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1 evated Rrs1 mRNA in HD compared with control postmortem brain.
2 ure models, HD transgenic mice, and human HD postmortem brain.
3 requires the detection of amyloid plaques in postmortem brain.
4 expression of the DYT1 gene in normal human postmortem brain.
5 ed with lower D2 short isoform expression in postmortem brain.
6 the neuronal and nonneuronal nuclei from the postmortem brain.
7 predicted increases in amyloid pathology in postmortem brain.
8 (CGI) that is highly methylated in the human postmortem brain.
9 d Western blots to study native htt in human postmortem brain.
10 ates from biological samples including human postmortem brains.
11 tor subunit 1 (GABAB1) splicing in alcoholic postmortem brains.
12 r RNA (mRNA) in a relatively small sample of postmortem brains.
13 that has historically only been conducted on postmortem brains.
14 cortical interneurons of schizophrenia (SZ) postmortem brains (10), suggesting that the availability
15 ing data with the standard of truth based on postmortem brain amyloid status for subjects in the auto
18 dynein heavy chain with the plaques in human postmortem brain and in a double transgenic AD mouse mod
20 , and cAMP was significantly decreased in HD postmortem brain and lymphoblastoid cells, attesting to
21 mulation of cytoplasmic TDP-43 aggregates in postmortem brain and spinal cord (SC), it has been sugge
22 has been highlighted by their presence in HD postmortem brains and by the fact that nuclear inclusion
23 from each of 8 schizophrenic and 11 control postmortem brains and immunohistochemistry for the phosp
24 been demonstrated in the substantia nigra of postmortem brains and several peripheral tissues obtaine
26 orrelated with RNA polymerase II activity in postmortem brain, and pharmacologic modulation of RNA po
27 escribed for dopaminergic markers in CSF and postmortem brain, and there exists a range of affective,
30 diseases are diagnosed definitively only in postmortem brains by the presence of key misfolded and a
31 ndria hours after death indicates that human postmortem brains can be an abundant source of viable mi
32 strate that overrepresented IgG sequences in postmortem brains can be used to produce functional reco
33 ng neurotransmitter receptors from the human postmortem brain, can be transplanted to frog oocytes, a
34 is review, we describe key findings in human postmortem brains, cultured cells, and animal models of
35 is to gene expression data from high-quality postmortem brains, examining 24-h cyclic patterns in six
38 ne genes and microglial transcripts occur in postmortem brain from alcoholics and animals exposed to
39 ved decreased synaptosomal F-actin levels in postmortem brain from mild cognitive impairment and AD p
40 mately 50% in various cortical structures of postmortem brain from patients diagnosed with schizophre
41 he total volume and neuron number of BA17 in postmortem brains from 10 subjects with schizophrenia an
42 CpG loci) in the orbital frontal cortices of postmortem brains from 22 younger (age <42 years) and 22
43 d cellular composition of the hippocampus in postmortem brains from 30 patients with DSM-IV-diagnosed
44 uronal and glial somal size were analyzed in postmortem brains from 9 patients with schizophrenia, 10
45 ents were carried out on coronal sections of postmortem brains from Alzheimer's disease patients and
46 and GAL peptide by RIA of the GAL system in postmortem brains from depressed persons who had committ
48 Western blot protein expression analysis in postmortem brains from patients diagnosed with schizophr
53 al models of PTSD, and review the human PTSD postmortem brain gene profiling studies performed to dat
54 molecules in isolated neuronal nuclei from a postmortem brain, generating 3227 sets of single-neuron
56 on control and severe AD samples from human postmortem brain in a single experimental run with a sin
58 of BDNF and/or trk B isoforms was altered in postmortem brain in subjects who commit suicide (hereaft
59 s of reduced expression of BDNF and trk B in postmortem brain in suicide subjects suggest that these
60 bridization studies of torsinA mRNA in human postmortem brain in which a more limited distribution wa
61 unique challenges associated with studies of postmortem brain, including limited sample sizes and var
62 nalyzed, blind, an entirely new cohort of 60 postmortem brains, including equal numbers of patients m
66 ctural and ultrastructural study in complete postmortem brains (n = 7) and in postmortem (n = 42) and
68 ed [3H]BTA-1 binding to crude homogenates of postmortem brain obtained from nine Alzheimer's disease
69 were examined in Brodmann's areas 8 and 9 of postmortem brains obtained from 18 teenage suicide subje
70 termined in the anterior cingulate cortex of postmortem brains obtained from controls and from patien
