ライフサイエンスコーパス: neurovascular

1 iously unrecognized effector of the damaging neurovascular actions of Abeta and unveil a new mechanis

2 Neurovascular alignment is a common anatomical feature o

3 may be profoundly influenced by the maturing neurovascular and autoregulatory systems of the neonatal

4 are broad, impacting processes ranging from neurovascular and cardiovascular health to cell migratio

5 ings unveil a pathogenic role of PVMs in the neurovascular and cognitive dysfunction associated with

6 y in hippocampus and other areas affected by neurovascular and neurodegenerative disorders.

7 derstanding the complex interactions between neurovascular and neuroinflammatory responses in aging a

8 We examined how neurovascular and neurometabolic couplings vary vertical

9 in a mouse incisor model and identified the neurovascular bundle (NVB) as an MSC niche.

10 ring to minimize lateral displacement of the neurovascular bundle and attenuate neurapraxia enables e

11 the existing imaging modalities to image the neurovascular bundle around the prostate pre, intra, and

12 life expectancy, better visualization of the neurovascular bundle around the prostate using novel ima

13 ssessed the extent of soft tissue component, neurovascular bundle involvement, epiphyseal and joint i

14 chieved due to a better visualization of the neurovascular bundle responsible for erectile function.

15 uch as prostate capsule, external sphincter, neurovascular bundle) has significant impact on preopera

16 on have led to a better appreciation of the neurovascular bundle, thus encouraging novel techniques

17 0 cm, and for tumors in close proximity to a neurovascular bundle.

18 al finesse to minimize stretch injury to the neurovascular bundle.

19 We identify these channels as neurovascular canals, that include parts of the trigemin

20 or spinal cord injury, SUR1 is increased in neurovascular cells at the site of injury.

21 lls and may be responsible for the augmented neurovascular changes.

22 depends on the precise molecular control of neurovascular co-patterning.

23 ights into region-specific specialization of neurovascular communication, with special implications f

24 oosted in vivo by manipulating Flna-mediated neurovascular communication.

25 nding of the molecular mechanisms that cause neurovascular complications, particularly in type 2 diab

26 rement, pain, loss of function and mobility, neurovascular compromise, and occasionally life-threaten

27 structures such as the mouse whisker system, neurovascular congruency does not follow the previous mo

28 Previous studies have suggested that neurovascular congruency in planar tissues such as skin

29 y act as an important mechanism to establish neurovascular congruency patterns that facilitate unique

30 Neurovascular constriction was enhanced approximately 1.

31 ension, an increased fibroblast growth rate, neurovascular contact at the rostral-ventrolateral medul

32 In summary, altered neurovascular control in human MetSyn is receptor specif

33 ral blood flow that range from physiological neurovascular coupling (hyperaemia) to pathological inve

34 The classical model of neurovascular coupling (NVC) implies that activity-depen

35 Neurovascular coupling (NVC) is the process whereby neur

36 Physiologically, neurovascular coupling (NVC) matches focal increases in

37 a proof of concept study aiming to quantify neurovascular coupling (NVC) using wavelet analysis of t

38 They play an important role in mediating neurovascular coupling (NVC) via several astrocytic Ca(2

39 Here we report that stress impairs neurovascular coupling (NVC), the process that matches n

40 sodilatory prostaglandins play a key role in neurovascular coupling (NVC), the tight link between neu

41 stent reduction in CBF, but not the impaired neurovascular coupling after CSD.

42 Furthermore, disturbed neurovascular coupling after stroke can confound hemodyn

43 tant vascular diseases, or medication on the neurovascular coupling and consequently the functional M

44 mutase (CuZnSOD) prevented the alteration in neurovascular coupling and endothelium-dependent respons

45 altered calcium signaling that could disrupt neurovascular coupling and gliotransmission.

46 may regulate experience-dependent changes in neurovascular coupling and myelination.

47 ions of mural cells in vascular development, neurovascular coupling and neuropathology.

