Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Seed-competent tau monomer initiates pathology in PS19 tauopathy mice

ABSTRACT: Tau Monomer from age controlled healthy and Alzheimer's Disease LUM2_C10053 LUM2_C10054 LUM2_C10055 LUM2_C10056 LUM2_C10057 LUM2_C10058 Tau fibril from Alzheimer's Disease LUM2_630897 Tau monomer from brain of PS19 mouse at age week 1, 2, 3, 4, 5, 6 LUM1_C11496 to LUM1_C11501 Tau monomer from brain of PS19 mouse at age 1 year LUM1_705666

INSTRUMENT(S): Orbitrap Fusion Lumos

ORGANISM(S): Homo Sapiens (ncbitaxon:9606)

SUBMITTER: Marc I Diamond

PROVIDER: MSV000088651 | MassIVE | Thu Jan 06 11:22:00 GMT 2022

REPOSITORIES: MassIVE

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Alzheimer's Disease Dataset

Project description:FK506 binding protein 51kDa (FKBP51/FKBP5) is part of a mature heat shock protein 90kDa (Hsp90) chaperone complex that preserves tau. Microarray analysis of human brains reveal that FKBP51 gene expression selectively increased with age and Alzheimer's disease, which correlated with demethylation of the regulatory regions in the FKBP5 gene. Moreover, FKBP51 levels significantly correlated with Braak pathological staging. In addition, we show that in brains devoid of FKBP51, tau levels are reduced. Recombinant FKBP51 and Hsp90 synergize to block tau clearance through the proteasome and produce T22-positive tau oligomers. Overexpression of FKBP51 in a tau transgenic mouse model revealed that FKBP51 preserved tau species, including phosphorylated and oligomeric tau that have been linked to Alzheimer's disease pathogenesis. FKBP51 blocked amyloid formation and decreased tangle load in the brain. These alterations in tau turnover and aggregate structure culminated in enhanced neurotoxicity. We propose a model where age-associated increases in FKBP51 levels can out-compete the association of other pro-degradation Hsp90 co-chaperones, resulting in neurotoxic tau accumulation. Thus, strategies aimed at attenuating FKBP51 levels or its interaction with Hsp90 could be therapeutically relevant for Alzheimer's disease and other tauopathies. These AD cases were processed simultaneously with the control cases (young and aged) included in GSE11882 Postmortem brain tissue was collected from ADRC brain banks. Cases were preferentially selected where 3 or more brain regions were available

2014-04-21 | E-GEOD-48350 | biostudies-arrayexpress

E-PROT-32

Project description:Proteomic signatures of brain regions affected by tau pathology in early and late stages of Alzheimer's disease

2021-05-25 | E-PROT-32 | ExpressionAtlas

E-PROT-35

Project description:Brain ureido degenerative protein modifications in Alzheimer's disease with cerebrovascular disease

2022-01-06 | E-PROT-35 | ExpressionAtlas

Tau posttranslational modifications

Project description:Human tauopathies including Alzheimer's disease are characterized by alterations in the post-translational modification (PTM) pattern of Tau, leading to the formation of insoluble aggregates, neuronal dysfunction and degeneration. We immunoprecipitated Tau from post-mortem brain tissue of early stage Alzheimer's disease patients and age-matched controls, and analyzed PTMs on this soluble pool of Tau protein. In addition to known serine, threonine and tyrosine phosphorylation events, we identified a number of previously unknown monomethylation events on lysines in both control and Alzheimer's patient tissues.

2021-09-09 | PXD017065 | Pride

E-PROT-31

Project description:Proteomic Atlas of the human brain in Alzheimer's disease

2021-05-25 | E-PROT-31 | ExpressionAtlas

E-PROT-61

Project description:Proteomic Atlas of the Human Brain in Alzheimer's Disease

2021-05-25 | E-PROT-61 | ExpressionAtlas

E-GEOD-48350

Project description:Microarray analysis of Alzheimer's disease patients across 4 brain regions

2025-01-24 | E-GEOD-48350 | ExpressionAtlas

Microbial infection instigates tau-related pathology in Alzheimer's disease via activating neuroimmune cGAS-STING pathway

Project description:Microbial infection, the strong trigger to directly induce inflammation in brain, is long considered a risk factor of Alzheimer's disease (AD), but how these infections contribute to neurodegeneration remains underexplored. To examine the effect of herpes simplex virus type 1 (HSV-1) infection on tauopathy in local hippocampus of P301S mice, we utilized a modified HSV-1 strain (mHSV-1) potentially relevant to AD, we found that its infection promotes tau-related pathology in part via activating neuroimmune cGAS-STING pathway in the tau mouse model. Specifically, Sting ablation causes the detectable improvement of neuronal dysfunction and loss in P301S mice, which is causally linked to lowered proinflammatory status in the brain. Administration of STING inhibitor H-151 alleviates neuroinflammation and tau-related pathology in P301S mice. These results jointly suggest that herpesviral infection, as the vital environmental risk factor, could induce tau-related pathology in AD pathogenesis partially via neuroinflammatory cGAS-STING pathway.

2024-04-11 | GSE229411 | GEO

Microbial infection instigates tau-related pathology in Alzheimer's disease via activating neuroimmune cGAS-STING pathway

2025-04-17 | GSE264504 | GEO

E-MTAB-6094

Project description:Whole genome transcriptional analysis of Alzheimer's disease patients compared with age-matched non-demented controls

2025-01-23 | E-MTAB-6094 | ExpressionAtlas