ライフサイエンスコーパス: neuropathological

1 deficits arise in parallel with a number of neuropathological abnormalities, including progressive n

2 accine to rhesus macaques does not result in neuropathological abnormalities, or aberrant behaviors,

3 of cases, mossy fiber sprouting was a common neuropathological abnormality, and somatostatin-immunore

4 chosis, consistent with dysconnectivity as a neuropathological account of symptom expression.

5 disease to cigarette smoke and analysed the neuropathological alterations in comparison with animals

6 Brain tissue HI was verified by neuropathological analysis and by Adenosine Triphosphate

7 Neuropathological analysis found greater neuronal loss i

8 a of mutation-positive individuals including neuropathological analysis in one instance.

9 Interestingly, neuropathological analysis of a Belgian FTD family carry

10 One week after treatment, neuropathological analysis of hemispheric and hippocampa

11 Neuropathological analysis of patients with NCL shows ac

12 Neuropathological analysis of post-mortem brain tissue d

13 Brain Bank archival collection and detailed neuropathological analysis of the selected cases.

14 Neuropathological analysis showed diffuse astrocytic gli

15 Neuropathological analysis showed extensive alpha-synucl

16 Neuropathological analysis showed significant levels of

17 at PGC-1alpha overexpression exacerbates the neuropathological and behavioral deficits that occur in

18 of motor and cognitive functional deficits, neuropathological and biochemical changes and levels of

19 active humoral and Treg) and analyzed using neuropathological and biochemical markers.

20 This study describes new neuropathological and biochemical observations in a seri

21 nic mice and characterized their behavioral, neuropathological and biochemical phenotypes.

22 We developed a mouse model to mimic both neuropathological and clinical c9FTD/ALS phenotypes.

23 oid-beta species accumulate and affect other neuropathological and clinical features in the disease.

24 To determine the neuropathological and clinical features of deceased foot

25 protease-sensitive prionopathy, followed by neuropathological and clinical review of candidate cases

26 for dystonia and should stimulate systematic neuropathological and imaging studies in carriers of TOR

27 Neuropathological and immunological studies support the

28 Neuropathological and in vivo studies have revealed a ti

29 of cortical brain development, with distinct neuropathological and neuroimaging patterns.

30 We propose this synthesis to prompt refined neuropathological and neuroimaging studies on the pivota

31 The present findings unveil particular neuropathological and neuroinflammatory profiles in FFI

32 cts of the DeltaE mutation at the molecular, neuropathological and organismal levels.

33 Focusing on neuropathological and physiological data from two phylog

34 njury to the pediatric brain reproduces many neuropathological and seizure-like hallmarks characteris

35 Recent neuropathological and structural neuroimaging data point

36 nt to cause electrophysiological, molecular, neuropathological, and behavioral changes related to SZ.

37 t causes a form of PD with unusual clinical, neuropathological, and biochemical features.

38 should be noted, however, that neurological, neuropathological, and neuropsychological studies have c

39 However, with profound clinical, prognostic, neuropathological, and now genetic heterogeneity, the co

40 data, MRI voxel-based morphometry (VBM) and neuropathological assessment from 64 C9P cases (ALS=31,

41 Neuropathological assessment of GM and WM disease burden

42 BLSA, 191 participants underwent autopsy and neuropathological assessment, and 75 non-demented indivi

43 gnitive assessments during life and detailed neuropathological assessments at death, such as the BLSA

44 Systematic neuropathological assessments documented the severity of

45 We performed clinical and neuropathological assessments of patients with and witho

46 e potential mechanism to ameliorate or delay neuropathological brain changes with aging.

47 he dissociation of cognitive performance and neuropathological burden are poorly understood, and ther

48 ent, amyloid burden and WMH likely represent neuropathological cascades with distinct etiologies and

49 worse prognosis for each increasing level of neuropathological change.