48 ron, a direction opposite to that of classic neurovascular coupling and referred to here as vasculo-n

49 esponses to investigate cocaine's effects on neurovascular coupling and to differentiate its effects

50 001), indicating that cocaine did not affect neurovascular coupling at rest and that the reduction in

51 The investigation of mechanisms underlying neurovascular coupling at the capillary level requires a

52 Neurovascular coupling between resting-state neural acti

53 Astrocytes play a critical role in neurovascular coupling by providing a physical linkage f

54 Here, we reexamined their role in neurovascular coupling by selectively expressing a genet

55 We conclude that neurovascular coupling depends critically on anesthesia

56 Neurovascular coupling describes the link between neuron

57 min after cocaine injection, indicating that neurovascular coupling during stimulation was temporaril

58 transcriptional regulator of SEMA3E-mediated neurovascular coupling in a mouse model of oxygen-induce

59 sis, and activity-induced neurometabolic and neurovascular coupling in adult (6 months) and aged (12

60 Wavelet coherence analysis of neurovascular coupling in NE may identify infants at ris

61 transcriptional regulator of SEMA3E-mediated neurovascular coupling in pathological retinal angiogene

62 hyperglycemia has a detrimental influence on neurovascular coupling in the brain-an effect linked to

63 direct proportionality of volumetric spatial neurovascular coupling in the cerebral cortex.

64 Here, we investigate spatial correlations of neurovascular coupling in three dimensions, by applying

65 -dependent Ca(2+) signaling does not mediate neurovascular coupling in visual cortex of awake, lightl

66 lity and consequences of conditions in which neurovascular coupling may be altered, including during

67 Inversion of neurovascular coupling may contribute to the decreased c

68 may fail in situations interfering with the neurovascular coupling mechanisms (drugs, anesthesia).

69 Here, we review current candidate neurovascular coupling mechanisms and propose that previ

70 is needed for improving our understanding of neurovascular coupling mechanisms and the related measur

71 standing of the signalling events underlying neurovascular coupling mechanisms in the brain is a cruc

72 , we determined whether pathological inverse neurovascular coupling occurred as a mechanism of second

73 concept from the current electrochemical and neurovascular coupling principles used for brain imaging

74 overed capillaries control vasomotion during neurovascular coupling remains controversial.

75 regulation of cerebral blood flow (CBF) and neurovascular coupling remains, however, under debate.

76 ling lead to a switch in the polarity of the neurovascular coupling response from vasodilation to vas

77 t improvement in cerebral blood flow and the neurovascular coupling response, as well as increased ex

78 ies such as Alzheimer's disease, would alter neurovascular coupling responses to sensory stimulation.

79 erebrovascular reactivity and whisker-evoked neurovascular coupling responses were measured at end po

80 nt for the full expression of sensory-evoked neurovascular coupling responses.

81 simultaneous PET/fMRI for investigations of neurovascular coupling that correlate neurochemistry wit

82 three patients exhibited dynamic changes in neurovascular coupling to depolarizations throughout the

83 These results establish inverse neurovascular coupling to spreading depolarization as a

84 This neurovascular coupling underlies blood oxygen level-depe

85 The mechanisms of neurovascular coupling underlying generation of BOLD fMR

86 Further, neurovascular coupling was intact in lightly sedated, re

87 We found that neurovascular coupling was similar across states and tha

88 mic responses consistent with more efficient neurovascular coupling within the left DLPFC.

89 d hemodynamics, a phenomenon referred to as "neurovascular coupling" (NVC).

90 cerebral blood flow to neuronal metabolism (neurovascular coupling).

91 d with release of arachidonic acid, impaired neurovascular coupling, and reduced cerebral blood flow

92 According to the current model of neurovascular coupling, blood flow is controlled regiona

93 ked neuronal activity.SIGNIFICANCE STATEMENT Neurovascular coupling, defined as the tight relationshi

94 orts a conceptual shift in the mechanisms of neurovascular coupling, from a unidimensional process in

95 he effects of wakefulness reflect changes in neurovascular coupling, not in neural activity.

96 ishing astrocytes as potential regulators of neurovascular coupling.

97 ulation, endothelial-mediated signaling, and neurovascular coupling.

98 nge in cerebral blood flow, a process termed neurovascular coupling.

99 ggesting that pericytes could have a role in neurovascular coupling.

100 gs, as well as a more principled modeling of neurovascular coupling.

101 tigators to probe the role of capillaries in neurovascular coupling.

