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Project description:TLDA miRNA Screen for Candidate AD Biomarkers in CSF from Living Donors
| PRJNA875952 | ENA
Project description:We used an independent cohort of patient CSF samples from living donors obtained from the Shiley-Marcos Alzheimer's Disease Research Center at the Univ of CA, San Diego to validate the expression of 36 candidate AD miRNA biomarkers. The miRNAs were quantified on custom Taqman Low Density miRNA Arrays from ThermoFisher Scientific; miRNA probes were consistent to those used in the UH2 discovery arrays.
2022-09-03 | GSE212623 | GEO
Project description:Validation Study for Candidate AD miRNA Biomarkers in Human CSF
| PRJNA876275 | ENA
Project description:Cross-sectional and longitudinal Analysis of CSF from controls and cases with AD
2015-07-15 | MSV000079192 | MassIVE
Project description:HIGHTLIGHTS-Improved protocol for ISF collection using microdialysis and CSF sampling in mice.-Combined LC‒MS/MS proteomics ISF and CSF analyses for the validation and description of potential new AD biomarkers.-ISF proteomics analysis to track disease progression at the neuronal and glial levels.-Identification of new biomarker candidates for Alzheimer’s disease.ABSTRACTBackground: Mass spectrometry (MS)-based cerebrospinal fluid (CSF) proteomics is an important method for discovering biomarkers of neurodegenerative diseases. CSF serves as a reservoir for interstitial fluid (ISF), and extensive communication between the two fluid compartments helps to remove waste products from the brain.New method: We performed proteomic analyses of both CSF and ISF fluid compartments using intracerebral microdialysis to validate and detect novel biomarkers of Alzheimer's disease (AD) in APPtg and C57Bl/6J control mice.Results: We identified up to 625 proteins in ISF and 4,483 proteins in CSF samples. By comparing the biofluid profiles of APPtg and C57Bl/6J mice, we detected 37 and 108 significantly up- and downregulated candidates, respectively. In ISF, 7 highly regulated proteins, such as Gfap, Aldh1l1, Gstm1, and Txn, have already been implicated in AD progression, whereas in CSF, 9 out of 14 highly regulated proteins, such as Apba2, Syt12, Pgs1 and Vsnl1, have also been validated to be involved in AD pathogenesis. In addition, we also detected new interesting regulated proteins related to the control of synapses and neurotransmission (Kcna2, Cacng3, and Clcn6) whose roles as AD biomarkers should be further investigated.Comparison with existing methods: This newly established combined protocol provides better insight into the mutual communication between ISF and CSF as an analysis of tissue or CSF compartments alone.Conclusions: The use of multiple fluid compartments, ISF and CSF, for the detection of their biological communication enables better detection of new promising AD biomarkers.KEYWORDSAlzheimer’s disease, CSF, ISF, proteomics, biomarkers, microdialysis, mass spectrometry, protein identification, neurodegeneration, brain fluids, expression profilesDATA AVAILABILITYDOI: 10.17605/OSF.IO/VWQ58PUBLICATIONS using this dataset:1)Gorska et al. 2024, Journal of Neuroscience Methodshttps://doi.org/10.1016/j.jneumeth.2024.1102392) to come
2024-08-28 | PXD048864 | Pride
Project description:Replication-deficient adenovirus (Ad) type 5 capsids induce potent host innate immune responses. One system pivotal in host innate immune defense is the complement system. Intriguingly, excessive or inappropriate complement activation can result in extreme tissue damage and systemic inflammatory responses similar to those noted immediately after high dose systemic Ad vector injections. To determine if the complement system has a significant role in intensifying Ad-associated acute toxicities, we compared complement deficient (C3-knockout (KO)) mice responses to those of wild type (WT) mice following systemic challenge with Ad vectors. We noted not only thrombocytopenia and rapid increases in plasma IL-6, IFN-γ, TNF-α, and IL-12 levels previously reported after high dose Ad injections into WT mice, but also induction of cytokines IL-2, IL-4, IL-5 and IL-10, G-CSF and GM-CSF, and chemokines KC (CXCL1) and MIP-1. This expanded innate response “profile” was significantly blunted in Ad injected C3-KO mice, with a near complete avoidance of thrombocytopenia. Further validation for complement’s critical role in perturbing these innate responses against Ad were noted after comparison of gene specific RNA transcription levels in C3-KO to WT mice livers. Finally, these disparities were not attributed to a diminished ability of the Ad vectors to transduce C3-KO mice hepatocytes. These results suggest that Ad capsid interaction with the mammalian complement system may exacerbate the toxicity of systemic Ad injections, and thus represents a future target for manipulation in efforts to improve the efficacy and safety profile of Ad mediated gene delivery. Keywords: adenovirus, complement system, time course, innate immune response, toxicity
2006-02-15 | GSE4128 | GEO
Project description:Very little studies have explored the role played by the specialized choroid plexus epithelial cells and the ependymal cells that line the ventricles. In normal and pathological (AD) ageing, reports of alterations in the blood brain CSF barrier (BCSFB) integrity and membrane transporters, accompanied by deficiencies in CSF production and an enlarged ventricular volume have been documented. The molecular sequelae of events driving these age-related pathological changes remains elusive. Given the pivotal role of the ventricular system in normal brain physiology, in this study we proposed to explore their contributing role towards AD pathogenesis. To address this, we used our state-of-the-art proteomic platform, a liquid chromatography/mass spectrometry (LC-MS) approach coupled with Tandem Mass Tag labeling technology to conduct a detailed characterization and assessment of molecular changes in protein expression levels from isolated tissue from the walls of the ventricles in autopsy AD cases, and two groups of age-matched control cases (non-agenarian’s with no AD pathology, and those with no clinical AD diagnosis but significant amyloid pathology and Braak staging).
