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Appears in Networks 3

In-Edges 4

deg(a(CHEBI:"amyloid-beta")) association p(HGNC:AQP4) View Subject | View Object

In addition, Jeffrey J. Iliff et al. have demonstrated that the Aβ in brain interstitium can be eliminated from the parenchyma by the bulk flow of interstitial fluid, which also depends on a water channel aquaporin-4 (AQP4) expressed in astrocyte endfeet PubMed:29626319

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

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

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

Out-Edges 7

act(p(HGNC:AQP4)) increases deg(a(CHEBI:"amyloid-beta")) View Subject | View Object

Activation of aquaporin 4 channels on perivascular astrocytes to aid the glymphatic elimination of cerebral Aβ and other toxic proteins is a potential strategy for stimulating clearance. PubMed:30116051

act(p(HGNC:AQP4)) decreases p(CHEBI:"amyloid-beta", loc(GO:"extracellular region")) View Subject | View Object

However, two-photon imaging studies from the past few years have suggested that ISF bulk flow—facilitated by astroglial aquaporin-4 (AQP4) channels and named the glymphatic (glial + lymphatic) system—contributes to a larger portion of eAβ clearance than previously thought. PubMed:26195256

p(HGNC:AQP4) increases 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

p(HGNC:AQP4) increases 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

p(HGNC:AQP4) association deg(a(CHEBI:"amyloid-beta")) View Subject | View Object

In addition, Jeffrey J. Iliff et al. have demonstrated that the Aβ in brain interstitium can be eliminated from the parenchyma by the bulk flow of interstitial fluid, which also depends on a water channel aquaporin-4 (AQP4) expressed in astrocyte endfeet PubMed:29626319

p(HGNC:AQP4) decreases a(CHEBI:"amyloid-beta") View Subject | View Object

Consistent with the conclusion above, there is evidence that glymphatic drainage of ISF bulk flow relying on water channel AQP4 can decrease the levels of Aβ in brain (Iliff et al. 2012) PubMed:29626319

p(HGNC:AQP4) decreases a(CHEBI:"amyloid-beta") View Subject | View Object

In the meanwhile, a study supported this idea that AQP4 deficiency can reduce the rate of Aβ clearance via glymphatic pathway (Iliff and Nedergaard 2013) PubMed:29626319

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.