50 ls of pre-apoptotic proteins, attenuated the neuropathological changes and apoptosis and decreased th

51 HI resulted in decreased ATP and PCr levels, neuropathological changes and increased levels of cytoch

52 inA hypofunction to the development of early neuropathological changes in distinct sensorimotor regio

53 their ability to mitigate the behavioral and neuropathological changes in experimental Alzheimer dise

54 n of C1q and C3 were analyzed in relation to neuropathological changes in myelinated and demyelinated

55 Prion strains induce specific neuropathological changes in selected brain areas.

56 Neuropathological changes in spinal cord are linked to C

57 hat DTI are potentially useful correlates of neuropathological changes in TBPQ64 rats and raise hope

58 eatment with iPPS did not reduce the overall neuropathological changes in the brain.

59 uch as gait ataxia, associated with multiple neuropathological changes including mutant ATXN3 inclusi

60 an excellent surrogate marker for assessing neuropathological changes that occur in Alzheimer's dise

61 TDP-43-DeltaNLS) in forebrain neurons evokes neuropathological changes that recapitulate several feat

62 elated motor dysfunction that is preceded by neuropathological changes, including gliosis, accumulati

63 s with MCI may be associated with underlying neuropathological changes, including prodromal AD, and m

64 , attention is shifting to understanding the neuropathological changes, particularly in the pre-front

65 in support of an association between severe neuropathological changes, robust macrophage and microgl

66 e further show an association between severe neuropathological changes, robust resident microglia inf

67 hich recapitulates deregulated Cdk5-mediated neuropathological changes, such as hyperphosphorylated t

68 the associations between APOE alleles and AD neuropathological changes, using the APOEepsilon3/epsilo

69 crucial mediator of tau-related clinical and neuropathological changes.

70 12 patients with alpha-synucleinopathies for neuropathological changes.

71 ographic, clinical, diagnostic, genetic, and neuropathological characteristics among racial/ethnic gr

72 series, and many clinical, neuroimaging and neuropathological characteristics are not well understoo

73 ell patterning cue models the behavioral and neuropathological characteristics of PD in a remarkable

74 with unique biochemical, morphological, and neuropathological characteristics.

75 Full neuropathological characterization has not been reported

76 nts in the Memory and Aging Project clinical neuropathological cohort study, 2004-2013.

77 We developed a neuropathological comorbidity (NPC) score and compared i

78 ings indicate axonal damage as an underlying neuropathological component of bipolar disorder, althoug

79 active astrogliosis is a critical process in neuropathological conditions and neurotrauma.

80 ctivation in psychiatry, and likely in other neuropathological conditions as well.

81 when overexpressed, often upregulated under neuropathological conditions with impaired learning and

82 een implicated in learning, development, and neuropathological conditions.

83 h, and as such, they play a role in numerous neuropathological conditions.

84 inks between dendritic spine impairments and neuropathological conditions.

85 been associated with cognitive decline under neuropathological conditions.

86 s during inflammatory events underlying many neuropathological conditions.

87 ation of neural cells, implicated in several neuropathological conditions.

88 er reports added to our understanding of the neuropathological consequences of a career in boxing, le

89 ation and the ensuing neurodevelopmental and neuropathological consequences.

90 tive impairments, uncontrolled drinking, and neuropathological cortical changes characterize alcohol

91 National Institute on Aging-Reagan Institute neuropathological criteria for AD.

92 opographical distribution is one of the core neuropathological criteria for the diagnosis of Alzheime

93 l Institute on Aging-Alzheimer's Association neuropathological criteria, and used multivariate regres

94 tematic review of patients' neuroimaging and neuropathological data allowed us to distinguish at leas

95 , we examined symptom onset, and genetic and neuropathological data from a cohort of patients with Le

96 Neuropathological data indicate that tau tangles in the

97 nsive clinical, cognitive, neuroimaging, and neuropathological data were collected from 69 patients w

98 heimer's disease dementia, and with complete neuropathological data, are included in our analyses.