71 II+III, in congruency to data obtained from postmortem brain of HD patients and from toxin models.
73 ined in medial temporal lobe sections in the postmortem brain of patients who experienced an episode
75 Levels of KYNA are elevated in CSF and the postmortem brain of schizophrenia patients, and these el
76 gh the activation of CREB are altered in the postmortem brain of subjects who commit suicide (hereaft
77 on and functional characteristics of CREB in postmortem brain of suicide subjects suggest that CREB m
79 f fornix was removed from each hemisphere of postmortem brains of 16 male and 13 female schizophrenic
80 s (MSNs) in the striatum was assessed in the postmortem brains of 5 TS subjects as compared with norm
81 By injecting pathological tau extracted from postmortem brains of AD (AD-tau), progressive supranucle
83 receptor subtypes have been observed in the postmortem brains of adult suicide victims; however, the
86 Ns and pyramidal neurons in layer V of FI in postmortem brains of four young patients with autism and
87 e ratio proBDNF/mature BDNF was confirmed in postmortem brains of HIV-positive subjects cognitively i
88 Here, we show that cell membranes from the postmortem brains of humans that suffered Alzheimer's di
89 We evaluated the abundance of PC mRNAs in postmortem brains of individuals exhibiting HIV-associat
92 aring white matter of the corpus callosum in postmortem brains of patients with multiple sclerosis, u
93 nt study, we first reevaluated the pH of the postmortem brains of patients with schizophrenia and bip
94 zheimer's disease-like neuropathology in the postmortem brains of patients with schizophrenia, normal
97 ls of tumor necrosis factor (TNF) in CSF and postmortem brains of PD patients and animal models of PD
100 ased expression of inflammatory mediators in postmortem brains of people with Alzheimer disease has b
102 ective cognate proteins is down-regulated in postmortem brains of schizophrenia and bipolar disorder
103 kt-473) has been observed in lymphocytes and postmortem brains of schizophrenia patients, and psychos
105 creased mitochondrial calcium uptake, and in postmortem brains of sporadic PD/PDD patients of both se
106 expressed levels of the PLC beta1 isozyme in postmortem brains of suicide subjects may have clinical
113 firmed in further ADLD-1-TO tissues and in a postmortem brain sample, where lamin B1 was increased in
115 the 5 dopamine receptors were quantified in postmortem brain samples from 16 schizophrenic patients
118 ase, catalase, and glutathione peroxidase in postmortem brain samples from 9 patients with sporadic a
119 subtypes are also differentially altered in postmortem brain samples from Alzheimer disease cases.
121 te into neurons there, we decided to examine postmortem brain samples from females who had received b
124 f reduction of nuclear Dnmt1 levels in human postmortem brain samples from PD and DLB patients as wel
125 cortical p11 protein levels were assessed in postmortem brain samples from PD patients and matched co
126 assays, and quantitative tau measurements in postmortem brain samples from two progressive supranucle
127 ping in chromatin extracted from hundreds of postmortem brain samples in cell-type-specific manner.
128 quencing, and identified DMPs were tested in postmortem brain samples obtained from patients with maj
129 drial MEF2D and ND6 levels were decreased in postmortem brain samples of patients with PD compared wi
130 -6 were significantly increased in blood and postmortem brain samples of patients with suicidality co
131 ne levels in blood, cerebrospinal fluid, and postmortem brain samples of patients with suicidality.
132 h the origin of this contrast, MRI data from postmortem brain samples were compared with electron mic
133 determined with and without nalbuphine, and postmortem brain samples were subjected to Western blot
135 her transcriptional levels of PCDH17 mRNA in postmortem brain samples, which is consistent with incre
140 nt labeling of Abeta plaques in the brain of postmortem brain sections of patients with confirmed AD.
