ライフサイエンスコーパス: postmortem brain

1 specific functional genomic studies in human postmortem brain.

2 predicted increases in amyloid pathology in postmortem brain.

3 (CGI) that is highly methylated in the human postmortem brain.

4 d Western blots to study native htt in human postmortem brain.

5 xpression was mostly unaltered in BD and SCZ postmortem brain.

6 evated Rrs1 mRNA in HD compared with control postmortem brain.

7 ure models, HD transgenic mice, and human HD postmortem brain.

8 requires the detection of amyloid plaques in postmortem brain.

9 expression of the DYT1 gene in normal human postmortem brain.

10 Mbnl1 auto-splicing also occurs in human FXS postmortem brain.

11 patiotemporal expression with respect to the postmortem brain.

12 the neuronal and nonneuronal nuclei from the postmortem brain.

13 ed with lower D2 short isoform expression in postmortem brain.

14 tor subunit 1 (GABAB1) splicing in alcoholic postmortem brains.

15 r RNA (mRNA) in a relatively small sample of postmortem brains.

16 that has historically only been conducted on postmortem brains.

17 of Shank3-deficient mice and autistic human postmortem brains.

18 antify identified pathologic features in the postmortem brains.

19 ates from biological samples including human postmortem brains.

20 consistently observed to be abnormal in SCZ postmortem brains.

21 cortical interneurons of schizophrenia (SZ) postmortem brains (10), suggesting that the availability

22 ing data with the standard of truth based on postmortem brain amyloid status for subjects in the auto

23 We further validated miRNA data using AD postmortem brains, amyloid precursor protein transgenic

24 Postmortem brain analyses documented increased GAS5 expr

25 Magnetic resonance imaging and postmortem brain analysis supports important roles for W

26 s been implicated in SZ by gene association, postmortem brain and animal studies.

27 case-control studies of human tissue (i.e., postmortem brain and bio-fluids) were considered: DNA me

28 Analyses of 93 samples from postmortem brain and blood found (i) the 4977 bp 'common

29 d from mouse models of stress and from human postmortem brain and genome-wide association studies ind

30 dynein heavy chain with the plaques in human postmortem brain and in a double transgenic AD mouse mod

31 The quality of HCV RNA from postmortem brain and liver was assessed and demonstrated

32 , and cAMP was significantly decreased in HD postmortem brain and lymphoblastoid cells, attesting to

33 mulation of cytoplasmic TDP-43 aggregates in postmortem brain and spinal cord (SC), it has been sugge

34 of 1,130,767 nuclei per cells from 149 adult postmortem brains and 72 organoid samples were used.

35 has been highlighted by their presence in HD postmortem brains and by the fact that nuclear inclusion

36 human nervous system with evidence from both postmortem brains and detection in cerebrospinal fluid o

37 from each of 8 schizophrenic and 11 control postmortem brains and immunohistochemistry for the phosp

38 D are enriched in those downregulated in ASD postmortem brains and in genes harboring de novo mutatio

39 been demonstrated in the substantia nigra of postmortem brains and several peripheral tissues obtaine

40 mouse cerebral cortex and spinal cord, human postmortem brain, and glioma biopsy specimens.

41 orrelated with RNA polymerase II activity in postmortem brain, and pharmacologic modulation of RNA po

42 escribed for dopaminergic markers in CSF and postmortem brain, and there exists a range of affective,

43 by deep sequencing (ChIP-seq) datasets from postmortem brains are needed.

44 essed in peripheral blood, muscle biopsy, or postmortem brain at the level of enzyme activity or subu

45 phenotype and clinical characterization, and postmortem brain banking data which includes these.

46 een investigated over the last century using postmortem brains but there has been little progress in

47 diseases are diagnosed definitively only in postmortem brains by the presence of key misfolded and a

48 ndria hours after death indicates that human postmortem brains can be an abundant source of viable mi

49 strate that overrepresented IgG sequences in postmortem brains can be used to produce functional reco

50 ng neurotransmitter receptors from the human postmortem brain, can be transplanted to frog oocytes, a

51 Sorted neurons/glia from a fourth postmortem brain collection (n = 58) were used for valid

52 Allocation of lineages in postmortem brain correlated with anterior-posterior axis

53 is review, we describe key findings in human postmortem brains, cultured cells, and animal models of

54 opathic ASD cases from controls across three postmortem brain data sets.

