Senescent-like microglia limit remyelination through the senescence associated secretory phenotype - Nature Communications The impact of senescent cells on remyelination is unknown. Here, the authors show that treatment with senolytics following demyelination enhances remyelination in young, but not aged mice, and these effects are mediated by senescence-associated secretory phenotype factors including CCL11.

Research Spotlight💡
A new study shows senescent cells accumulate in lesions and impair #myelin repair—especially with age. Senolytics improved remyelination in younger mice, highlighting #senescence as a key barrier in aging & #MultiplesSclerosis.
https://www.nature.com/articles/s41467-025-57632-w

We built in the US the best scientific industry in world history and it is dying.

Fixing just the damage done since Jan 20 would take years. Maybe a decade. The program staff, SROs, and brilliant talent is not coming back.

Thanks! Complimentary results to what you found in EAE

Senolytic therapy in mild Alzheimer’s disease: a phase 1 feasibility trial - Nature Medicine The first feasibility study of orally delivered senolytic therapy in Alzheimer’s disease reports favorable safety data and penetrance of dasatinib into the brain with a modest impact on Alzheimer’s an...

Thanks! So far I think information is limited on D/Q ability to cross the BBB, but this study here (doi.org/10.1038/s415...) shows elevated levels in csf of D but not Q. Newer next generation senolytics that target apoptosis pathways better may cross better though.

Senescent-like microglia limit remyelination through the senescence associated secretory phenotype - Nature Communications The impact of senescent cells on remyelination is unknown. Here, the authors show that treatment with senolytics following demyelination enhances remyelination in young, but not aged mice, and these e...

‪Congratulations Phil @philgrossphd.bsky.social and a huge thank you to all the lab members and collaborators for their contributions to our project on the role of senescence in remyelination, which has now been published in @naturecomms.bsky.social! 😀 www.nature.com/articles/s41...

Check out this exciting work by @philgrossphd.bsky.social in the @jkhuang.bsky.social lab! Thanks for asking us to be a part of it

A big thank you to my mentor @jkhuang.bsky.social and members of the lab @zeebamehrin.bsky.social and all of our collaborators who were amazing to work with @mengmengfu.bsky.social @jrplemel.bsky.social

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We find this is (partially) mediated by CCL11, which we find is sufficient to limit oligodendrocyte maturation, and has been shown to impair neuro-regeneration w/ age and is involved in long covid neurological deficits (as shown by @michellemonje.bsky.social, among others)

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Senescent-like microglia limit remyelination through the senescence associated secretory phenotype - Nature Communications The impact of senescent cells on remyelination is unknown. Here, the authors show that treatment with senolytics following demyelination enhances remyelination in young, but not aged mice, and these e...

Excited to finally have this published! Out today in @naturecomms.bsky.social, we show that following demyelination in a mouse model of Multiple Sclerosis, treatment of senescent microglia with senolytics leads to improved remyelination. www.nature.com/articles/s41...

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Very excited that Phil Gross @PSGrossScience @georgetown #IPN #GUBiology has successfully defended his PhD thesis on the role of cellular senescence in CNS remyelination. Next stop a postdoc at the NIH. Congratulations Dr. Gross! 🎉🎉🎉🍾🍾🍾