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1 ent contrasts in different tissue types of a post mortem brain.
2 f-principle NODDI estimates in a whole human post-mortem brain.
3 o define the tau PTM landscape present in AD post-mortem brain.
4 in protein changes similar to schizophrenia post-mortem brain.
5 confirmed by pathological analysis of their post mortem brains.
6 ronal vulnerability previously identified in post-mortem brains.
7 s have been detected in Huntington's disease post-mortem brains.
8 could be detected in patient cell lines and post-mortem brains.
9 iplexed immunofluorescence on HD and control post-mortem brains.
10 required to form the aggregates observed in post-mortem brains.
11 mation, demyelination and remyelination from post-mortem brains.
12 d 159 clinico-pathologically diagnosed human post-mortem brains (48 controls, 47 AD, 25 DLB, 20 mixed
13 hesis has gained indirect support from human post-mortem brain analyses and genetic studies, little i
17 been informed by both direct analysis of the post-mortem brain and by study of the biological consequ
18 pes predicted levels of NPY messenger RNA in post-mortem brain and lymphoblasts, and levels of plasma
21 athy in two distinct ALS mouse models and in post-mortem brain and spinal cord tissues of ALS patient
22 ve MS (PPMS) using a cross-tissue (blood and post-mortem brain) and multilayered data (genetic, epige
23 ogenic human induced pluripotent stem cells, post-mortem brain, and APOE targeted replacement mice.
24 single-cell transcriptomic analyses of human post-mortem brains are important for documentation of pa
27 and TRIM33 in the human prefrontal cortex of post-mortem brains between subjects with and those witho
29 se models as well as increased binding in HD post-mortem brains, compared to first generation ligands
36 ines and demonstrate its upregulation in the post-mortem brain from 15q11-13 duplication patients for
37 NMR) spectroscopy, we biochemically profiled post-mortem brain from mice that suffered mild TBI (N =
38 mately 50% in various cortical structures of post-mortem brain from patients diagnosed with schizophr
39 d protein are reduced in multiple regions of post-mortem brain from patients diagnosed with schizophr
40 ation of GFAP and AQP4 immunoreactivities in post-mortem brains from adult baboons with cerebral hypo
42 prefrontal cortex in an extensive series of post-mortem brains from fetal development through ageing
43 motor cortex, hippocampus and cerebellum of post-mortem brains from HD individuals, particularly in
44 ide microRNA (miRNA) expression profiling in post-mortem brains from individuals with ASD and control
45 eq and meRIP-seq in middle frontal cortex of post-mortem brains from individuals with or without AD,
46 tilize non-targeted mass spectrometry on 316 post-mortem brains from participants in the Religious Or
47 P2X(7)R protein levels increase in human AD post-mortem brain, in agreement with an upregulation of
49 scovery and proteomics approach by comparing post-mortem brain material from schizophrenia patients a
50 eocortical neuronal subtypes lost with AD in post-mortem brain middle temporal gyri from non-diseased
53 r from an independent (Oxford, UK) cohort of post-mortem brains (n = 74), we confirmed the significan
56 f Long COVID patients, have been detected in post-mortem brain of COVID patients, and exhibit neuroin
57 estigated large-scale gene expression in the post-mortem brain of MDD subjects paired with matched co
58 le of the immune system in a large sample of post-mortem brain of patients with schizophrenia: RNA se
62 cortical, limbic and subcortical areas, from post-mortem brains of familial Alzheimer's disease (n =
64 d-type PSEN1 allele expression is reduced in post-mortem brains of human EOfAD mutation carriers (and
65 ruitment and activation was also observed in post-mortem brains of humans that died after myocardial
66 r cingulate cortex and amygdala samples from post-mortem brains of individuals with BD and neurotypic
67 ast growth factor (FGF) system is altered in post-mortem brains of individuals with major depressive
70 occludin, in 12 brain regions dissected from post-mortem brains of normal ageing (n = 10), pathologic
71 gomers in brain lysates prepared from frozen post-mortem brains of normal, Alzheimer's disease and DL
73 erived sarkosyl-insoluble tau fractions from post-mortem brains of patients with progressive supranuc
74 clein mRNA and soluble protein in five human post-mortem brain regions from four groups of individual
75 ) to measure metabolites and metals in seven post-mortem brain regions of nine AD patients and nine c
77 pecific genes differentially expressed in HD post-mortem brains relative to controls using snRNAseq w
78 Analysis of three independent data sets of post-mortem brains revealed signs of increased methylati
79 ay approach for gene expression profiling in post mortem brain samples from patients with cirrhosis w