55 We examined the concentration of lactate in postmortem brain (dorsolateral prefrontal cortex) in sub

56 is to gene expression data from high-quality postmortem brains, examining 24-h cyclic patterns in six

57 Here we report the first postmortem brain findings of a phase I clinical stroke t

58 association study (EWAS) of smoking in human postmortem brain, focusing on nucleus accumbens (NAc) as

59 genotype and histopathological assessment of postmortem brains for CAA severity.

60 ne genes and microglial transcripts occur in postmortem brain from alcoholics and animals exposed to

61 ved decreased synaptosomal F-actin levels in postmortem brain from mild cognitive impairment and AD p

62 mately 50% in various cortical structures of postmortem brain from patients diagnosed with schizophre

63 he total volume and neuron number of BA17 in postmortem brains from 10 subjects with schizophrenia an

64 CpG loci) in the orbital frontal cortices of postmortem brains from 22 younger (age <42 years) and 22

65 d cellular composition of the hippocampus in postmortem brains from 30 patients with DSM-IV-diagnosed

66 uronal and glial somal size were analyzed in postmortem brains from 9 patients with schizophrenia, 10

67 Sulfhydration of AKT was detected in the postmortem brains from AD patients; thus, it represents

68 ents were carried out on coronal sections of postmortem brains from Alzheimer's disease patients and

69 and GAL peptide by RIA of the GAL system in postmortem brains from depressed persons who had committ

70 genome-wide circRNA expression profiling in postmortem brains from individuals with ASD and controls

71 nical, genomic, and neuroimaging data, and 6 postmortem brains from neurotypical individuals in the A

72 Studies on postmortem brains from Parkinson's patients reveal eleva

73 Western blot protein expression analysis in postmortem brains from patients diagnosed with schizophr

74 stochemistry to compare RTP801 expression in postmortem brains from PD and control patients.

75 ssion of GluN2C subunit has been reported in postmortem brains from schizophrenia patients.

76 In postmortem brains from Veterans/military Servicemembers

77 In rapidly acquired postmortem brains from women with AD, we found greatly r

78 pH has been shown to have a large effect on postmortem brain gene expression patterns.

79 need for age stratification in schizophrenia postmortem brain gene expression studies.

80 al models of PTSD, and review the human PTSD postmortem brain gene profiling studies performed to dat

81 molecules in isolated neuronal nuclei from a postmortem brain, generating 3227 sets of single-neuron

82 ial candidate gene expression studies of the postmortem brain have evolved into genome wide profiling

83 Transcriptomic analyses of postmortem brains have begun to elucidate molecular abno

84 In an in vitro binding assay using postmortem brain homogenates of Alzheimer's patients and

85 schizophrenia by convergent data from human postmortem, brain imaging, RNA-sequencing, and genome-wi

86 on control and severe AD samples from human postmortem brain in a single experimental run with a sin

87 To circumvent the limitations of using postmortem brain in molecular assays, we used avidin-bio

88 of BDNF and/or trk B isoforms was altered in postmortem brain in subjects who commit suicide (hereaft

89 s of reduced expression of BDNF and trk B in postmortem brain in suicide subjects suggest that these

90 bridization studies of torsinA mRNA in human postmortem brain in which a more limited distribution wa

91 unique challenges associated with studies of postmortem brain, including limited sample sizes and var

92 nalyzed, blind, an entirely new cohort of 60 postmortem brains, including equal numbers of patients m

93 tical layer-specific protein levels in human postmortem brain is highly desirable.

94 Analysis of human postmortem brain lysates by SDS-PAGE and Western blot re

95 cal MRI n = 4180) along with high-resolution postmortem brain microarray data from Allen Brain Atlas

96 Furthermore, we show that postmortem brain mitochondria retain their DeltaPsi(mem)

97 Extensive research of AD postmortem brains, mouse and fly models, including tripl

98 In 3 collections of human postmortem brain (n = 206) and 1 collection of blood sam

99 ctural and ultrastructural study in complete postmortem brains (n = 7) and in postmortem (n = 42) and

100 Using postmortem brain neuritic plaque density data as a truth

101 rgic system, drawing upon studies from human postmortem brain, neuroimaging, and drug challenge inves

102 ed [3H]BTA-1 binding to crude homogenates of postmortem brain obtained from nine Alzheimer's disease

103 were examined in Brodmann's areas 8 and 9 of postmortem brains obtained from 18 teenage suicide subje

104 termined in the anterior cingulate cortex of postmortem brains obtained from controls and from patien

105 ive paired helical filaments (PHFs) from the postmortem brain of a patient with Alzheimer's disease,

106 e in both models of depression as well as in postmortem brain of depressed individuals.

