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95 results for “Neuropathology”
Brain functional connectivity data in anesthetized participants and patients with neuropathological or psychiatric diagnoses
<p>Five fMRI datasets were collected from independent research sites including: propofol deep sedation (PDS; drug effect site concentration= ~2.4 μg/ml) in Dataset-1, propofol general anesthesia (PGA; drug effect site concentration= 4.0 μg/ml) in Dataset-2, ketamine anesthesia (KA) in Dataset-3, unresponsive wakefulness syndrome (UWS) in Dataset-4, and schizophrenia (SCHZ), bipolar disorder (BD), and attentional deficit hyperactivity disorder (ADHD) in Dataset-5. Following fMRI data preprocessing, the fMRI time courses were extracted from 400 cortical areas according to a well-established brain parcellation scheme (Schaefer's 400 ROIs). A connectivity matrix was then calculated using Pearson correlation resulting in a 400x400 connectivity matrix for each participant and each condition.</p>
Multiplexed and scalable cellular phenotyping toward the standardized three-dimensional human neuropathology
<p>The dataset for the publication. Cite the publication if you use the datasets.</p>
dataset related to article: " Cerebrospinal fluid neuropathological biomarkers in beta-propeller protein-associated neurodegeneration, with complicated parkinsonian phenotype"
<p>analysis sanger electropherograms in the patient's in .abi format and segregation in the family (mother; father and sister</p>
Humans share features of Alzheimer's neuropathology with other mammalian species
<p>Summary of relevant publications describing Aβ and tau neuropathology in carnivores collated into tables.</p> <p>Table 1. Alzheimer-like neuropathology in carnivore species. Occurrence of Aβ deposits in plaques in the brain and vessels (CAA) plaques and tauopathy (including NFTs and the earlier pTau) in select carnivore (Carnivora) species (primarily focusing on cats and dogs) compared to humans. The age of occurrence and prevalence of these pathologies is reported for each study.</p> <p>Supplementary Table 1 (S1). Occurrence and distribution of plaque and tangle types in carnivore species. Extended version of Table 1 to include the type of plaques, CAA (Aβ residues), and Tau pathology and their distribution across the cerebral cortex and other areas of the brain. </p> <p>For more information about the classification of mature versus early-stage plaques, see the 'Table legend and Key' tab in the extended table workbook (S1). </p> <p>Summary of the key findings from the data collated in Table 1 and S1: Dogs, but not cats, have Alzheimer-like mature senile plaques. Other felids (Felidae), such as cheetahs and Tsushima leopard cats, also do not have mature plaques, but other carnivore species, such as sea lions, did display this type of senile plaques. Cats have less cerebral amyloid angiopathy (CAA) in the meninges than dogs and humans. However, there were a higher number of observations of hyperphosphorylated tau in the cat studies we collated than in those studying dogs. Nonetheless, dogs and cats had a similar number of positive reports for neurofibrillary tangles (NFTs), and these were found to be at a lower prevalence than that in humans. </p> <p> </p> <p> </p>
miRNA counts identified by RNA seq in the caudate nucleus of patients neuropathologically diagnosed with late-onset Alzheimer's disease (non-carriers and carriers of intermediate expansions in the HTT gene) and healthy subjects.
<p>These data include the raw miRNA counts identified by RNA-seq in <em>post mortem</em> caudate nucleus samples. Samples with identifier <strong>A</strong> belong to patients with a neuropathological diagnosis of late-onset Alzheimer's disease. Group <strong>B</strong> samples belong to patients with the same neuropathological diagnosis, but carrying CAG expansions in the intermediate range (27-35 CAG) in the <em>HTT</em> gene. Finally, group <strong>C </strong>samples belong to healthy subjects without neuropathological diagnosis. </p> <p> </p>
Differential methylation analysis in neuropathological confirmed dementia with Lewy bodies
<p>Authors: Paolo Reho, Sara Saez-Atienzar, Sultana Solaiman, Zalak Shah, Ruth Chia, Karri Kaivola, Bryan J. Traynor, Bension S. Tilley, Steve M. Gentleman, Angela K. Hodges, Dag Aarsland, Edwin S. Monuki, Kathy L. Newell, Randy Woltjer, Marilyn S. Albert, Ted M. Dawson, Liana S. Rosenthal, Juan C. Troncoso, Olga Pletnikova, Geidy E. Serrano, Thomas G. Beach, Hariharan P. Easwaran, Sonja W. Scholz</p> <p>Epigenome-wide association study investigating epigenetic modulations in a cohort of neuropathologically confirmed dementia with Lewy bodies cases and neurologically healthy controls.</p>
Data-driven versus consensus diagnosis of MCI: enhanced sensitivity for detection of dementia progression, biomarker status, and neuropathological outcomes