80 time-dependent changes in gene expression in post mortem brain samples is critical for the interpreta
81 sequencing data from male Grade 1 HD patient post-mortem brain samples and male zQ175 and R6/2 mouse
83 We analyzed MSUT2 protein in age-matched post-mortem brain samples from AD patients and observe a
85 compared DSCR1 (Adapt78) mRNA expression in post-mortem brain samples from Alzheimer's disease patie
87 ed these to a series of fibroblast lines and post-mortem brain samples from individuals with either a
88 tant HTT and its oligomeric intermediates in post-mortem brain samples from patients with Huntington'
89 APT H1/H2 haplotypes on tau transcription in post-mortem brain samples from patients with Lewy body d
90 from the anterior cingulate cortex in human post-mortem brain samples from patients with PD and heal
91 pression of chosen nuclear import factors in post-mortem brain samples from patients with TDP-43 posi
94 Over the past 25 years, studies analyzing post-mortem brain samples have found evidence of aberran
95 omplexes of Abeta and COX-2 were detected in post-mortem brain samples in greater amounts in AD tissu
97 nular osmiophilic material in skin biopsy or post-mortem brain samples of affected members in the Swe
98 By analyzing gene expression data in human post-mortem brain samples, from the prenatal period to l
99 e-wide DNA methylation was quantified in 262 post-mortem brain samples, representing tissue from four
100 anoids from dup15q patient-derived iPSCs and post-mortem brain samples, we identify increased glycoly
108 We applied our approach to RNA-seq data of post-mortem brains that compared the Alcohol Use Disorde
112 oups, though, as with any method for imaging post mortem brain tissue, care should be taken when inte
115 ble protein aggregates in vitro and in human post-mortem brain tissue but the cellular dynamics of th
117 of OXD-2115 were synthesized and screened in post-mortem brain tissue for tau affinity against [(3)H]
118 expression of TSPO was further described in post-mortem brain tissue from 20 cases with secondary pr
119 mmunohistochemical analysis was performed on post-mortem brain tissue from 26 cases with primary prog
120 rs PI2620, RO948, MK6240 and JNJ067 in human post-mortem brain tissue from a cohort of 25 dementia ca
121 at function in sound source localization, in post-mortem brain tissue from autistic individuals.
123 f alpha-synuclein with PSEN1 was detected in post-mortem brain tissue from cognitively normal cases a
124 vidence from cerebrospinal fluid samples and post-mortem brain tissue from individuals with multiple
125 ped with an up-regulated gene set from human post-mortem brain tissue from individuals with schizophr
128 r improved MX-Raman methodology, we utilized post-mortem brain tissue from several neurodegenerative
130 Tof-MS) and chemometrics for the analysis of post-mortem brain tissue from subjects with Alzheimer's
131 d 407 individuals with an antemortem MRI and post-mortem brain tissue from the Mayo Clinic Alzheimer'
135 ningeal IgA(+), IgM(+) and IgG(+) B cells in post-mortem brain tissue of 20 MS patients and 6 control
136 ies revealed increased levels of sortilin in post-mortem brain tissue of AD patients and that overexp
137 ongitudinal retrospective study, we analysed post-mortem brain tissue of all individuals with an Alzh
138 More TGF-beta1 messenger RNA was present in post-mortem brain tissue of Alzheimer's patients than in
140 recognized intracellular inclusions in human post-mortem brain tissue of Lewy body disease cases, but
142 ans and ruminants relies on the detection in post-mortem brain tissue of the protease-resistant form
143 CT), positron emission tomography (PET), and post-mortem brain tissue RNA analysis or pathological an
145 roteomics and metabolomics were performed on post-mortem brain tissue to identify potential pathways
147 ously been employed to biochemically profile post-mortem brain tissue, and the novel methods describe
148 values with normative gene expressions from post-mortem brain tissue, we constructed a grade-related
156 we conducted whole transcriptome analysis of post-mortem brain tissues (cingulate cortex) from SCZ, B
157 nd fluorescent LMTK2 immunohistochemistry on post-mortem brain tissues and compared them to age-match
160 roblasts, induced pluripotent stem cells and post-mortem brain tissues from six controls and six pati
161 ng to pathologic alpha-syn aggregates in MSA post-mortem brain tissues was significantly higher than
165 integrate SVs with RNA-sequencing from human post-mortem brains to quantify their dosage and regulato
166 lood methylomic data and post-disease onset (post-mortem) brain transcriptional data, we have identif
168 distribution of neurofibrillary pathology in post-mortem brains was used to classify SPET scans taken
169 d in vitro model of the BBB and T2DM patient post-mortem brains, we show the translatable applicabili