107 II+III, in congruency to data obtained from postmortem brain of HD patients and from toxin models.

108 In the postmortem brain of individuals with AD, astrocytic GABA

109 ined in medial temporal lobe sections in the postmortem brain of patients who experienced an episode

110 vely correlated with pCREB expression in the postmortem brain of persons with AD.

111 Levels of KYNA are elevated in CSF and the postmortem brain of schizophrenia patients, and these el

112 gh the activation of CREB are altered in the postmortem brain of subjects who commit suicide (hereaft

113 on and functional characteristics of CREB in postmortem brain of suicide subjects suggest that CREB m

114 latory activities of protein kinase A in the postmortem brain of suicide victims.

115 f fornix was removed from each hemisphere of postmortem brains of 16 male and 13 female schizophrenic

116 s (MSNs) in the striatum was assessed in the postmortem brains of 5 TS subjects as compared with norm

117 By injecting pathological tau extracted from postmortem brains of AD (AD-tau), progressive supranucle

118 d its expression and activity are reduced in postmortem brains of AD patients.

119 receptor subtypes have been observed in the postmortem brains of adult suicide victims; however, the

120 S-100 beta is increased in the postmortem brains of both DS and Alzheimer's disease.

121 evidence for similar mechanisms occurring in postmortem brains of depressed humans.

122 exhibits disturbed circadian rhythms in the postmortem brains of depressed patients.

123 Ns and pyramidal neurons in layer V of FI in postmortem brains of four young patients with autism and

124 e ratio proBDNF/mature BDNF was confirmed in postmortem brains of HIV-positive subjects cognitively i

125 Here, we show that cell membranes from the postmortem brains of humans that suffered Alzheimer's di

126 We evaluated the abundance of PC mRNAs in postmortem brains of individuals exhibiting HIV-associat

127 ntal cortex and superior temporal gyrus from postmortem brains of individuals with and without schizo

128 PV expression have been observed in both the postmortem brains of individuals with ASD and in animal

129 Postmortem brains of mild cognitive impairment (MCI) rat

130 Postmortem brains of neonatal brain injury were investig

131 trocytes was found to be a common feature in postmortem brains of neonatal brain injury.

132 enveloping NA-containing neuritic plaques in postmortem brains of patients with AD.

133 aring white matter of the corpus callosum in postmortem brains of patients with multiple sclerosis, u

134 nt study, we first reevaluated the pH of the postmortem brains of patients with schizophrenia and bip

135 zheimer's disease-like neuropathology in the postmortem brains of patients with schizophrenia, normal

136 protein levels are substantially reduced in postmortem brains of patients with schizophrenia.

137 hether the molecular epigenetic signature of postmortem brains of patients with SZ, SZA, and BP disor

138 molecular changes similar to changes seen in postmortem brains of patients with SZ.

139 ls of tumor necrosis factor (TNF) in CSF and postmortem brains of PD patients and animal models of PD

140 ed alterations found in PD animal models and postmortem brains of PD patients.

141 were co-localized in Lewy bodies (LB) in the postmortem brains of PD patients.

142 ased expression of inflammatory mediators in postmortem brains of people with Alzheimer disease has b

143 nosine (A-to-I) editing in a large cohort of postmortem brains of people with ASD.

144 re in several ways similar to those found in postmortem brains of psychotic patients.

145 ective cognate proteins is down-regulated in postmortem brains of schizophrenia and bipolar disorder

146 kt-473) has been observed in lymphocytes and postmortem brains of schizophrenia patients, and psychos

147 al targeting; and its levels are elevated in postmortem brains of schizophrenics.

148 creased mitochondrial calcium uptake, and in postmortem brains of sporadic PD/PDD patients of both se

149 expressed levels of the PLC beta1 isozyme in postmortem brains of suicide subjects may have clinical

150 Altered 5-HT2CR editing has been reported in postmortem brains of suicide victims.

151 n expression of PLC isozymes are abnormal in postmortem brains of teenage suicide subjects.