99 ed in brain, and their loss in mice leads to neuropathological deficits that are reminiscent of Hunti

100 This condition has a clear neuropathological definition but the relationship betwee

101 Among these participants, 50% had neuropathological diagnoses of Alzheimer disease (AD), a

102 Neuropathological diagnoses of neurodegenerative disease

103 scribed (Mesulam et al., 2008) but had their neuropathological diagnoses updated to fit current crite

104 Compared to neuropathological diagnoses, clinical diagnosis had high

105 adults and the mismatch between clinical and neuropathological diagnoses.

106 Our results confirm the high prevalence of neuropathological diagnosis in older adults and the mism

107 Accurately predicting the underlying neuropathological diagnosis in patients with behavioural

108 tion (behavioural Alzheimer's disease) and a neuropathological diagnosis of high-likelihood Alzheimer

109 also described and compared the frequency of neuropathological diagnosis to clinical diagnosis of dem

110 -four percent of the sample met criteria for neuropathological diagnosis.

111 flects underlying genetic, environmental and neuropathological differences.

112 tion of hp-Tau is implicated in more than 20 neuropathological diseases including Alzheimer's disease

113 DNA lesion, have been associated with three neuropathological diseases: ataxia oculomotor apraxia 1,

114 ntal processes can result in microcephaly, a neuropathological disorder characterized by a reduction

115 in the management of type 2-diabetes and/or neuropathological disorders.

116 olds potential interest for the treatment of neuropathological disorders.

117 brain injury, cerebral hemorrhage, and other neuropathological disorders.

118 ture aiming to establish neuroanatomical and neuropathological (e.g. amyloid and tau deposition) dime

119 L-1) mediates diverse neurophysiological and neuropathological effects in the CNS through type I IL-1

120 ype alpha-synuclein could exert dopaminergic neuropathological effects.

121 Various underlying neuropathological entities lead to the frontotemporal de

122 Neuropathological evaluations and retrospective telephon

123 r brains for research, a high proportion had neuropathological evidence of CTE, suggesting that CTE m

124 Neuropathological evidence suggests that demyelination c

125 Neuropathological examination confirmed the PSP diagnosi

126 Neuropathological examination during end-stage disease s

127 We also provide the first detailed neuropathological examination of a child with extreme me

128 underwent postmortem examination, including neuropathological examination of the brain.

129 Brain and spinal cord neuropathological examination of two cases with SLC52A3

130 Neuropathological examination revealed widespread Lewy b

131 Neuropathological examination showed astrocytic and micr

132 Neuropathological examination showed that NPT100-18A dec

133 2.8) years, died, and underwent a postmortem neuropathological examination that provided estimates of

134 Detailed neuropathological examination using 70mum and traditiona

135 Neuropathological examination was conducted in nine pati

136 mpal sclerosis and prion disease) based on a neuropathological examination with or without cerebrovas

137 s in substantia nigra pars compacta is a key neuropathological feature in Parkinson disease.

138 Inflammation is a common neuropathological feature in several neurological disord

139 -beta (Abeta)-containing plaques are a major neuropathological feature of Alzheimer's disease (AD).

140 Defective axonal transport is an early neuropathological feature of amyotrophic lateral scleros

141 The core clinical and neuropathological feature of the autosomal dominant spin

142 ggests that reduction in myelin is a primary neuropathological feature of Wolfram syndrome.

143 efficacy of bezafibrate in ameliorating both neuropathological features and disease phenotype in BACH

144 The identified neuropathological features closely resembled those in br

145 ioral deficits correlated with mitigation of neuropathological features commonly observed in HD.

146 rable to amyloid-beta accumulation and other neuropathological features in familial Alzheimer's disea

147 rt genetic, clinical, neuroradiological, and neuropathological features of 50 children from 30 famili

148 Because neuropathological features of AD can be present several

149 tides into protein fibres is one of the main neuropathological features of Alzheimer's disease (AD).

150 ur findings expand the genetic, clinical and neuropathological features of Brown-Vialetto-Van Laere s

151 al diagnosis of PD made by a neurologist and neuropathological features of PD.

152 and neuronal death, thus recapitulating key neuropathological features of TDP-43 proteinopathies.

153 in tumors that do not fully recapitulate the neuropathological features of the human condition.

