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33 results for “CSF biomarkers”
A Pilot Study of the Effects of BCG Immunization on CSF and Blood-based Biomarkers in Older Adults.
ClinicalTrials.gov study NCT04507126. IPD Sharing: NO. Countries: 1. Publications: 0.
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>
Multivariate GWAS of Alzheimer's disease CSF biomarker profiles implies GRIN2D in synaptic functioning: Summary statistics
<p>Summary statistics for a genome-wide association study (GWAS) of Alzheimer's disease CSF biomarkers principal components (PCs). This dataset accompanies the publication "Multivariate GWAS of Alzheimer’s disease CSF biomarker profiles implies GRIN2D in synaptic functioning". The article is currently in press at Genome Medicine. A link will be provided upon publication, but see the medRxiv preprint in the meantime:</p> <p>Neumann, A., Ohlei, O., Küçükali, F., Bos, I. J., Vos, S., Prokopenko, D., ... & Kristel Sleegers & Lars Bertram. (2022). Multivariate GWAS of Alzheimer’s disease CSF biomarker profiles implies GRIN2D in synaptic functioning. <em>medRxiv</em>, 2022-08. https://doi.org/10.1101/2022.08.02.22278185</p> <p>A GWAS was performed for five different PC biomarkers.</p> <p>PC1: Tau pathology/degeneration</p> <p>PC2: Aβ Pathology</p> <p>PC3: Injury/inflammation</p> <p>PC4: Non-AD inflammation</p> <p>PC5: Non-AD synaptic functioning</p> <p>Each GWAS was performed in either males and females ("all"), in females only ("female"), or in males only ("male"). In addition, we also ran an interaction model with sex as moderator ("interaction"). Each file includes output of the meta-analysis between the EMIF-AD study and ADNI.</p> <p>The files contain following columns:</p> <p>CHROM: Chromosome</p> <p>POS: Position according to Build 37</p> <p>ID: Chromosome:Position</p> <p>A1: Effect allele</p> <p>A2: Other allele</p> <p>BETA: Effect of one copy of the effect allele on biomarker PCs in SD. In case of sex interaction, the effect specific to females.</p> <p>SE: Standard Error</p> <p>P: p-value</p> <p>D: Direction in ADNI and EMIF-AD respectively</p> <p>Het: Heterogeneity statistics (I<sup>2</sup>, and corresponding χ<sup>2</sup>, degrees of freedom and p-value)</p>
The Canadian Multicentre CSF Monitoring and Biomarker Study
ClinicalTrials.gov study NCT01279811. IPD Sharing: Not stated. Countries: 2. Publications: 2.
Alzheimer Biomarkers on CSF of Elderly Patients Undergoing Surgery
ClinicalTrials.gov study NCT03977025. IPD Sharing: UNDECIDED. Countries: 1. Publications: 20.
CSF Biomarkers in Idiopathic Intracranial Hypertension
ClinicalTrials.gov study NCT05647837. IPD Sharing: Not stated. Countries: 1. Publications: 2.