152 -HT(2A) receptor subtypes are altered in the postmortem brains of teenage suicide victims.

153 In addition, postmortem brains or spinal cords from 22 cases with or

154 In a different set of postmortem brains, p11 mRNA expression was measured in d

155 In the present study, we show that postmortem brain pH is similar across different brain re

156 lyze publicly available expression data from postmortem brain regions across humans, chimpanzees, and

157 ated data from deep RNA-seq and GWAS of four postmortem brain regions from 30 subjects with AUD and 3

158 S mouse model DEGs with human idiopathic ASD postmortem brain RNA-sequencing data and found significa

159 firmed in further ADLD-1-TO tissues and in a postmortem brain sample, where lamin B1 was increased in

160 levels, and microglia activation in the same postmortem brain sample.

161 Postmortem brain samples came from 32 subjects including

162 applied to RNA-Seq data collected from human postmortem brain samples collected within the ROS/MAP an

163 the 5 dopamine receptors were quantified in postmortem brain samples from 16 schizophrenic patients

164 Postmortem brain samples from 220 individuals were genot

165 Postmortem brain samples from 9 cases of MSA were fracti

166 ase, catalase, and glutathione peroxidase in postmortem brain samples from 9 patients with sporadic a

167 subtypes are also differentially altered in postmortem brain samples from Alzheimer disease cases.

168 authors also studied beta2*-nAChR binding in postmortem brain samples from depressed subjects.

169 te into neurons there, we decided to examine postmortem brain samples from females who had received b

170 In postmortem brain samples from human alcoholics we found

171 METHOD: Postmortem brain samples from human subjects (N=78) and

172 f reduction of nuclear Dnmt1 levels in human postmortem brain samples from PD and DLB patients as wel

173 cortical p11 protein levels were assessed in postmortem brain samples from PD patients and matched co

174 We combined RNA-seq data from 537 postmortem brain samples from the CommonMind Consortium

175 ross 364 schizophrenia cases and 383 control postmortem brain samples from the CommonMind Consortium,

176 egation analysis and Southern blotting using postmortem brain samples from two affected individuals a

177 assays, and quantitative tau measurements in postmortem brain samples from two progressive supranucle

178 We compiled data from 1408 postmortem brain samples in 3 collections to identify se

179 ping in chromatin extracted from hundreds of postmortem brain samples in cell-type-specific manner.

180 quencing, and identified DMPs were tested in postmortem brain samples obtained from patients with maj

181 drial MEF2D and ND6 levels were decreased in postmortem brain samples of patients with PD compared wi

182 -6 were significantly increased in blood and postmortem brain samples of patients with suicidality co

183 ne levels in blood, cerebrospinal fluid, and postmortem brain samples of patients with suicidality.

184 h the origin of this contrast, MRI data from postmortem brain samples were compared with electron mic

185 determined with and without nalbuphine, and postmortem brain samples were subjected to Western blot

186 The mRNA and protein levels in postmortem brain samples, genetic association with schiz

187 her transcriptional levels of PCDH17 mRNA in postmortem brain samples, which is consistent with incre

188 cortex, and primary visual cortex) in human postmortem brain samples.

189 (MAP) kinase pathway in schizophrenics using postmortem brain samples.

190 es have shown evidence of inflammation in BD postmortem brain samples.

191 Application of this antibody in postmortem brain sections indicated the presence of casp

192 Autoradiography studies of postmortem brain sections of a patient with Down's syndr

193 Autoradiography of postmortem brain sections of human Alzheimer's disease p

194 nt labeling of Abeta plaques in the brain of postmortem brain sections of patients with confirmed AD.

195 Immunohistochemical studies of postmortem brain sections revealed decreased staining by

196 ns of the entorhinal cortex were examined in postmortem brain specimens from 10 schizophrenic subject

197 , and glutamic acid decarboxylase (GAD67) in postmortem brain specimens from 15 pairs of subjects wit

198 upracallosal anterior cingulate cortex in 60 postmortem brain specimens from 4 groups of 15 subjects,

199 Postmortem brain specimens from 9 schizophrenic patients

200 A total of 200 postmortem brain specimens were studied, including 65 fr

201 linergic function and cholinergic markers in postmortem brain specimens.