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Nanostring mRNA expression profiling of P7 Arx(GCG)10+7 neonatal cortex using nCounter® mouse Neuropathology Plus Panel
<p>X-linked infantile spasms syndrome (ISSX) is a clinically devastating developmental epileptic encephalopathy with life-long impact. <em>Arx<sup>(GCG)10+7</sup></em>, a mouse model of the most common triplet-repeat expansion mutation of ARX, exhibits neonatal spasms, electrographic phenotypes and abnormal migration of GABAergic interneuron subtypes. Neonatal presymptomatic treatment with 17β-estradiol (E2) in <em>Arx<sup>(GCG)10+7</sup></em> reduces spasms and modifies progression of epilepsy. Cortical pathology during this period, a crucial point for clinical intervention in ISSX, has largely been unexplored, and the pathogenic cellular defects that are targeted by early interventions are unknown. In the first postnatal week, we identified a transient wave of elevated apoptosis in <em>Arx<sup>(GCG)10+7</sup></em> mouse cortex that is non-Arx cell autonomous, since mutant Arx-immunoreactive (Arx+) cells are not preferentially impacted by cell death. NeuN+ (also known as Rbfox3) survival was also not impacted, suggesting a vulnerable subpopulation in the immature <em>Arx<sup>(GCG)10+7</sup></em> cortex. Inflammatory processes during this period might explain this transient elevation in apoptosis; however, transcriptomic and immunohistochemical profiling of several markers of inflammation revealed no innate immune activation in <em>Arx<sup>(GCG)10+7</sup></em> cortex. Neither neonatal E2 hormone therapy, nor ACTH(1-24), the frontline clinical therapy for ISSX, diminished the augmented apoptosis in <em>Arx<sup>(GCG)10+7</sup></em>, but both rescued neocortical Arx+ cell density. Since early E2 treatment effectively prevents seizures in this model, enhanced apoptosis does not solely account for the seizure phenotype, but may contribute to other aberrant brain function in ISSX. However, since both hormone therapies, E2 and ACTH(1-24), elevate the density of cortical Arx+-interneurons, their early therapeutic role in other neurological disorders hallmarked by interneuronopathy should be explored.</p>
Associations of fully-automated CSF and novel plasma biomarkers with Alzheimer's disease neuropathology at autopsy
<p>The objective of this study was to study cerebrospinal fluid (CSF) biomarkers of Alzheimer's disease (AD) analyzed by fully automated Elecsys immunoassays in comparison to neuropathologic gold standards, and compare their accuracy to plasma phosphorylated tau (p-tau181) measured using a novel Simoa method. We studied <i>ante-mortem</i> Elecsys-derived CSF biomarkers in 45 individuals who underwent standardized <i>post-mortem</i> assessments of AD and non-AD neuropathologic changes at autopsy. In a subset of 26 participants, we also analysed <i>ante-mortem</i> levels of plasma p-tau181 and neurofilament light (NfL). Reference biomarker values were obtained from 146 amyloid-PET-negative healthy controls (HC). All CSF biomarkers clearly distinguished pathology-confirmed AD dementia (N=27) from HC (AUCs=0.86-1.00). CSF total-tau (t-tau), p-tau181, and their ratios with Aβ<sub>1-42</sub>, also accurately distinguished pathology-confirmed AD from non-AD dementia (N=8; AUCs=0.94-0.97). In pathology-specific analyses, intermediate-to-high Thal amyloid phases were best detected by CSF Aβ<sub>1-42</sub> (AUC[95% CI]=0.91[0.81-1]), while intermediate-to-high CERAD neuritic plaques and Braak tau stages were best detected by CSF p-tau181 (AUC=0.89[0.79-0.99] and 0.88[0.77-0.99], respectively). Optimal Elecsys biomarker cut-offs were derived at 1097/229/19 pg/ml for Aβ<sub>1-42</sub>, t-tau, and p-tau181. In the plasma subsample, both plasma p-tau181 (AUC=0.91[0.86-0.96]) and NfL (AUC=0.93[0.87-0.99]) accurately distinguished pathology-confirmed AD (N=14) from HC. However, only p-tau181 distinguished AD from non-AD dementia cases (N=4; AUC=0.96[0.88-1.00]), and showed a similar, though weaker, pathologic specificity for neuritic plaques (AUC=0.75[0.52-0.98]) and Braak stage (AUC=0.71[0.44-0.98]) as CSF p-tau181. Elecsys-derived CSF biomarkers detect AD neuropathologic changes with very high discriminative accuracy<i> in-vivo</i>. Preliminary findings support the use of plasma p-tau181 as an easily accessible and scalable biomarker of AD pathology. This study provides Class II evidence that fully-automated CSF t-tau and p-tau181measurements discriminate between autopsy-confirmed Alzheimer's disease and other dementias.</p>
Neuropathology of Spasmodic Dysphonia
ClinicalTrials.gov study NCT00118586. IPD Sharing: Not stated. Countries: 1. Publications: 3.
Neuropathological Changes of the Intestinal Wall in Patients With Bowel Evacuation Disorders
ClinicalTrials.gov study NCT05016700. IPD Sharing: YES. Countries: 1. Publications: 10.
