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  3. path(MESH:"Brain Injuries, Traumatic")

path(MESH:"Brain Injuries, Traumatic")

Equivalencies: 0 | Classes: 0 | Children: 0 | Explore

Entity

Name
Brain Injuries, Traumatic
Namespace
mesh
Namespace Version
20180906
Namespace URL
https://raw.githubusercontent.com/pharmacome/terminology/b46b65c3da259b6e86026514dfececab7c22a11b/external/mesh-names.belns

Appears in Networks 6

Tau protein aggregation is associated with cellular senescence in the brain v1.0.0

Tau oligomers-Cytotoxicity, propagation, and mitochondrial damage v1.0.0

Tau oligomers-Cytotoxicity, propagation, and mitochondrial damage from Shafiei et al., 2017

Clearance systems in the brain-implications for Alzheimer disease. v1.0.1

Clearance of Amyloid Beta and Tau in Alzheimer’s Disease:from Mechanisms to Therapy v1.0.1

The role of inflammasome in Alzheimer’s disease v1.0.3

Nuclear Factor Kappa-light-chain-enhancer of Activated B Cells (NF-κB) - a Friend, a Foe, or a Bystander - in the Neurodegenerative Cascade and Pathogenesis of Alzheimer's Disease v1.0.0

In-Edges 3

p(HGNC:MAPT) association path(MESH:"Brain Injuries, Traumatic") View Subject | View Object

Tau protein accumulation is the most common pathology among degenerative brain diseases, including Alzheimer’s disease (AD), progressive supranuclear palsy (PSP), traumatic brain injury (TBI) and over twenty others PubMed:30126037

Appears in Networks:
Annotations
Confidence
High

a(HBP:"Tau oligomers") increases path(MESH:"Brain Injuries, Traumatic") View Subject | View Object

These tau oligomers potentiate neuronal damage, leading to neurodegeneration and traumatic brain injury (Hawkins et al., 2013; Gerson et al., 2014a, 2016; Sengupta et al., 2015). Moreover, they have been implicated in synaptic loss as shown in studies of wild-type human tau transgenic mice (Spires et al., 2006; Berger et al., 2007; Clavaguera et al., 2013) PubMed:28420982

Appears in Networks:
Annotations
Confidence
High
MeSH
Cerebral Cortex

p(HBP:"tau aggregates") association path(MESH:"Brain Injuries, Traumatic") View Subject | View Object

These findings support the link between TBI and tau aggre- gation, with resulting neurodegeneration similar to that seen in AD and chronic traumatic encephalopathy PubMed:26195256

Appears in Networks:
Annotations
MeSH
Choroid Plexus

Out-Edges 11

path(MESH:"Brain Injuries, Traumatic") association p(HGNC:MAPT) View Subject | View Object

Tau protein accumulation is the most common pathology among degenerative brain diseases, including Alzheimer’s disease (AD), progressive supranuclear palsy (PSP), traumatic brain injury (TBI) and over twenty others PubMed:30126037

Appears in Networks:
Annotations
Confidence
High

path(MESH:"Brain Injuries, Traumatic") association p(HBP:"tau aggregates") View Subject | View Object

These findings support the link between TBI and tau aggre- gation, with resulting neurodegeneration similar to that seen in AD and chronic traumatic encephalopathy PubMed:26195256

Appears in Networks:
Annotations
MeSH
Choroid Plexus

path(MESH:"Brain Injuries, Traumatic") decreases p(HGNC:AQP4) View Subject | View Object

Unfortunately, the glymphatic system may be impaired due to the loss of AQP4 after traumatic brain injury (Iliff et al. 2014) PubMed:29626319

Appears in Networks:

path(MESH:"Brain Injuries, Traumatic") decreases act(p(HGNC:AQP4)) View Subject | View Object

After traumatic brain injury (TBI), the expression and location of AQP4 will change, inducing its dysfunction (Ren et al. 2013) PubMed:29626319

Appears in Networks:

path(MESH:"Brain Injuries, Traumatic") decreases p(HGNC:AQP4) View Subject | View Object

It has been reported that ISF tau can be eliminated by the glymphatic system and the function of this clearance mechanism may be impaired due to the loss of AQP4 after TBI, which ultimately accelerates tau accumulation (Iliff et al.2014) PubMed:29626319

Appears in Networks:
Annotations
MeSH
Extracellular Fluid

path(MESH:"Brain Injuries, Traumatic") decreases a(HP:"glymphatic system") View Subject | View Object

Unfortunately, the glymphatic system may be impaired due to the loss of AQP4 after traumatic brain injury (Iliff et al. 2014) PubMed:29626319

Appears in Networks:

path(MESH:"Brain Injuries, Traumatic") decreases a(HP:"glymphatic system") View Subject | View Object

It has been reported that ISF tau can be eliminated by the glymphatic system and the function of this clearance mechanism may be impaired due to the loss of AQP4 after TBI, which ultimately accelerates tau accumulation (Iliff et al.2014) PubMed:29626319

Appears in Networks:
Annotations
MeSH
Extracellular Fluid

path(MESH:"Brain Injuries, Traumatic") increases p(HGNC:MAPT) View Subject | View Object

It has been reported that ISF tau can be eliminated by the glymphatic system and the function of this clearance mechanism may be impaired due to the loss of AQP4 after TBI, which ultimately accelerates tau accumulation (Iliff et al.2014) PubMed:29626319

Appears in Networks:
Annotations
MeSH
Extracellular Fluid

path(MESH:"Brain Injuries, Traumatic") increases bp(GO:"cell death") View Subject | View Object

In human astrocytes, ATP released from damaged or dying cells after traumatic brain injury activates the NLRP2 inflammasome, leading to the maturation of both IL-1β and IL-18 (Minkiewicz et al., 2013) PubMed:24561250

Appears in Networks:
Annotations
Cell Ontology (CL)
astrocyte
Confidence
Medium
NeuroMMSigDB
Interleukin signaling subgraph

path(MESH:"Brain Injuries, Traumatic") increases act(complex(GO:"NF-kappaB complex")) View Subject | View Object

Physiological, pathophysiological, and biochemical stimuli known to induce proliferation of NPC via NF-κB activation include cerebral infarction [165], traumatic brain injury [166], reactive oxygen species [167], hypoxia [168-172], sAPPα [147], and sphingosine-1-phosphate [173] PubMed:28745240

Appears in Networks:
Annotations
MeSH
Hippocampus
MeSH
Alzheimer Disease

path(MESH:"Brain Injuries, Traumatic") increases bp(GO:neurogenesis) View Subject | View Object

Physiological, pathophysiological, and biochemical stimuli known to induce proliferation of NPC via NF-κB activation include cerebral infarction [165], traumatic brain injury [166], reactive oxygen species [167], hypoxia [168-172], sAPPα [147], and sphingosine-1-phosphate [173] PubMed:28745240

Appears in Networks:
Annotations
MeSH
Hippocampus
MeSH
Alzheimer Disease

About

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.