202 , in the defined pathological areas of human postmortem brains, starting from early stages of AD (Bra

203 Earlier platelet and postmortem brain studies have found alterations in serot

204 Evidence from postmortem brain studies have indicated that early prena

205 Postmortem brain studies have shown that HDAC1-a lysine

206 reveal autism-specific signatures similar to postmortem brain studies, indicating a potential common

207 ere are significant challenges with studying postmortem brain, such as the postmortem interval, it co

208 In postmortem brain, T allele carriers had greater expressi

209 greater than that observed in rats in which postmortem brain temperature was not maintained.

210 We identify genetic variants within the postmortem brains that map to the CPG2 promoter region,

211 Human postmortem brain tissue and fibroblasts from subjects wi

212 We first analyzed human postmortem brain tissue and found robust up-regulation o

213 Immunohistochemical studies on postmortem brain tissue confirmed the presence of transg

214 Increased PK11195 binding in vivo and in postmortem brain tissue correlated with abundance of mac

215 ease in human-specific L1 DNA copy number in postmortem brain tissue derived from ataxia telangiectas

216 zed in the lumen of postcapillary venules in postmortem brain tissue derived from cases of HIV-1-asso

217 We evaluated postmortem brain tissue for adaptive immune cells and im

218 Loss of M1R has been found in postmortem brain tissue for several neuropsychiatric dis

219 d DNA methylation (DNAm) in a pilot study of postmortem brain tissue from 19 autism cases and 21 unre

220 ide (CNPS) in the pathogenesis of human CME, postmortem brain tissue from 21 patients with CME (13 AI

221 Postmortem brain tissue from 22 patients with MS (age 27

222 lum of experimental MSUD animals, as well as postmortem brain tissue from a child that died of leucin

223 ssed this region in an independent sample of postmortem brain tissue from affected individuals and co

224 ssion in Alexander disease model mice and in postmortem brain tissue from Alexander disease patients,

225 rotein levels are significantly decreased in postmortem brain tissue from BD patients, as compared to

226 ssed in demyelinated white matter lesions of postmortem brain tissue from human subjects with multipl

227 Rare postmortem brain tissue from individuals with 22q11.2DS

228 sence of published confirmation, we obtained postmortem brain tissue from late-onset Alzheimer's dise

229 torhinal cortex and hippocampal formation of postmortem brain tissue from normal human subjects and f

230 tamen, globus pallidus and cerebellum in the postmortem brain tissue from one patient compared to thr

231 n a mouse alpha-synucleinopathy model and in postmortem brain tissue from patients with alpha-synucle

232 ino-terminal fragments of Htt in extracts of postmortem brain tissue from patients with Huntington di

233 , SV2C expression is dramatically altered in postmortem brain tissue from PD cases but not in Alzheim

234 [(125)I]SIL23 binds alpha-syn fibrils in postmortem brain tissue from PD patients as well as an a

235 This linkage was also observed in postmortem brain tissue from subjects with mild cognitiv

236 ies in iPSC models, knock-in mice, and human postmortem brain tissue have demonstrated that APOE4 exp

237 Assays of human postmortem brain tissue have revealed that smokers have

238 w adenylyl cyclase activity in platelets and postmortem brain tissue of depressed individuals.

239 in cyclic gene expression in six regions of postmortem brain tissue of depressed patients matched wi

240 yelitis murine model of demyelination and in postmortem brain tissue of patients with AD.

241 d its downstream targets are reduced both in postmortem brain tissue of patients with Alzheimer's dis

242 on has been reported to be attenuated in the postmortem brain tissue of patients with schizophrenia.