154 halidomide involving in the mitigation of AD neuropathological features remains unclear.

155 lpha-synuclein homeostasis and a spectrum of neuropathological features that implicate RAB39B in the

156 These neuropathological features were also found in transgenic

157 challenge to the identification of unifying neuropathological features.

158 ncurrent cerebrovascular disease is a common neuropathological finding in aged subjects with dementia

159 Cerebral amyloid angiopathy is a common neuropathological finding in the ageing human brain, ass

160 inical approach, differential diagnosis, and neuropathological findings are discussed.

161 m brain analysis available for assessment of neuropathological findings associated with prion disease

162 d imaging are presented here, in addition to neuropathological findings from two cases with novel mut

163 We report on the neuropathological findings in a case of vCJD treated wit

164 Additional neuropathological findings included bilateral hippocampa

165 Here we show that Arsg KO mice share common neuropathological findings with other Sanfilippo syndrom

166 s, evident from neuroimaging, biomarker, and neuropathological findings, and a high incidence of cogn

167 In light of these new neuropathological findings, GCIs and neuronal cytoplasmi

168 LIPPERS aetiologies by neuroradiological and neuropathological findings.

169 lored this association in more detail at the neuropathological, genetic and clinical level.

170 influencing residual cognition, we leveraged neuropathological, genetic, epigenetic, and transcriptio

171 Through a multistep analysis of cognitive, neuropathological, genomic, epigenomic, and transcriptom

172 e HD patients were compared with HD striatal neuropathological grade, and symptom scores of motor imp

173 neration correlated with increasing striatal neuropathological grade.

174 zen tissue was recognized retrospectively on neuropathological grounds alone.

175 uce amyloid plaque formation in the brain, a neuropathological hallmark of AD.

176 d beta protein in extracellular plaques is a neuropathological hallmark of Alzheimer disease.

177 d from amyloid precursor protein (APP), is a neuropathological hallmark of Alzheimer's disease (AD).

178 ulation of beta-amyloid (Abeta) is the major neuropathological hallmark of Alzheimer's disease (AD).

179 amyloid-beta (Abeta) in amyloid plaques is a neuropathological hallmark of Alzheimer's disease (AD).

180 ing of deposited beta-amyloid (Abeta), are a neuropathological hallmark of Alzheimer's Disease (AD).

181 Amyloid plaques, a neuropathological hallmark of Alzheimer's disease, are l

182 The neuropathological hallmark of HD is the loss of neurons

183 eased the number of huntingtin aggregates, a neuropathological hallmark of HD, but did not influence

184 unction and often signs of parkinsonism; the neuropathological hallmark of MSA is glial cytoplasmic i

185 f nigrostriatal dopamine (DA) neurons is the neuropathological hallmark of Parkinson's disease (PD).

186 Intracellular tau aggregates are the neuropathological hallmark of several neurodegenerative

187 d tau in neurofibrillary tangles (NFTs) is a neuropathological hallmark of tauopathies, including Alz

188 ed formation of alpha-synuclein fibrils, the neuropathological hallmark of the disease.

189 One of the neuropathological hallmarks of AD is the accumulation of

190 ccumulation of amyloid-beta and tau, the two neuropathological hallmarks of AD.

191 id-beta protein (Abeta) and synapse loss are neuropathological hallmarks of Alzheimer disease (AD).

192 One of the primary neuropathological hallmarks of Alzheimer disease is the

193 n (alpha-syn)-rich Lewy bodies are the major neuropathological hallmarks of Alzheimer's disease (AD)

194 Key neuropathological hallmarks of Alzheimer's disease (AD)

195 he form of Lewy bodies and Lewy neurites are neuropathological hallmarks of Parkinson's disease.

196 e are remarkably similar to the clinical and neuropathological hallmarks of Parkinson's disease.

