Research group interested in neuroinflammation, de- and regeneration in the injured or aged CNS. Headed by Prof. Dr. Moons @BiologyKULeuven @KU_Leuven, Belgium

Leuven
Joined November 2020
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Preprint out! 📄🥳🥳 Using the killifish optic nerve, we show that aging alone is sufficient to trigger the emergence of interferon-responsive oligodendrocytes, a cell state shared with neurodegenerative and demyelinating diseases. biorxiv.org/content/10.64898…
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Don't miss this amazing meeting in Austria! Deadline 20 May 2026!! #EMBORegeneration2026
The registration deadline for #EMBORegeneration2026 is approaching: May 20 !!! Don't miss this amazing meeting on the banks of the Danube in Austria: meetings.embo.org/event/26-t…
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To reduce the extensive scarring, we performed a partial optic nerve transection in young adults, leaving a portion of the nerve uninjured. This approach indeed limited scar formation, and it allowed regenerating axons to reach the brain and reinnervate their targets. ✅
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Why does this happen? 🔎 A gliofibrotic scar forms at the injury site, an injury response typically associated with mammals. So the axons keep growing, but they physically and chemically can’t overcome the barrier. The result: permanent vision loss.
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Even more intriguing: the retinal ganglion cells in killifish retain their intrinsic growth potential. 🧐 However, instead of navigating towards the brain, they misdirect and loop within the retina (yellow arrowheads).
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Adult killifish — both young and old — fail to reinnervate their brain target after complete optic nerve transection. 🐠🧠👁️ This is surprising, as most teleost fish are able to fully restore neural circuitry and regain visual function after this type of injury.
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A new preprint from our lab is out! 🥳 Huge congrats to @AnyiZhang2 and @LucaMasin for this great paper titled: Repressed mTORC1 signaling and transient dendritic pruning support axonal regeneration! Grateful for the fruitful collaboration with the @filodelbene and @Poulain lab!
🚨New preprint out!🚨 I’m excited to share the latest work by @AnyiZhang2 and me, which shows that mTORC1-dependent transient dendritic pruning is essential for efficient axonal regeneration in spontaneously regenerating zebrafish neurons. biorxiv.org/content/10.64898…
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With transcriptomic and functional data, @lucamasin.bsky.social et al. @labmoons.bsky.social show that local glycolysis supports injury-induced axonal regeneration. hubs.la/Q03SCLtG0 📕 In Cellular Neurobiology collection hubs.la/Q03SCy560 #SfN25
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Proud to be one of the best poster presenters of GRC CNS injury and repair meeting 🥳 Big thanks to the organisers giving me this opportunity! Also big thanks to our lab members @LabMoons, especially our excellent post doc @LucaMasin. I could not achieve this without him 😊
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All these data were generated by an updated version of RGCode, RGCode2. An automated cell counting platform able to reliable count murine, zebrafish and killifish retinal ganglion cells using RBPMS and Rbpms2 as marker! RGCode2 is publicly available gitlab.com/NCDRlab/rgcode2
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Killifish, an aging model shown to lose its regenerative capacity with age, displays a unique biphasic RGC loss profile. Both young adult and old killifish present with a similar degree of RGC loss during the first wave. Old fish, however, lose more RGCs during the second wave.
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After optic nerve crush (ONC), mice lose ~80% of their RGC by 14 days post injury (dpi). In contract, zebrafish retain nearly all RGC during the first two weeks, before presenting with late RGC degeneration (~13%) by 21dpi.
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Comparing mice, zebrafish and killifish, we were able to determine the differences in retinal ganglion cell (RGC) density between species. Fish species of an equivalent life stage have a five-fold higher density compared to mice. With age, RGC density decreases in killifish.
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We have a 3 year postdoc position using the killifish to study retinal ageing available in my lab. Based in London, UK and visa eligible. We’re interested in glial mechanisms underpinning age-related neurodegeneration. If you, or someone you know, is interested please reach out.
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Killifish, an aging model shown to lose its regenerative capacity with age, displays a unique biphasic RGC loss profile. Both young adult and old killifish present with a similar degree of RGC loss during the first wave. Old fish, however, lose more RGCs during the second wave.
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After optic nerve crush (ONC), mice lose ~80% of their RGC by 14 days post injury (dpi). In contract, zebrafish retain nearly all RGC during the first two weeks, before presenting with late RGC degeneration (~13%) by 21dpi.
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