243 c neurons of the PD animal models as well as postmortem brain tissue of PD patients, and is responsib

244 ate glycerophosphocholine have been found in postmortem brain tissue of persons with Alzheimer's dise

245 resolution mapping of epigenetic markings in postmortem brain tissue or neural cultures derived from

246 Postmortem brain tissue revealed classic loss of midbrai

247 is of RNA-sequencing data performed in human postmortem brain tissue revealed MYRACL to be among the

248 Postmortem brain tissue samples from AD patients, transg

249 and UBL post-translational modifications in postmortem brain tissue samples from persons with schizo

250 Studies of postmortem brain tissue showed that the changes in overf

251 Postmortem brain tissue specimens were collected from in

252 microdialysis, and neurochemical measures of postmortem brain tissue to investigate the effects of ag

253 of alpha7 mRNA and receptor protein in human postmortem brain tissue was examined by in situ hybridiz

254 Additionally, neurogranin expression in postmortem brain tissue was studied.

255 cleus (CN) and accumbens nucleus (NAC)) from postmortem brain tissue were compared between 6 OCD and

256 case-control genetic association analysis of postmortem brain tissue, genotype CC (rs2234693) and hap

257 With the use of postmortem brain tissue, mouse models of defeat stress,

258 We hypothesized that in postmortem brain tissue, OXTR binding in the hippocampal

259 within individual cortical layers from human postmortem brain tissue, providing a powerful tool in th

260 isition and characterization of high-quality postmortem brain tissue, RNA extraction, and preparation

261 monoacylglycerol lipase (MAGL) expression in postmortem brain tissue, such that regions with higher M

262 Using spectrophotometric assays in postmortem brain tissue, we found evidence of impaired o

263 studies of MDD employed bulk homogenates of postmortem brain tissue, which obscures gene expression

264 pairment (MCI), and dementia stages of AD in postmortem brain tissue.

265 nding site expression in bipolar disorder in postmortem brain tissue.

266 rological disorders often involve the use of postmortem brain tissue.

267 publicly available RNA expression data from postmortem brain tissue.

268 ied in ALS and frontotemporal dementia (FTD) postmortem brain tissue.

269 alleles and higher C4A transcript levels in postmortem brain tissue.

270 s with pathological diagnosis of AD in human postmortem brain tissue.

271 and controls from both blood (N = 1132) and postmortem brain tissues (N = 61 samples from Brodmann A

272 Biochemical examination of PD postmortem brain tissues also suggested deregulated mTOR

273 nding the pathophysiology of the illness, as postmortem brain tissues collected from individuals with

274 Using postmortem brain tissues from an INCL patient and tissue

275 Using human postmortem brain tissues from both lentivirus-infected e

276 onstructed gene-regulatory networks in 1,647 postmortem brain tissues from LOAD patients and nondemen

277 critical for mitochondrial fragmentation, in postmortem brain tissues from patients with AD and brain

278 We examined postmortem brain tissues from patients with sporadic dee

279 Postmortem brain tissues from subjects with schizophreni

280 LRP4 was reduced in postmortem brain tissues of AD patients.

281 nt huntingtin inhibits Sp1 binding to DNA in postmortem brain tissues of both presymptomatic and affe

282 mal and pathological specimens obtained from postmortem brain tissues of patients with multiple scler

283 littermates as well as in mitochondria from postmortem brain tissues of unaffected individuals and H

284 We also used mitochondria isolated from postmortem brain tissues of unaffected individuals and H

285 alable to non-human primate brains and human postmortem brain tissues, and can visualize neuronal pro

286 including schizophrenia, rely on the use of postmortem brain tissues, in which an understanding of t

287 By analyzing Lewy body pathology in the same postmortem brain tissues, we found that alpha-synuclein

288 s further corroborated with investigation of postmortem brain tissues.

289 eases in humans was gathered from studies in postmortem brain tissues.

290 xpression, splicing and protein abundance in postmortem brain tissues.

291 iption patterns and histological features of postmortem brain to fresh human neocortex isolated immed

292 Herein, we perform a meta-analysis of 8 PD postmortem brain transcriptome studies by employing a mu

293 Large-scale analysis of gene expression in postmortem brain using microarray technology has the pot

294 cortex and substantia nigra of control human postmortem brains, using the 454 GS FLX Titanium pyroseq

295 stem, a rodent depression model, and a human postmortem brain, we investigated the role of a brain-en

296 itative immunohistochemical methods in human postmortem brain, we sought to examine the relative cont

297 By comparative analysis in human postmortem brains, we found that ubiquitin immunoreactiv

298 ise measurements of frontal lobe volume from postmortem brains were derived by defining the posterior

299 Furthermore, qRT-PCR analysis of the AD postmortem brains with different Braak stages also showe

300 Postmortem brains with HIV-1 encephalitis exhibit increa