102 rlying neuronal activity by a process termed neurovascular coupling.

103 Roy and Sherrington, 1890), a process termed neurovascular coupling.

104 e been proposed to play a role in functional neurovascular coupling.

105 V4 channels are engaged in and contribute to neurovascular coupling.

106 endfoot microdomain and assess their role in neurovascular coupling.

107 e synthase is involved in astrocyte-mediated neurovascular coupling.

108 erent conditions of neuronal stimulation and neurovascular coupling.

109 ha, and ultimately lead to the impairment of neurovascular coupling.

110 rocytes, and arterioles-causing inversion of neurovascular coupling.

111 derstand temporal correlations that describe neurovascular coupling.

112 a longer time span and is less dependent on neurovascular coupling.

113 t release Ca(2+) from stores does not affect neurovascular coupling.

114 y visual cortex to investigate the limits of neurovascular coupling.

115 hese networks, over and above the effects on neurovascular coupling.

116 red hippocampal cytoarchitectonics; impaired neurovascular coupling; attenuated prepulse inhibition (

117 mechanism is essential to preserving healthy neurovascular coupling; however, to our knowledge, no st

118 Ca(2+) signaling within the endfoot mediates neurovascular coupling; thus, these functional microdoma

119 Under nitroprusside infusion, a neurovascular-coupling inhibitor, the diffusion response

120 del that incorporates internalization into a neurovascular-coupling relationship.

121 Thus, this study revealed neurovascular crosstalk and unprecedented cellular regul

122 ial stretching, which is ideal in the use in neurovascular curved arteries.

123 In vivo MRI evaluated both the neurovascular damage and the protective effect of exerci

124 nstrate the protective effect of exercise on neurovascular damage in the ageing brain of ApoE(-/-) mi

125 e devastating consequences of stroke-induced neurovascular damage.

126 Concomitant with age-related neurovascular decline and complement activation, astrocy

127 rcise had little to no effect on age-related neurovascular decline or microglia/monocyte activation i

128 Neurovascular decline was sufficient to cause vascular l

129 idlife to old age prevented this age-related neurovascular decline, reduced C1QA+ microglia/monocytes

130 ed in an excellent outcome without secondary neurovascular deficits in this rare case of traumatic co

131 Neurovascular deficits lead over time to impaired neuron

132 Ca(2+) signaling, but display no neuronal or neurovascular deficits, implying that astrocyte Ca(2+) f

133 bra was achieved and there were no secondary neurovascular deficits.

134 her, the protective role of GAPDH in retinal neurovascular degeneration after I/R injury provides a b

135 I/R injury induced neurovascular degeneration, energy failure, DNA damage,

136 role of GAPDH in retinal I/R injury-induced neurovascular degeneration, the injured retinas of GAPDH

137 lar telangiectasia type 2; MacTel) is a rare neurovascular degenerative retinal disease.

138 poses new questions about the mechanisms of neurovascular development and its role in both normal an

139 BBB endothelial phenotype is induced during neurovascular development by surrounding cells of the CN

140 We propose a mechanism for coordinated neurovascular development within pancreatic islets, in w

141 PGRN has been implicated in neurovascular development, inflammation, and Wnt signali

142 iggers a strong immune response and disrupts neurovascular development, resulting in postnatal microc

143 gh endothelial WNT signaling is required for neurovascular development, too much endothelial WNT sign

144 Despite the importance of neurovascular disease and subsequent injury after ischem

145 gravating motor neuron damage, identifying a neurovascular disease signature for ALS.

146 Acute cerebral ischemia and chronic neurovascular diseases share various common mechanisms w

147 is prevalent in humans and is implicated in neurovascular diseases, including recently in certain re

148 monitoring and therapeutic interventions of neurovascular diseases.

149 f treating age-related neurodegenerative and neurovascular diseases.

150 Blood-brain barrier (BBB) pathology leads to neurovascular disorders and is an important target for t

151 roved diagnosis, treatment and management of neurovascular disorders, including stroke.

152 resulting cerebrovascular damage, leading to neurovascular dysfunction and cognitive deficits.