Prospective Quantification of CSF Biomarkers in Antibody-Mediated Encephalitis
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Associations of fully-automated CSF and novel plasma biomarkers with Alzheimer's disease neuropathology at autopsy
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Data from: Sex differences in CSF biomarkers vary by Alzheimer’s disease stage and APOE epsilon 4 genotype
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Data from: White matter hyperintensities and CSF AD biomarkers in preclinical Alzheimer's disease
Objective: Recent studies suggest that white matter hyperintensities (WMH) on MRI, which primarily reflect small vessel cerebrovascular disease, may play a role in the evolution of Alzheimer's disease (AD). In a longitudinal study, we investigated whether WMH promote the progression of AD pathology, or alter the association between AD pathology and risk of progression from normal cognition to mild cognitive impairment (MCI). Methods: Two sets of analyses were conducted. The relationship between whole brain WMH load, based on FLAIR MRI images, obtained in initially cognitively normal participants (n=274) and time to onset of symptoms of MCI (n=60) was examined using Cox regression models. In a subset of the participants with both MRI and CSF data (n=204), the interaction of WMH load and CSF AD biomarkers was also evaluated. Results: Baseline WMH load interacted with CSF t-tau with respect to symptom onset, but not with CSF abeta1-42 or p-tau181. WMH volume was associated with time to symptom onset of MCI among individuals with low t-tau [HR=1.35, CI=1.06-1.73, p=0.013], but not those with high t-tau [HR=0.86,CI=0.56-1.32, p=0.47]. The rate of change in the CSF biomarkers over time was not associated with the rate of change in WMH volumes. Conclusions and Relevance: These results suggest that WMH primarily affect the risk of progression when CSF measures of neurodegeneration or neuronal injury (as reflected by t-tau) are low. However, CSF biomarkers of amyloid and p-tau and WMH appear to have largely independent and non-synergistic effects on the risk of progression to MCI.
Data from: Increased CAIDE dementia risk, cognition, CSF biomarkers and vascular burden in healthy adults
Objective: To investigate the cognitive profile of healthy individuals with increased CAIDE dementia risk score, and to explore whether this association is related to vascular burden and CSF biomarkers of amyloidosis and neurodegeneration. Method: Cognitively normal participants (mean age = 57.6 years) from the Gipuzkoa Alzheimer Project study were classified as having high risk (HR, n = 82) or low risk (LR, n = 293) for dementia according to a CAIDE score cut off of 9. Cognitive composites were compared between groups. We explored the role of APOE genotype, MRI white matter hyperintensities (WMH) and CSF (n = 218) levels of amyloid-β1-42 (Aβ1-42), total tau (t-tau) and phosphorylated tau (p-tau) in the association between CAIDE and cognition conducting generalized linear models. Results: HR participants obtained lower scores on executive function (EF) (p = .001) and visual perception and construction (VPC) (p < .001) composites. EFc was associated with CAIDEp-tau (p = .001), CAIDEt-tau (p = .001) and WMH (p = .003). VPCc was associated with APOE (p = .001), Aβ1-42 (p = .004), the interaction APOEAβ1-42 (p = .003), and WMH (p = .004). Performance on global memory was associated with Aβ1-42 (p = .006), APOE (p = .008), and their interaction (p = .006). Analyses were adjusted for age, education, sex, premorbid intelligence and stress. Conclusion: Healthy participants at increased dementia risk, based on CAIDE scores, show lower performance in executive function and visual perception and construction. This difference is related to APOE, WMH and Alzheimer's biomarkers.
CSF synaptic biomarkers in the preclinical stage of Alzheimer's disease and their association with MRI and PET markers of neurodegeneration: a cross-sectional study
