Browse
Submit Data
Databases
API
Help

Dataset Information

229 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Human Cerebrospinal fluid mass-spec

ABSTRACT: Cerebrospinal fluid from Alzheimer patients affects cell-mediated nerve growth factor production and cell survival in vitroCerebrospinal fluid from Alzheimer patients affects cell-mediated nerve growth factor production and cell survival in vitro

INSTRUMENT(S): 6330 Ion Trap LC/MS

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Cerebrospinal Fluid

DISEASE(S): Lewy Body Dementia,Memory Impairment,Alzheimer's Disease

SUBMITTER: Homira Behbahani

LAB HEAD: Homira Behbahani

PROVIDER: PXD010230 | Pride | 2018-08-13

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Publications

Cerebrospinal fluid from Alzheimer patients affects cell-mediated nerve growth factor production and cell survival in vitro.

Eriksdotter Maria M Navarro-Oviedo Manuel M Mitra Sumonto S Wahlberg Lars L Linderoth Bengt B Tjernberg Lars O LO Behbahani Homira H

Experimental cell research 20180806 1

Alzheimer's disease (AD) is characterized by early degeneration of cholinergic neurons and decreased levels of nerve growth factor (NGF). Thus, increasing the NGF levels by for instance encapsulated cell bio-delivery (ECB) is a potential treatment strategy. The results from our previous first-in-human studies on ECB of NGF to the basal forebrain cholinergic neurons were promising, but indicated some variability of long-term viability of the encapsulated cells and associated reduced NGF-release. ...[more]

PMID: 30092220

Similar Datasets

Modulation of brain dead induced inflammation by vagus nerve stimulation

Project description:Because the vagus nerve is implicated in control of inflammation, we investigated if brain death causes impairment of the parasympathetic nervous system, hence contributing to inflammation. Brain death (BD) was induced in rats. Anaesthetised ventilated rats (NBD) served as control. Heart rate variability (HRV) was assessed by ECG. The vagus nerve was electrically stimulated (BD+STIM) during BD. Intestine, kidney, heart and liver were harvested after 6h. Affymetrix chip- analysis was performed on intestinal RNA. Quantitative PCR was performed on all organs. Serum was collected to assess TNFÎ± concentrations. Renal transplantations were performed to address the influence of vagus nerve stimulation on graft outcome. HRV was significantly lower in BD animals. Vagus nerve stimulation inhibited the increase in serum TNFÎ± concentrations and resulted in down-regulation of a multiplicity of pro-inflammatory genes in intestinal tissue. In renal tissue vagal stimulation significantly decreased the expression of E-selectin, IL1Î² and ITGA6. Renal function was significantly better in recipients that received a graft from a BD+STIM donor. Our study demonstrates impairment of the parasympathetic nervous system during BD and inhibition of serum TNFÎ± through vagal stimulation. Vagus nerve stimulation variably affected gene expression in donor organs and improved renal function in recipients. Gene expression in brain dead (BD) induced rat (with and without vagal stimulation) was compared with that of Non brain-dead ventilated control (NBD)

2010-05-19 | E-GEOD-16483 | biostudies-arrayexpress

Comparative proteomics analysis of growth-primed adult dorsal root ganglia reveals key molecular mediators for peripheral nerve regeneration

Project description:Peripheral nerve injuries due to physical insults or chronic diseases are quite common, yet no pharmacological therapies are available for the effective repair of injured nerves. The slow growth rate of adult nerves and insufficient access to growth factors pose major hurdles in timely reinnervating target tissues and restoring functions after nerve injuries. A better understanding of the molecular changes that occur during the immediate regenerative reprogramming of neurons, stated here as in vivo priming, following nerve injury may reveal ideal candidates for future therapies. Hence, molecular profiling of neuronal soma within the first week of nerve injury has been the gold standard for revealing molecular candidates critical for nerve regeneration. A complementary in vitro regenerative priming approach was recently shown to induce enhanced outgrowth in adult sensory neurons. In this work, we exploited the in vitro priming model to reveal novel candidates for adult nerve regeneration. We performed the whole tissue proteomics analysis of in vitro primed DRGs and compared their molecular profile with that of the in vivo primed, and control DRGs. Through this approach, we identified several commonly and uniquely altered molecules in the in vitro and in vivo primed DRGs that have the potential to modulate adult nerve regrowth. We further validated the growth inducing potential of mesencephalic astrocyte-derived neurotrophic factor (MANF), one of the hits identified in our proteomics analysis, in primary adult sensory neurons. Overall, this study showed that in vitro priming partially reproduces the molecular features in in vivo primed adult sensory neurons. The shortlisted candidates presented here from the two priming approaches may serve as potential therapeutic targets for adult nerve regeneration.