197 These findings indicate that biochemical and neuropathological hallmarks of tauopathies are accuratel

198 Although neuropathological hallmarks such as gliosis, globoid cel

199 TATEMENT Tauopathies show great clinical and neuropathological heterogeneity, despite the fact that t

200 ltifunctional protein p62 is associated with neuropathological inclusions in several neurodegenerativ

201 , preserves BBB permeability, and attenuates neuropathological indices more effectively than non-targ

202 Detailed neuropathological information on the structural brain le

203 to P3 models the characteristic white matter neuropathological injury, gray matter volume loss, and m

204 alus formation is a frequent complication of neuropathological insults associated with neuroinflammat

205 c biomarker, but caution is indicated in the neuropathological interpretation of its binding.

206 These neuroimaging and neuropathological investigations provide converging evid

207 t in dendrites and if Lewy bodies, the major neuropathological lesion found in PD brains, exacerbate

208 hical distribution of the defining molecular neuropathological lesions among 10 neurodegenerative dis

209 Associations between neuropathological lesions and cognitive impairment were

210 nd tau, the two major proteins composing the neuropathological lesions detected in brain tissue of Al

211 cy of neurodegenerative and vascular-related neuropathological lesions in 1,092 Brazilian admixed old

212 rly presentation of Alzheimer's disease (AD) neuropathological lesions including degeneration of the

213 have remarkably different clinical signs and neuropathological lesions.

214 consider these as leads for the treatment of neuropathological lysosomal storage disorders.

215 es mediated by IL-1beta and the clinical and neuropathological manifestations of EAE disappeared in m

216 The relationship between dementia and common neuropathological markers (Alzheimer-type, infarcts and

217 etermining associations between dementia and neuropathological markers of dementia in patients with a

218 In summary, CART treatment reduced multiple neuropathological measures and improved memory in APP/PS

219 However, the neuropathological mechanism is unclear.

220 These findings suggest a novel neuropathological mechanism of early AD, which is initia

221 Further, the neuropathological mechanism of risk appears to primarily

222 x, multifactorial disease in which different neuropathological mechanisms are likely involved, includ

223 We identified the underlying neuropathological mechanisms in male and female shaky mi

224 ay induce epigenetic modifications affecting neuropathological mechanisms in the brain leading to inc

225 Our findings provide novel insight into the neuropathological mechanisms of ASPD.

226 Despite decades of extensive research, the neuropathological mechanisms responsible for the develop

227 s extremely useful tools for elucidating the neuropathological mechanisms that underlie different dis

228 ac3 heterodimer, which may shed light on the neuropathological mechanisms triggered by Sac3 dysfuncti

229 ifest stage of HD, which are relevant to the neuropathological mechanisms underlying the development

230 Together, these data support a neuropathological model in which sleep disruption may co

231 Here, we generated a comprehensive neuropathological, molecular, and transcriptomic charact

232 nse as a possible contributory factor in the neuropathological nature of Dync1h1 mutations, despite g

233 lted in significant reversal of biochemical, neuropathological, neurophysiological, and behavioural d

234 Together our findings define divergent neuropathological outcomes arising from different classe

235 To determine clinical and neuropathological outcomes following a clinical diagnosi

236 l to examine the chronic neurobehavioral and neuropathological outcomes following single and repetiti

237 The neuropathological overlap with amyotrophic lateral scler

238 rative disorders with clinical, genetic, and neuropathological overlap.

239 forms) and a skepticism for the brain-based neuropathological paradigm of psychiatric research then

240 Main Outcomes and Measures: Neuropathological parameters and changes in hippocampal

241 he retired players suggested the presence of neuropathological patterns consistent with models of con

242 Few details are known about the neuropathological phenotype of these unique cases that m

243 nical, neurochemical and, for the most part, neuropathological phenotype that is indistinguishable fr

244 Multiple research groups have observed neuropathological phenotypes and molecular symptoms in v

245 Nlk expression suppresses the behavioral and neuropathological phenotypes in SCA1 knock-in mice.

246 Treatment with HV-3 reduces behavioural and neuropathological phenotypes of HD in both fragment- and

247 ssed alpha-syn that closely recapitulate the neuropathological phenotypes of Lewy neurites found in h

248 Further neuropathological phenotypes of these mutants provide no

249 Clinical, cognitive, and neuropathological phenotypes were collected in 3 prospec

250 The frequency of PD and its neuropathological presentation remain unknown in this co

251 risk factor for early-onset PD with variable neuropathological presentation reminiscent of LRRK2-asso

252 alone are sufficient to account for diverse neuropathological presentations, similar to those that d

253 ction, collectively known as synaptopathy, a neuropathological process contributing to excitotoxic ne

254 pulation of cerebrospinal fluid drainage and neuropathological processes in the CNS.