153 le link between astrocytic Apoe, age-related neurovascular dysfunction and microglia/monocyte activat

154 uch as Alzheimer's disease may contribute to neurovascular dysfunction and neurodegeneration associat

155 eses that have been proposed include trauma, neurovascular dysfunction and transient hyperemia.

156 However, the molecular mechanisms underlying neurovascular dysfunction during BBB breakdown remain el

157 udying microvascular pathologic findings and neurovascular dysfunction in the eye and retina.

158 Neurovascular dysfunction is present in normal APOE4 car

159 AD), a neurological disorder associated with neurovascular dysfunction, abnormal elevation of amyloid

160 ceptor involved in Abeta trafficking, in the neurovascular dysfunction, cognitive deficits, and amylo

161 Neurovascular dysregulation in putaminal and pallidal re

162 rovascular, memory and epilepsy clinics, and neurovascular emergency services, emphasizing the need f

163 To assess neurovascular encasement, contact between tumor and arte

164 y monocytes with stress adhered to IL-1R1(+) neurovascular endothelial cells and this interaction was

165 induced endothelial morphogenesis produced a neurovascular environment.

166 Accordingly, we propose that enlarged neurovascular facial canals shouldn't be used to exclusi

167 both the neural interactions and a flexible neurovascular forward model.

168 nings of hypertension-induced alterations in neurovascular function during cold exposure is clinicall

169 tension, no studies have examined integrated neurovascular function during cold stress in HTN.

170 tension, no studies have examined integrated neurovascular function during cold stress in hypertensiv

171 This position allows them to regulate key neurovascular functions of the brain.

172 l cells, astrocytes and neurons that control neurovascular functions.

173 A neurovascular guiding factor, Semaphorin 3c (Sema3c), is

174 ifactorial, disabling, recurrent, hereditary neurovascular headache disorder.

175 perience has profound and complex effects on neurovascular health and disease.

176 supports emerging concepts that maintaining neurovascular health promotes brain health.

177 pericytes play important roles in regulating neurovascular homeostasis by secreting soluble factors,

178 a novel mechanism for how pericytes regulate neurovascular homeostasis.

179 According to the neurovascular hypothesis, impairment of low-density lipo

180 promoted anxiogenesis through stimulation of neurovascular IL-1R1 by IL-1beta.

181 themes of modern stroke care are the use of neurovascular imaging and speed of diagnosis and treatme

182 t that the impact of ischemia/reperfusion on neurovascular injury and functional outcome especially i

183 ischemia; and (3) acute glycemic control on neurovascular injury and functional outcome in diabetic

184 ent methods and capture the full spectrum of neurovascular injury and its clinical effect.

185 potential role for thrombin contributing to neurovascular injury and several potential avenues for n

186 is a key target for treating APOE4-mediated neurovascular injury and the resulting neuronal dysfunct

187 tPA is known to worsen neurovascular injury by amplifying matrix metalloprotein

188 ood-borne coagulation factor, contributes to neurovascular injury during acute focal ischemia.

189 development of intracerebral haemorrhage and neurovascular injury in experimental stroke.

190 investigate the role of PGE2 EP1 receptor in neurovascular injury in stroke.

191 ed the effects of these compounds on retinal neurovascular injury induced by hyperglycemia.

192 ombin receptor, appeared to mediate ischemic neurovascular injury.

193 ban, a direct thrombin inhibitor, alleviated neurovascular injury.

194 effects of chronic exercise on cognition to neurovascular integrity during aging.

195 ho signalling is required for maintenance of neurovascular integrity, unravelling a mechanism by whic

196 t injury after neonatal stroke by preserving neurovascular integrity, we subjected postnatal day 7 (P

197 We find Mekk3 deficiency impairs neurovascular integrity, which is partially dependent on

198 Here, we identified a noncanonical neurovascular interaction in eye development and disease

199 ha modulates semaphorin 3E transcription and neurovascular interaction in pathological retinal angiog

200 Neurovascular interactions are essential for proper brai

201 ar link." Most of the evidence demonstrating neurovascular interactions derives from studies outside

202 lar networks reveals an important feature of neurovascular interactions.

203 evaluation confirmed osseous, articular, and neurovascular invasion in 8.6%, 2.9%, and 25.3% of patie

204 n of MEKK3:CCM2 interaction leads to similar neurovascular leakage.