2023-01-06 | PXD031927 | Pride

Proteomics of Alzheimer's Disease mouse models

Project description:Alzheimer’s disease (AD) is a neurodegenerative disease displaying plaques formed by the neurotoxic amyloid β-peptide (Aβ) and intracellular neurofibrillary tangles consisting of protein tau. However, how these pathologies relates to the massive neuronal death that occurs in AD brains remain elusive. To identify proteins, the levels of which are affected by increased Aβ levels, we performed a proteomic analysis of the AD mouse model APPsw and compared it to that of APPsw mice lacking the major Aβ degrading enzyme neprilysin. This was achieved by establishing an LC-MS/MS method to analyze brain homogenate, using an 18O-labeled internal standard to accurately quantify the protein levels. By this approach we identified approximately 600 proteins and could quantify the levels of 300 of these. Interestingly, several proteins, including some not previously reported to be associated with AD, were identified. The relevance of these proteins for AD warrants further research.

2015-07-29 | PXD000968 | Pride

Comparative genomic hybridization of human malignant peripheral nerve sheath tumors and normal reference DNA

Project description:DNA copy number profiling of malignant peripheral nerve sheath tumours

2009-02-25 | E-MEXP-869 | biostudies-arrayexpress

Proteomics of Alzheimer's Disease mouse models - control dataset

Project description:Alzheimer’s disease (AD) is a neurodegenerative disease displaying plaques formed by the neurotoxic amyloid β-peptide (Aβ), and intracellular neurofibrillary tangles consisting of protein tau. However, how these pathologies relates to the massive neuronal death that occurs in AD brains remain elusive. Neprilysin is the major A degrading enzyme and a lack thereof increases A levels in the brain twofold. To identify altered protein expression levels induced by increased Aβ levels, we performed a proteomic analysis of the brain of the AD mouse model APPsw and compared it to that of APPsw mice lacking neprilysin. To this end we established an LC-MS/MS method to analyze brain homogenate, using an 18O-labeled internal standard to accurately quantify the protein levels. To distinguish between alterations in protein levels directly caused by increased A levels and those induced by neprilysin deficiency independently of A, the brain proteome of neprilysin deficient APPsw mice was compared to that of neprilysin deficient mice. By this approach we identified approximately 600 proteins and could quantify the levels of 300 of these. Pathway analysis showed that many of the proteins with altered expression were involved in neurological disorders, and that tau, presenilin and APP were key regulators in the identified networks. The data have been deposited to the ProteomeXchange Consortium with identifier PXD000968. Interestingly, the levels of several proteins, including some not previously reported to be associated with AD, were associated with increased A levels.

2015-07-29 | PXD001786 | Pride

Expression data from rat regenerating livers after autonomic nervous system is disrupted

Project description:Autonomic nervous system is widely distributed in liver, and some reserchers have found that disruppted autonomic nerves will delay liver regeneration. We used microarrays to further highlight the regulatory role of autonomic nervous system in liver regeneration at gene transcription level. Surgical operations of rat partial hepatectomy (PH) and its operation control (OC), sympathectomy combining partial hepatectomy (SPH), vagotomy combining partial hepatectomy (VPH), and total liver denervation combining partial hepatectomy (TDPH) were performed, and the expression profiles of regenerating liver at 2h were detected using Rat Genome 230 2.0 array. Then the significantly changed genes related to liver regeneration (LR)-, injury-, splanchnic nerve-LR-, vagal nerve-LR-, and autonomic nerve-LR-related genes were identified, respectively. The relevance of gene expression profiles and biological processes was analyzed by bioinformatics and systems biology.

2010-12-18 | E-GEOD-26138 | biostudies-arrayexpress

RNA-seq of human plasma microRNAs in Alzheimer Disease

Project description:MicroRNAs (miRNAs) could play an important role as potential Alzheimer Disease (AD) biomarkers. Plasma samples were collected from participants: Mild cognitive impairment (MCI) due to AD patients (n= 20), preclinical AD patients (n= 8) and healthy controls (n= 20). Then, small RNA sequencing analysis, followed by miRNA differential expression analysis comparing different methods (DESeq2, edgeR, NOISeq) were carried out.

