Thanks, Silvia!

Thanks, Sandro - hope you're well!

Overall, our work supports that TIMP2 (and likely other unexplored youth-associated factors) could be important for reducing microglial dysfunction in age-related disorders. Thanks for reading! (end).

TIMP2 ⬇️ microglial activation, ⬆️ phagocytosis, and ⬇️ the proportion of microglia associated with deleterious processes, including pro-inflammatory processes and senescence—essentially reversal of several age-associated microglial phenotypes. (5/n)

Since key changes in microglia are seen regardless of which TIMP2 pool is targeted, we wondered if ⬆️the extracellular pool mitigates age-related microglial changes. Since TIMP2 gets into brain f/ blood, we gave aged mice systemic TIMP2 injections. (4/n)

TIMP2 deficiency ⬆️microgliosis, ⬇️phagocytosis, and induces transcriptomic changes associated w/ activation + cytokine production. Hippocampal microdialysis revealed that TIMP2 loss ⬆️cellular stress and inflamm. proteins in the extracellular space. (3/n)

We prev. found that TIMP2 regulates hippocampal plasticity. Since microglia regulate plasticity, we looked at how differing TIMP2 sources affect microglial state and function by targeting global, neuronal, and microglial contributions to the TIMP2 pool. (2/n)

Special thanks to her fantastic committee, incl. her committee chair Anne Schaefer (pictured), @scottrussophd.bsky.social , @mcalpinelab.bsky.social , and @cheadlelab.bsky.social for invaluable guidance. She's seeking postdoc opps. in the Boston area (incl. NH/RI)—reach out if interested!

Congrats, Nick!

Congrats to you and the whole team!! 👏🍾

Fantastic study - congrats!!!

Great pack - can you please add me?

I'd love to be added - thanks for organizing the list!

Thx - good to see you here!