Evidences a(MESH:"Lymphatic Vessels") to p(MGI:Vegfc)

Collectively, these data point to no apparent meningeal lymphatic dysfunction in transgenic mice with Alzheimer’s disease at younger ages, which might explain the inefficacy of mVEGF-C treatment

We have previously shown that treatment with recombinant VEGF-C increases the diameter of meningeal lymphatic vessels

Furthermore, delivery of VEGF-C by adenoviral gene therapy was previously found to efficiently boost peripheral lymphatic sprouting and function

Treatment of young mice with AAV1-CM-mVEGF-C resulted in a significant increase in meningeal lymphatic vessel diameter, without affecting blood vessel coverage (Extended Data Fig. 6k–m)

Treatment of old mice (at 20–24 months) with AAV1-CMV-mVEGF-C also resulted in increased lymphatic vessel diameter (compared to AAV1-CMV-eGFP) without detectable off-target effects on the meningeal blood vasculature coverage and on meningeal and/or brain vascular haemodynamics (Fig. 2e–h and Extended Data Fig. 6n–p)

This VEGF-C treatment led to a significant increase in the function of meningeal lymphatic vessels in old mice, whereas young–adult mice did not respond to the treatment (Extended Data Fig. 7d, e), probably due to the ceiling effect of their existing capacity to drain OVA-A647

Moreover, viral expression of mVEGF-C did not significantly affect the diameter of meningeal lymphatic vessels, the level of amyloid-β in the CSF, or amyloid-β deposition in the hippocampus (Extended Data Fig. 8g–n)

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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.