and rates of cerebral palsy by gestational age and to identify potent

239 Cerebral palsy describes the most common physical disabi

240 Twenty-four children with unilateral cerebral palsy had physiological and anatomical measures

241 ssociation between maternal BMI and rates of cerebral palsy in full-term children was mediated throug

242 Cerebral palsy is the most frequent cause of severe phys

243 Individuals with cerebral palsy often exhibit crouch gait, a debilitating

244 The incidence of cerebral palsy or other major neurological impairments w

245 turn are associated with increased risks of cerebral palsy.

246 The strength of cerebellar-to-cerebral pathways for a given muscle may reflect aspects

247 Cerebral Performance Categories (CPC) at 1 year was the

248 Good outcome (Cerebral Performance Categories 1 and 2) and mortality p

249 e neurological outcome, defined as Pediatric Cerebral Performance Categories 1 to 3 or no worse than

250 c level was an independent predictor of poor Cerebral Performance Category (Cerebral Performance Cate

251 %) of 62 patients were discharged alive with Cerebral Performance Category 1 or 2 versus 26 (15.3%) o

252 in neurologic outcome (45% of patients with cerebral performance category 1-2 in both groups) were o

253 A cerebral performance category score of 1 (mild or no neu

254 ictor of poor Cerebral Performance Category (Cerebral Performance Category, 3-5) with an odds ratio (

255 ogic outcome after 6 months, referred to as "Cerebral Performance Category." Thirty-six sites in Euro

256 We determined the association of cerebral perfusion (mL/100mL/min) with risk of dementia

257 ciated with unfavorable outcome (odds ratio %cerebral perfusion pressure < lower limit of reactivity,

258 tracranial pressure, percentage of time with cerebral perfusion pressure less than lower limit of rea

259 enoted automatically the "lower" and "upper" cerebral perfusion pressure limits of reactivity, respec

260 ively constant level despite fluctuations of cerebral perfusion pressure or arterial blood pressure.

261 The cerebral perfusion pressure values at which this "U-shap

262 METHODS AND MAIN Cerebral perfusion pressure-pressure reactivity index cu

263 onship between pressure reactivity index and cerebral perfusion pressure.

264 and into neural cells is critical for normal cerebral physiologic function.

265 (Cerebral Protection in Transcatheter Aortic Valve Replac

266 postmortem tau pathology averaged from three cerebral regions (angular gyrus, mid-frontal cortex, and

267 pheric counterparts of various task-relevant cerebral regions that are known to exhibit lateralizatio

268 ework for characterizing the maintenance and cerebral representation of different types of mind wande

269 n BP and cerebral ischemia (relative drop in cerebral saturation >15%) and explored the lower limit o

270 esence of cognitive impairment, but also for cerebral small vessel disease (CSVD) and Abeta-positivit

271 id from the brain and may reflect underlying cerebral small vessel disease (SVD).

272 The resulting cerebral small vessel disease and heart failure may cont

273 e imaging (MRI) are a neuroimaging marker of cerebral small vessel disease.

274 rivascular spaces may reflect the underlying cerebral small vessel disease.

275 riolar and venular diameter, and markers for cerebral small vessel disease.

276 ventricles and spinal cord to circulate the cerebral spinal fluid (CSF).

277 Notice of retraction: the article "Role of Cerebral Spinal Fluid in Space Flight Induced Ocular Cha

278 cal lissencephaly is characterized by smooth cerebral surface and cortical thickening that result in

279 mean 37 weeks (late), we compared the fetal cerebral T2* in 28 fetuses without heart defects to that

280 ed-tau levels are positively associated with cerebral tau burden in FTLD.

281 showed independent negative associations of cerebral tau neurofibrillary tangles score with the inte

282 SF phosphorylated tau levels with postmortem cerebral tau pathology in FTLD (Beta = 1.3; 95% confiden

283 ndex (BMI)] and greater odds of large-vessel cerebral vascular disease or history of cardiovascular d

284 microinfarcts (CMIs), a novel MRI marker of cerebral vascular disease, have not been studied, to dat

285 cular disease but lower odds of small-vessel cerebral vascular disease.

286 n the RTN is the opposite to the rest of the cerebral vascular tree is novel and fundamentally import

287 have been developed to study changes in the cerebral vasculature in numerous neuropathological proce

288 control as well as metabolic regulations of cerebral vasculature in response to changes in pressure

289 syndrome (RPLS), is a neurotoxic syndrome of cerebral vasoregulation classically characterized by bil

290 sphenoparietal sinus, and superficial middle cerebral vein was graded by one neuroradiologist, as fol

291 typical JCPyV encephalopathy associated with cerebral venous sinus thrombosis and disseminated primar

292 gic hydrocephalus (PHH), an expansion of the cerebral ventricles due to CSF accumulation following in

293 Large and small cerebral vessel disease can trigger stroke and contribut

294 olved in maintaining the resting tone of the cerebral vessels by releasing ATP and COX-1 derivatives.

295 Cerebral vessels play a major role in AD, as Abeta is cl

296 e Abeta transport across bioengineered human cerebral vessels.

297 repair mechanisms, including regeneration of cerebral white matter and improvement in neurocognitive

298 Cerebral white matter from a patient with TUBB4A Asn414L

299 rphism (rs12445022) was also associated with cerebral white matter hyperintensities (OR [95% CI] = 1.

300 rders leading to progressive degeneration of cerebral white matter.