255 nges in the cerebral vasculature in numerous neuropathological processes including subarachnoid hemor

256 or cognitive processes modify the effect of neuropathological processes on cognitive outcomes.

257 Therefore, neuropathological processes other than beta-amyloidosis

258 need for adjunctive therapy that targets the neuropathological processes that persist in antiretrovir

259 to identify biomarkers reflecting underlying neuropathological processes that predict clinical/behavi

260 ed interest in their possible involvement in neuropathological processes, yet little is known about t

261 MDA receptors (NMDARs) contribute to several neuropathological processes.

262 describe the unusual clinical and molecular-neuropathological profile of a case of Gerstmann-Strauss

263 d most frequent cognitive, neuroimaging, and neuropathological profile.

264 in HdhQ150 mice at both time points, with no neuropathological progression across time and a selectiv

265 levels of amyloid-beta peptide (Abeta) with neuropathological progression in Alzheimer's disease (AD

266 The biochemical and neuropathological properties of bovine spongiform enceph

267 Many of the strain-specified biochemical and neuropathological properties of BSE and vCJD prions, inc

268 or of second RNA-recognition motif (RRM2) of neuropathological protein TDP43 under the effect of oxid

269 n enduring long-term effects on behavior and neuropathological sequelae.

270 E, based on defined diagnostic criteria; CTE neuropathological severity (stages I to IV or dichotomiz

271 Neuropathological severity of CTE was distributed across

272 e in GFP-control mice, suggesting no obvious neuropathological side effects of the drug.

273 Clinical and neuropathological similarities between dementia with Lew

274 that both diseases likely belong to the same neuropathological spectrum.

275 and the utility of this system to study the neuropathological spread of tau aggregates.SIGNIFICANCE

276 ential pattern that permits recognition of 4 neuropathological stages consistent with the hypothesis

277 the ALS group that coincided with postmortem neuropathological stages.

278 , following from recent understanding of the neuropathological stages.

279 atterns similar to those prescribed by Braak neuropathological staging of tau pathology.

280 profiles of these disorders and to serve as neuropathological standards for emerging molecular neuro

281 Our data are consistent with neuropathological studies and further suggest that entor

282 Neuropathological studies are showing structural and con

283 Prion protein gene sequence, molecular, and neuropathological studies confirmed the diagnosis of spo

284 Moreover, few neuropathological studies have addressed whether blast e

285 Previous neuropathological studies have revealed a series of alte

286 In multiple sclerosis, neuropathological studies have shown widespread changes

287 Neuropathological studies in multiple sclerosis have sug

288 We also detail findings from neuropathological studies of brain areas associated with

289 alidates the potential of imaging for future neuropathological studies.

290 fferential disruption of a common primordial neuropathological substrate causes these differences in

291 TDP-43 and FUS have joined tau as common neuropathological substrates of the disease.

292 ortical tubers are believed to represent the neuropathological substrates of these disabling manifest

293 y patterns on MRI can reliably predict three neuropathological subtypes of Alzheimer's disease (AD):

294 bodies that are characteristic of different neuropathological subtypes of the disease.

295 of CD8(+) T lymphocytes, leading to a lethal neuropathological syndrome.

296 called strains, are associated with distinct neuropathological syndromes.

297 level profiles that mirrored key features of neuropathological tau progression including profiles con

298 ertain loci may influence multiple different neuropathological traits, including tau, amyloid beta pl

299 Our results support the proposed neuropathological trajectory in PD and establish novel m

300 ss-sectional study, we describe clinical and neuropathological variables related to cognitive impairm