142 ns of the entorhinal cortex were examined in postmortem brain specimens from 10 schizophrenic subject
143 , and glutamic acid decarboxylase (GAD67) in postmortem brain specimens from 15 pairs of subjects wit
144 upracallosal anterior cingulate cortex in 60 postmortem brain specimens from 4 groups of 15 subjects,
147 , in the defined pathological areas of human postmortem brains, starting from early stages of AD (Bra
150 ere are significant challenges with studying postmortem brain, such as the postmortem interval, it co
155 Increased PK11195 binding in vivo and in postmortem brain tissue correlated with abundance of mac
156 ease in human-specific L1 DNA copy number in postmortem brain tissue derived from ataxia telangiectas
157 zed in the lumen of postcapillary venules in postmortem brain tissue derived from cases of HIV-1-asso
159 d DNA methylation (DNAm) in a pilot study of postmortem brain tissue from 19 autism cases and 21 unre
160 ide (CNPS) in the pathogenesis of human CME, postmortem brain tissue from 21 patients with CME (13 AI
162 lum of experimental MSUD animals, as well as postmortem brain tissue from a child that died of leucin
163 ssed this region in an independent sample of postmortem brain tissue from affected individuals and co
164 ssion in Alexander disease model mice and in postmortem brain tissue from Alexander disease patients,
165 ssed in demyelinated white matter lesions of postmortem brain tissue from human subjects with multipl
167 sence of published confirmation, we obtained postmortem brain tissue from late-onset Alzheimer's dise
168 torhinal cortex and hippocampal formation of postmortem brain tissue from normal human subjects and f
169 tamen, globus pallidus and cerebellum in the postmortem brain tissue from one patient compared to thr
170 n a mouse alpha-synucleinopathy model and in postmortem brain tissue from patients with alpha-synucle
171 ino-terminal fragments of Htt in extracts of postmortem brain tissue from patients with Huntington di
172 , SV2C expression is dramatically altered in postmortem brain tissue from PD cases but not in Alzheim
173 [(125)I]SIL23 binds alpha-syn fibrils in postmortem brain tissue from PD patients as well as an a
177 in cyclic gene expression in six regions of postmortem brain tissue of depressed patients matched wi
178 d its downstream targets are reduced both in postmortem brain tissue of patients with Alzheimer's dis
179 on has been reported to be attenuated in the postmortem brain tissue of patients with schizophrenia.
180 c neurons of the PD animal models as well as postmortem brain tissue of PD patients, and is responsib
181 ate glycerophosphocholine have been found in postmortem brain tissue of persons with Alzheimer's dise
182 resolution mapping of epigenetic markings in postmortem brain tissue or neural cultures derived from
185 and UBL post-translational modifications in postmortem brain tissue samples from persons with schizo
188 microdialysis, and neurochemical measures of postmortem brain tissue to investigate the effects of ag
189 of alpha7 mRNA and receptor protein in human postmortem brain tissue was examined by in situ hybridiz
190 case-control genetic association analysis of postmortem brain tissue, genotype CC (rs2234693) and hap
192 isition and characterization of high-quality postmortem brain tissue, RNA extraction, and preparation
197 nding the pathophysiology of the illness, as postmortem brain tissues collected from individuals with
200 onstructed gene-regulatory networks in 1,647 postmortem brain tissues from LOAD patients and nondemen
201 critical for mitochondrial fragmentation, in postmortem brain tissues from patients with AD and brain
203 nt huntingtin inhibits Sp1 binding to DNA in postmortem brain tissues of both presymptomatic and affe
204 mal and pathological specimens obtained from postmortem brain tissues of patients with multiple scler
205 alable to non-human primate brains and human postmortem brain tissues, and can visualize neuronal pro
206 including schizophrenia, rely on the use of postmortem brain tissues, in which an understanding of t
209 Large-scale analysis of gene expression in postmortem brain using microarray technology has the pot
210 cortex and substantia nigra of control human postmortem brains, using the 454 GS FLX Titanium pyroseq
211 stem, a rodent depression model, and a human postmortem brain, we investigated the role of a brain-en
212 itative immunohistochemical methods in human postmortem brain, we sought to examine the relative cont
214 ise measurements of frontal lobe volume from postmortem brains were derived by defining the posterior
215 Furthermore, qRT-PCR analysis of the AD postmortem brains with different Braak stages also showe
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