PXD005785 is an
original dataset announced via ProteomeXchange.
Dataset Summary
| Title | The effect of chronic inflammation on molecular pathways of long-term potentiation in an APP/PS1 mouse model of Alzheimer Disease |
| Description | Alzheimer Disease (AD) is the most common cause of dementia and neuroinflammation, initiated by systemic bacterial infection, is believed to contribute significantly to its pathogenesis. Lipopolysaccharide (LPS) is an endotoxin, which stimulates inflammatory reactions by increasing the levels of pro-inflammatory cytokines through binding to Toll like receptor-4 (TLR-4) and CD14, in an NF-κΒ-dependent fashion. These receptors are expressed in the circumventricular organs, choroid plexus and leptomeninges as well as on microglia cells, thereby providing an entry for an innate immune reaction to spread through the cerebral tissue. Here, 9 months old APP695/PS1ΔE9 (APP/PS1) double transgenic mice and wild type littermates were treated with weekly intraperitoneal injections of LPS or PBS over 13 weeks to evaluate the effect of repeated infections on the innate immune response of the hippocampal proteome. The effect on the proteome was evaluated using a quantitative iTRAQ 8-plex proteomics approach, with 3D-LC-MS/MS to gain a deep coverage of the hippocampal proteome. Furthermore, the effect of long-term inflammation on amyloid beta (Aβ) protein level was evaluated using stereological plaque load estimation followed by investigation of protein levels of Aβ40 and Aβ42 by Mesoscale. An effect of infection on proteins involved in long-term potentiation was observed, including p-MAPK, p-CREB and phosphorylation motifs of PKA and 14-3-3. Furthermore the complement system, redox reactions and the activation of retinoid receptors were found significantly changed in APP/PS1 mice infected with LPS. This study provides new insight into the effect of bacterial infections in the development of AD. |
| HostingRepository | PRIDE |
| AnnounceDate | 2024-10-22 |
| AnnouncementXML | Submission_2024-10-22_04:35:48.529.xml |
| DigitalObjectIdentifier | |
| ReviewLevel | Peer-reviewed dataset |
| DatasetOrigin | Original dataset |
| RepositorySupport | Unsupported dataset by repository |
| PrimarySubmitter | Stefan J. Kempf |
| SpeciesList | scientific name: Mus musculus (Mouse); NCBI TaxID: 10090; |
| ModificationList | iTRAQ8plex-116 reporter+balance reagent acylated residue; iodoacetamide derivatized residue |
| Instrument | Orbitrap Fusion Lumos; Orbitrap Fusion |
Dataset History
| Revision | Datetime | Status | ChangeLog Entry |
| 0 | 2017-01-26 02:02:04 | ID requested | |
| 1 | 2018-11-21 16:24:47 | announced | |
| 2 | 2018-11-23 06:49:32 | announced | Updated publication reference for PubMed record(s): 30459560. |
| ⏵ 3 | 2024-10-22 04:35:50 | announced | 2024-10-22: Updated project metadata. |
Publication List
| 10.3389/fncel.2018.00397; |
| Thygesen C, Ilkj, æ, r L, Kempf SJ, Hemdrup AL, von Linstow CU, Babcock AA, Darvesh S, Larsen MR, Finsen B, Transgenic Mice Implicate Cathepsin Z in Alzheimer's Disease. Front Cell Neurosci, 12():397(2018) [pubmed] |
Keyword List
| curator keyword: Biomedical |
| submitter keyword: neuroinflammation, brain, LTP,LPS |
Contact List
| Martin R. Larsen |
| contact affiliation | Department of Biochemistry and Molecular Biology, University of Southern Denmark, Odense, Denmark |
| contact email | mrl@bmb.sdu.dk |
| lab head | |
| Stefan J. Kempf |
| contact affiliation | University of Southern Denmark |
| contact email | kempf-stefan@t-online.de |
| dataset submitter | |
Full Dataset Link List
Dataset FTP location
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| PRIDE project URI |
Repository Record List
[ + ]
[ - ]
- PRIDE
- PXD005785
- Label: PRIDE project
- Name: The effect of chronic inflammation on molecular pathways of long-term potentiation in an APP/PS1 mouse model of Alzheimer Disease