<p>Objective: To determine whether CSF synaptic biomarkers are altered in the early preclinical stage of the Alzheimer's <i>continuum</i> and associated with Alzheimer's disease (AD) risk factors, primary pathology, and neurodegeneration markers.</p> <p>Methods: Cross-sectional study in the ALFA+ cohort, comprising middle-aged cognitively unimpaired participants. CSF neurogranin and GAP-43 were measured using immunoassays and SNAP-25 and synaptotagmin-1 using immunoprecipitation mass spectrometry. AD CSF biomarkers Aβ42/40, p-tau and t-tau, and the neurodegeneration biomarker NfL were also measured. Participants underwent structural MRI, and <span>fluorodeoxyglucose and</span> Aβ<span> PET imaging. General linear modeling was used to test the associations between CSF synaptic biomarkers and risk factors, </span>Aβ<span> pathology, tau pathology, and neurodegeneration markers.</span></p> <p>Results: All CSF synaptic biomarkers increased with age. CSF neurogranin was higher in females, while CSF SNAP-25 was higher in <i>APOE-</i>ε4 carriers. All CSF synaptic biomarkers increased with higher Aβ load (as measured by CSF Aβ42/40 and Aβ PET Centiloid values) and, importantly, the synaptic biomarkers were increased even in individuals in the earliest stages of Aβ deposition. Higher CSF synaptic biomarkers were also associated with higher CSF p-tau and NfL. Higher CSF neurogranin and GAP-43 were significantly associated with higher brain metabolism, but lower cortical thickness in AD-related brain regions.</p> <p>Conclusion: CSF synaptic biomarkers increase in early preclinical stages of the Alzheimer's <i>continuum </i>even when a low burden of Aβ pathology is present, and they differ in their association with age, sex, <i>APOE-</i>ε4<i>,</i> and markers of neurodegeneration.</p>
Association of CSF biomarkers with hippocampal-dependent memory in preclinical Alzheimer disease
<p><b>Objective: </b>To determine if memory tasks with demonstrated sensitivity to hippocampal function can detect variance related to preclinical Alzheimer's disease (AD) biomarkers, we examined associations between performance in three memory tasks and CSF Ab<sub>42</sub>/Ab<sub>40 </sub>and p-tau<sub>181</sub> in cognitively unimpaired older adults (CU).</p> <p><b>Methods: </b>CU enrolled in the Stanford Aging and Memory Study (N=153; age 68.78 ± 5.81 yrs; 94 female) completed a lumbar puncture and memory assessments. CSF Ab<sub>42</sub>,<sub> </sub>Ab<sub>40</sub>, and phosopho-tau<sub>181</sub> (p-tau<sub>181</sub>) were measured with the automated Lumipulse G system in a single-batch analysis. Episodic memory was assayed using a delayed recall composite, paired associate (word-picture) cued recall, and a mnemonic discrimination task that involves discrimination between studied 'target' objects, novel 'foil' objects, and perceptually similar 'lure' objects. Analyses examined cross-sectional relationships between memory performance, age, and CSF measures, controlling for sex and education.</p> <p><span><b>Results: </b>Age and lower Ab<sub>42</sub>/Ab<sub>40 </sub>were independently associated with elevated p-tau<sub>181</sub>. Age, Ab<sub>42</sub>/Ab<sub>40,</sub> and p-tau<sub>181</sub> were each associated with a) poorer associative memory and b) diminished improvement in mnemonic discrimination performance across levels of decreased task difficulty (i.e., target-lure similarity). P-tau mediated the effect of Ab<sub>42</sub>/Ab<sub>40 </sub>on memory. Relationships between CSF proteins and delayed recall were similar but non-significant. CSF Ab<sub>42 </sub>was not significantly associated with p-tau<sub>181 </sub>or memory. </span></p> <p><b>Conclusions: </b>Tests designed to tax hippocampal function are sensitive to subtle individual differences in memory among CU, and correlate with early AD-associated biomarker changes in CSF. These tests may offer utility for identifying cognitively unimpaired older adults with preclinical AD pathology.<b> </b></p>
Prazosin and Cerebrospinal Fluid (CSF) Biomarkers in Mild Traumatic Brain Injury (mTBI)
ClinicalTrials.gov study NCT03221751. IPD Sharing: NO. Countries: 1. Publications: 0.
Data from: Increased CAIDE dementia risk, cognition, CSF biomarkers and vascular burden in healthy adults
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Data from: CSF biomarkers of neuroinflammation and cerebrovascular dysfunction in early Alzheimer's disease
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Data from: White matter hyperintensities and CSF AD biomarkers in preclinical Alzheimer’s disease
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Association of CSF biomarkers with hippocampal-dependent memory in preclinical Alzheimer disease
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CSF synaptic biomarkers in the preclinical stage of Alzheimer’s disease and their association with MRI and PET markers of neurodegeneration: a cross-sectional study
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CSF Biomarker and PIB-PET Derived Beta-Amyloid Signature Predicts Metabolic, Grey Matter and Cognitive Changes in Non-Demented Subjects
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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.