205 rnous malformations (CCMs) are predominantly neurovascular lesions and are associated with mutations

206 s impaction syndromes, stress fractures, and neurovascular lesions.

207 s known about the specific properties of the neurovascular link in the brain.

208 ulatory effects of molecules involved in the neurovascular link on angiogenesis in the periphery and

209 nt levels of complexity has been termed the "neurovascular link." Most of the evidence demonstrating

210 evers, early-onset lacunar strokes and other neurovascular manifestations, livedoid rash, hepatosplen

211 Both TGF-beta1 and MMP-9 are major neurovascular mediators, and therefore, our current find

212 s is of relevance to neurologists working in neurovascular, memory and epilepsy clinics, and neurovas

213 re evaluated, along with skeletal muscle and neurovascular models.

214 ocytes are critical regulators of neural and neurovascular network communication.

215 weeks of diabetes, the vasoreactivity of the neurovascular network to CO2 was abolished and was not r

216 r mapping the hemodynamic signal through the neurovascular network with specificity at the level of i

217 sion, Imaging, Metabolic Disorders & Lipids, Neurovascular & Neurodegenerative Disorders, Rhythm Diso

218 sion, Imaging, Metabolic Disorders & Lipids, Neurovascular & Neurodegenerative Disorders, Rhythm Diso

219 is of a CD31-enriched cell population of the neurovascular niche showed that endothelial Stat3 ablati

220 ularis, a group of syndromes associated with neurovascular, ophthalmological, overgrowth, and maligna

221 gy in fatal cases, information about in vivo neurovascular pathogenesis is scarce because brain tissu

222 bservations give important information about neurovascular pathophysiology in pediatric CM.

223 helial growth factor (VEGFA, VEGF) regulates neurovascular patterning.

224 In summary, our findings suggest a neurovascular protective effect of GHRH analogs during t

225 We investigated the potential neurovascular protective effect of hydrogen inhalation e

226 These neurovascular protective effects of EP1 inactivation are

227 s are critical in driving the alterations in neurovascular regulation and attendant cognitive impairm

228 cts were reflected by marked improvements in neurovascular regulation and cognitive performance.

229 nrecognized mechanism by which Abeta impairs neurovascular regulation and suggest that TRPM2 channels

230 cates that distinct processes might underlie neurovascular regulation for both stimulation and sponta

231 mer disease, induces profound alterations in neurovascular regulation through the innate immunity rec

232 confirming the role of ETB receptors in the neurovascular remodeling actions of IRL-1620.

233 e astrocytes and EPCs wherein HMGB1 promotes neurovascular remodeling and functional recovery after s

234 also participate in endogenous processes of neurovascular remodeling and recovery after cerebral isc

235 Are such angiocrine signals relevant to neurovascular remodeling and recovery in other neurologi

236 s endothelial progenitor cell (EPC)-mediated neurovascular remodeling during stroke recovery.

237 However, the effect of IRL-1620 on neurovascular remodeling following cerebral ischemia has

238 K inhibition suppressed surrogate markers of neurovascular remodeling, including matrix metalloprotei

239 Nrf2 in reprogramming ischemic tissue toward neurovascular repair via Sema6A regulation, providing a

240 ur findings have broad implications for both neurovascular research and longitudinal fMRI studies tha

241 that cortical spreading depolarization, the neurovascular response, cerebrovascular autoregulation,

242 doses revealed a monotonic coupling between neurovascular responses and receptor occupancies.

243 as compared to WT mice may explain impaired neurovascular responses in the mutant, and these alterat

244 ss central to cerebral malaria pathogenesis: neurovascular sequestration.

245 are confounded by age-related changes in the neurovascular signaling.

246 s review discusses the role of astrocytes in neurovascular signalling in both physiology and patholog

247 nhanced immunoreactivity was observed on the neurovascular structure around hematoma at 24 hrs after

248 Collectively, our data shows that neurovascular structures decline with age, a process tha

249 Given the diversity of neurovascular structures in different tissues, guidance

250 ging leads to a significant deterioration of neurovascular structures including basement membrane red

251 f defects that expose tendon, joints, and/or neurovascular structures is necessary to preserve optima

252 may exhibit tumor growth involving critical neurovascular structures or diffuse growth, resulting in

253 atomic landmark that hosts numerous critical neurovascular structures.