Brain Tissue Collection for Neuropathological Studies
ClinicalTrials.gov study NCT00001260. IPD Sharing: Not stated. Countries: 1. Publications: 7.
Neuropathological features associated with basal forebrain atrophy in Alzheimer’s disease
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Nanostring mRNA expression profiling of P7 Arx(GCG)10+7 neonatal cortex using nCounter® mouse Neuropathology Plus Panel
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Associations of fully-automated CSF and novel plasma biomarkers with Alzheimer's disease neuropathology at autopsy
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Supplementary results for: Visit-to-visit blood pressure variability, neuropathology and cognitive function
<p><b>Objective</b> Large systolic blood pressure (SBP) variability has been proposed as a novel risk factor for dementia above and beyond SBP levels, but the underlying neuropathology is largely unknown. We investigated the relationship among visit-to-visit SBP variability, cognitive deterioration and underlying neuropathological changes.</p> <p><b>Methods </b>We used longitudinal data (between 2005 and 2019) from the National Alzheimer's Coordinating Center. 13,284 dementia-free participants aged≥50 years were followed over a median of 5.0 (interquartile range: 3.1-7.6) years. Neuropathology data were available in 1,400 autopsied participants. Visit-to-visit SBP variability was quantified from repeated annual SBP measurements. Cognitive deterioration was defined as conversion from normal cognition to mild cognitive impairment (MCI) or dementia, or from MCI to dementia.</p> <p><b>Results</b> Larger visit-to-visit SBP variability was associated with cognitive deterioration (adjusted odds ratio comparing extreme quintiles: 2.64; 95%CI:2.29-3.04, P <0.001). It was also associated with a higher burden of vascular pathology (including microinfarcts, white matter lesion, atherosclerosis of the circle of Willis and arteriolosclerosis) and with neurofibrillary tangle pathology assessed by Braak staging (All P < 0.05). The association with cognitive deterioration and vascular pathology appeared stronger among those with normal cognition versus MCI at baseline. These findings were observed after adjusting for age, sex, mean SBP and other confounding variables. Similar results were observed for diastolic BP variability.</p> <p><b>Conclusion </b>Larger visit-to-visit SBP variability was associated with cognitive deterioration. It was also associated with cerebrovascular pathology and neurofibrillary tangles. These results suggest the intertwined role of vascular and Alzheimer's disease pathology in the etiology of dementia.</p>
Data from: Gene-wise association of variants in four lysosomal storage disorder genes in neuropathologically confirmed Lewy Body disease
Objective: Variants in GBA are associated with Lewy Body (LB) pathology. We investigated whether variants in other lysosomal storage disorder (LSD) genes also contribute to disease pathogenesis. Methods: We performed a genetic analysis of four LSD genes including GBA, HEXA, SMPD1, and MCOLN1 in 231 brain autopsies. Brain autopsies included neuropathologically defined LBD without Alzheimer Disease (AD) changes (n = 59), AD without significant LB pathology (n = 71), Alzheimer disease and lewy body variant (ADLBV) (n = 68), and control brains without LB or AD neuropathology (n = 33). Sequencing of HEXA, SMPD1, MCOLN1 and GBA followed by 'gene wise' genetic association analysis was performed. To determine the functional effect, a biochemical analysis of GBA in a subset of brains was also performed. GCase activity was measured in a subset of brain samples (n = 64) that included LBD brains, with or without GBA mutations, and control brains. A lipidomic analysis was also performed in brain autopsies (n = 67) which included LBD (n = 34), ADLBV (n = 3), AD (n = 4), PD (n = 9) and control brains (n = 17), comparing GBA mutation carriers to non-carriers. Results: In a 'gene-wise' analysis, variants in GBA, SMPD1 and MCOLN1 were significantly associated with LB pathology (p range: 0.03–4.14 x10-5). Overall, the mean levels of GCase activity were significantly lower in GBA mutation carriers compared to non-carriers (p<0.001). A significant increase and accumulation of several species for the lipid classes, ceramides and sphingolipids, was observed in LBD brains carrying GBA mutations compared to controls (p range: p<0.05-p<0.01). Interpretation: Our study indicates that variants in GBA, SMPD1 and MCOLN1 are associated with LB pathology. Biochemical data comparing GBA mutation carrier to non-carriers support these findings, which have important implications for biomarker development and therapeutic strategies.
Data from: Gene-wise association of variants in four lysosomal storage disorder genes in neuropathologically confirmed Lewy Body disease
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Supplementary results for: Visit-to-visit blood pressure variability, neuropathology and cognitive function
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Infection-induced vascular inflammation in COVID-19 links focal microglial dysfunction with neuropathologies through IL-1/IL-6-related systemic inflammatory states
GEO Series GSE234720. Homo sapiens. 4 samples. Type: Expression profiling by high throughput sequencing.
ScienceDex guides
Understand access before you commit
These curated guides explain access requirements, typical timelines, costs, and reuse considerations for widely used research datasets.
Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.