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Appears in Networks 6

In-Edges 6

a(CHEBI:"amyloid-beta") increases path(MESH:Gliosis) View Subject | View Object

These Aβ deposits lead to subsequent molecular and cellular alterations, such as NTFs, neuronal dystrophy, or microgliosis, i.e., pathological events that are closer to dementia and more relevant to neuronal dysfunction. PubMed:29196815

path(MESH:"Prion Diseases") increases path(MESH:Gliosis) View Subject | View Object

Prion disease neuropathology is characterized by widespread neuronal death, accompanied by spongiform vacuolation and astrogliosis, usually combined with widespread deposits of extracellular amyloid aggregates. PubMed:14556719

p(HGNC:NPEPPS) decreases path(MESH:Gliosis) View Subject | View Object

In addition, a non-functional PSA mutant exacerbated tau pathology in a Drosophila model of tauopathy, while overexpressing PSA ameliorated the tau phenotype and diminished tau levels (10). Overexpressing PSA had a similar effect in the TAUP301L mice, reducing the pathologic phenotype (delaying paralysis, increasing motor neuron density in the spinal cord, decreasing gliosis) and decreasing tau levels (12). PubMed:24027553

p(MGI:Tfeb) decreases path(MESH:Gliosis) View Subject | View Object

Overall, these results show that astroglial TFEB overexpression reduces tau pathology and gliosis in the hippocampus of PS19 tauopathy mice. PubMed:30108137

path(MESH:"Supranuclear Palsy, Progressive") increases path(MESH:Gliosis) View Subject | View Object

PSP is an age-associated tauopathy that clinically manifests as parkinsonism with additional motor abnormalities and cognitive dysfunction (Orr et al., 2017), and is neuropathologically defined by accumulation of four-repeat (4R) tau, NFTs, gliosis and neurodegeneration (Flament et al., 1991) PubMed:30126037

a(CHEBI:Anatabine) decreases path(MESH:Gliosis) View Subject | View Object

We have shown previously that anatabine displays some anti-inflammatory properties and reduces microgliosis and tau phosphorylation in a pure mouse model of tauopathy. PubMed:26010758

Out-Edges 0

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BEL Commons is developed and maintained in an academic capacity by Charles Tapley Hoyt and Daniel Domingo-Fernández at the Fraunhofer SCAI Department of Bioinformatics with support from the IMI project, AETIONOMY. It is built on top of PyBEL, an open source project. Please feel free to contact us here to give us feedback or report any issues. Also, see our Publishing Notes and Data Protection information.

If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.