254 thesia is widely employed in animal fMRI and neurovascular studies, however anesthetics are known to

255 trial and other studies have shown that the neurovascular thrombectomy improves outcomes at 90 days

256 INTERPRETATION: At 12 months follow-up, neurovascular thrombectomy reduced post-stroke disabilit

257 ing intravenous alteplase when eligible) and neurovascular thrombectomy with Solitaire FR or medical

258 e present study, we aimed at constructing 3D neurovascular tissues by combining in vitro neurogenesis

259 ture models and succeeded in constructing 3D neurovascular tissues with an optimized seeding conditio

260 ic component of inhibitory neuromuscular and neurovascular transmission, increased release of purines

261 Neurovascular uncoupling by cocaine during stimulation b

262 Neurovascular uncoupling could contribute to cocaine's n

263 responses to neuronal stimuli, resulting in neurovascular uncoupling, reduced oxygen supply to the b

264 Neurovascular unit (NVU) is a basic unit in the brain, i

265 ithin the greater context of a multicellular neurovascular unit (NVU) that includes neurons, astrocyt

266 Age-related changes to the neurovascular unit (NVU), and their consequences for cer

267 The concept of the neurovascular unit (NVU), formalized at the 2001 Stroke

268 ailed model of potassium flow throughout the neurovascular unit (synaptic region, astrocytes, and art

269 TEMENT: Pericytes are a key component of the neurovascular unit and are essential for normal BBB func

270 Given the role of APOE in maintaining the neurovascular unit and as an anti-inflammatory molecule,

271 s support bidirectional signaling within the neurovascular unit and astrocytes as key modulators of P

272 ator (t-PA) can modulate permeability of the neurovascular unit and exacerbate injury in ischemic str

273 tion between different cell types within the neurovascular unit and intact blood-brain barrier (BBB)

274 e well established action of estrogen in the neurovascular unit and its potential interaction with re

275 ighly interactive processes that involve the neurovascular unit and neural stem cells.

276 phenotype, it plays a pathogenic role in the neurovascular unit and triggers neuronal hyperexcitabili

277 They are positioned centrally in the neurovascular unit between endothelial cells, astrocytes

278 CNS pericytes are uniquely positioned in the neurovascular unit between endothelial cells, astrocytes

279 s well documented that all components of the neurovascular unit contribute to the restrictive nature

280 issue of the JCI points to perturbations of neurovascular unit coupling caused by perivascular macro

281 erived multipotent regenerative cells to the neurovascular unit during angiogenesis.

282 Intravenously injected DAG peptide homes to neurovascular unit endothelial cells and to reactive ast

283 e essential for maintaining integrity of the neurovascular unit following brain ischemia.

284 ese cells to the structural integrity of the neurovascular unit has not hitherto been assessed.

285 s because of progressive degeneration of the neurovascular unit in the retina, a condition known as d

286 The neurovascular unit is a coordinated and interactional sy

287 to be present in all major components of the neurovascular unit of both R6/2 mice and HD patients.

288 miR-155 is expressed at the neurovascular unit of individuals with MS and of mice wi

289 astrocytes, and microglia, cell types in the neurovascular unit that can secrete MMPs.

290 contribution to cellular interactions at the neurovascular unit that influence the overall function o

291 scular endothelial cells, which comprise the neurovascular unit within the central nervous system (CN

292 mmunication between the affected brain area, neurovascular unit, and peripheral immune cells.

293 At the neurovascular unit, brain endothelial cells, astrocytes,

294 ay, we searched for molecular markers of the neurovascular unit, including endothelial cells and astr

295 Within the neurovascular unit, pericytes play important roles in re

296 profoundly impacts communication within the neurovascular unit-neurons, astrocytes, and arterioles-c

297 multiple cellular involvement affecting the neurovascular unit.

298 onal model of bidirectional signaling in the neurovascular unit.

299 etween neurons, vasculature, and glia within neurovascular units are critical for maintenance of the

300 ons, the amacrine and horizontal cells, form neurovascular units with capillaries in 2 of the 3 retin