2022-05-08 | E-MTAB-11103 | biostudies-arrayexpress

Microdissected pyramidal cell proteomics of Alzheimer brain reveals alterations in Creatine Kinase B, 14-3-3-g and Heat Shock Cognate 71

Project description:Novel insights on proteins involved in Alzheimer disease (AD) are needed. Since multiple cell types and matrix components are altered in AD, bulk analysis of brain tissue may be difficult to interpret. In the current study, we isolated pyramidal cells from the CA1 region of the hippocampus from five AD and five neurologically healthy donors using laser capture microdissection. The samples were analysed by proteomics using 18O labeled internal standard and nano-HPLC MS/MS for relative quantification. Fold change between AD and control was calculated for the proteins that were identified in at least two individual proteomes from each group. From the ten cases analyzed, sixty-two proteins were identified in at least two AD cases and two control cases. Creatine Kinase B-type (CKB), 14-3-3-g and Heat Shock Cognate 71 (Hsc71) which have not been extensively studied in the context of human AD brain previously, were selected for further studies by immunohistochemistry (IHC). In hippocampus, semi-quantitative measures of IHC staining of the three proteins confirmed the findings from our proteomic analysis. Studies of the same proteins in frontal cortex revealed that the alterations remained for CKB and 14-3-3-g but not for Hsc71. Protein upregulation in CA1 neurons of final stage AD is either a result from detrimental, pathological effects, or from cell specific protective response mechanisms in surviving neurons. Based on previous findings from experimental studies, CKB and Hsc71 likely exhibit protective effects, whereas 14-3-3-g represents a detrimental path. These new players could represent pathways of importance for development of new therapeutic strategies.

2022-02-15 | PXD028282 | Pride

AP-MS of helicase Upf1 in PC12 cells

Project description:DNA/RNA helicase Upf1 seems to interact with axonal transcripts in response to nerve growth factor (NGF, A. Ludanyi, M. Gaspari and A. Riccio, unpublished data). In order to shed light on Upf1 mechanism of action and to identify potential associations with molecules having cleavage activity, we performed an AP-MS experiment comprising Upf1 immunoprecipitation, on-beads digestion, isotopic labelling (18O) and quantitative LC-MS/MS analysis.

2021-09-10 | PXD023586 | Pride

Immunodominant myelin basic protein fragments induce mechanical hypersensitivity.

Project description:An insulating myelin sheath ensures saltatory conduction of mechanosensory A afferents. Myelin damage results in the electrical instability of A fibers and the ability to generate pain in response to light touch/pressure (mechanical allodynia). We have hypothesized and then established that the release of T cell epitopes of myelin basic protein (MBP) enables nociceptive circuitry in myelinated fibers. Thus, mass spectrometry analysis of the rat sciatic nerve proteome followed by bioinformatics examination of the datasets revealed a loss of MBP and activation of T-helper cell signaling in the nerves undergoing chronic constriction injury (CCI). Matrix metalloproteinase-9 (MMP-9) proteolysis resulted in the MBP digest peptides, including the MBP84-104 and MBP68-86 regions, which exhibit prominent immunogenic epitopes. Myelin-forming Schwann cells and paranodal areas accumulated MHCII, MMP-9 and the degraded MBP at the sciatic nerve injury site. Administration of the immunodominant MBP84-104 and MBP68-86 peptides but not of the control peptides in a naïve rat sciatic nerve produced robust mechanical allodynia. Allodynia was accompanied by the T cell infiltration and an increase in MHCII, IL-17A and TNF- levels at the nerve injection site and the segmental ganglia. The pro-nociceptive activity of the synthetic MBP84-104 diminished in athymic nude rats lacking T cells. SB-3CT, an antagonist of MMP-9, inhibited mechanical allodynia, neuroinflammation and spinal sensitization after CCI. Collectively, our novel data implicate, for the first time, MMP-mediated cleavage of MBP and the resulting MBP digest fragments as a major cause of neuropathic pain. Gene extression profiling of total RNAs extracted from rat sciatic nerves, dorsal root ganglion and spinal cords after MBP84-104 peptide injection

2012-03-03 | E-GEOD-34868 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data