2021-09-08 | PXD012059 | Pride
Project description:ObjectiveTo compare the annual change in MRI and CSF biomarkers in cognitively normal (CN), amnestic mild cognitive impairment (aMCI), and Alzheimer disease (AD). Comparisons were based on intergroup discrimination, correlation with concurrent cognitive/functional changes, relationships to APOE genotype, and sample sizes for clinical trials.MethodsWe used data from the Alzheimer's Disease Neuroimaging Initiative study consisting of CN, aMCI, and AD cohorts with both baseline and 12-month follow-up CSF and MRI. The annual change in CSF (total-tau [t-tau], Abeta(1-42)) and MRI (change in ventricular volume) was obtained in 312 subjects (92 CN, 149 aMCI, 71 AD).ResultsThere was no significant average annual change in either CSF biomarker in any clinical group except t-tau in CN; moreover, the annual change did not differ by clinical group in pairwise comparisons. In contrast, annual increase in ventricular volume increased in the following order, AD > aMCI > CN, and differences were significant between all clinical groups in pairwise comparisons. Ventricular volume increase correlated with concurrent worsening on cognitive/functional indices in aMCI and AD whereas evidence of a similar correlation with change in CSF measures was unclear. The annual changes in MRI differed by APOE epsilon4 status overall and among aMCI while annual changes in CSF biomarkers did not. Estimated sample sizes for clinical trials are notably less for MRI than the CSF or clinical measures.ConclusionsUnlike the CSF biomarkers evaluated, changes in serial structural MRI are correlated with concurrent change on general cognitive and functional indices in impaired subjects, track with clinical disease stage, and are influenced by APOE genotype.
| S-EPMC2905929 | biostudies-literature
Project description:BackgroundLoss of brain capillary pericyte is involved in the pathologies and cognitive deficits in Alzheimer's disease (AD). The role of pericyte in early stage of AD pathogenesis remains unclear.MethodsWe investigated the dynamic changes of soluble platelet-derived growth factor receptor β (sPDGFRβ) in cerebrospinal fluid (CSF), a marker of brain pericyte injury, in transition from normal ageing to early AD in a cognitively unimpaired population aged 20 to 90 years. Association between sPDGFRβ and ATN biomarkers were analyzed.ResultsIn lifetime, CSF sPDGFRβ continually increased since age of 20 years, followed by the increases of phosphorylated tau-181 (P-tau181) and total tau (T-tau) at the age of 22.2 years and 31.7 years, respectively; CSF Aβ42 began to decline since the age of 39.6 years, indicating Aβ deposition. The natural trajectories of biomarkers suggest that pericyte injury is an early event during transition from normal status to AD, even earlier than Aβ deposition. In AD spectrum, CSF sPDGFRβ was elevated in preclinical stage 2 and participants with suspected non-AD pathophysiologies. Additionally, CSF sPDGFRβ was positively associated with P-tau181 and T-tau independently of Aβ42, and significantly strengthened the effects of Aβ42 on P-tau181, suggesting that pericyte injury accelerates Aβ-mediated tau hyperphosphorylation.ConclusionsOur results suggest that pericyte injury contributes to AD progression in the early stage in an Aβ-independent pathway. Recovery of pericyte function would be a target for prevention and early intervention of AD.
| S-EPMC8760673 | biostudies-literature