Please join us TOMORROW at 11.30 at UZH Irchel or online for talks by @seppedeschepper.bsky.social on the gut–brain axis in Parkinson’s disease and @laura-moberbichler.bsky.social
on the IRF5–PPARγ axis in neuroinflammation. See the flyer for more details.
Microglial CD31 suppresses Aβ clearance and promotes Alzheimer pathology in 5×FAD mice
www.nature.com/articles/s41...
The #buechlerlab is looking for #postdoc(s) to study how #fibroblasts control #inflammation and #immunity. Please see below and reach out if you are interested~ www.buechlerlab.com
Immunity
TGF-β: A master regulator of tissue-resident macrophage identity and function #immunology
Tour du force on how #fibroblast subsets can drive rheumatoid arthritis in #natureimmunology. Huge congrats to @arthritisbham, Mark Coles and team at #Oxford. Check it out: www.nature.com/articles/s41...
Swiss Myeloid League (SMyLe)
Astrocyte-microglia crosstalk via CSF1 and IFN-β promotes central nervous system repair
hello world.
Excited to launch the Ingelfinger Lab account! We’re a young lab in Germany’s Black Forest tackling key questions in immunology with innovative single-cell technologies.
Follow us for updates on systems immunology, machine learning & translational oncology.
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Andrew Octavian Sasmita
BuechlerLab
BuechlerLab
Alzheimer’s Society has announced £5.45m to fund 17 new research awards @alzheimerssoc.bsky.social
Join us live at 11am BST on Thurs 25 June as Alice Carstairs introduces the awardees with short talks from funded researchers on their new projects.
www.dementiaresearcher.nihr.ac.uk/introducing-...
Trends in Immunology
Now online! Persistent and transient senescent cells contribute to brain-barrier development
Cell Reports
Ingelfinger Lab
Cell - a Cell Press journal
Dementia Researcher
Altered astrocyte-microglia interactions have been implicated in the pathogenesis of Alzheimer’s disease, but the underpinning mechanisms remain unclear. Zhang and colleagues show that astrocytic PAD2-mediated citrullination of vimentin activates microglia, worsens Aβ accumulation, and exacerbates cognitive deficits. These findings highlight astrocyte-microglia crosstalk as a potential therapeutic target for Alzheimer’s disease.
