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This looks like important evidence. It’s not only very interesting that VCAM1 has been identified as a player in these processes, but even more so that there seems to be an opportunity for therapy (I honestly would not have been optimistic about the latter, but I’m glad to be wrong). It’s also worth noting that circulating VCAM1 is increased in many other chronic disease states in humans, as well as with aging in general, and it’s exciting to consider that this might be one of the too-much-inflammation bad actors that can be targeted. There’s still a lot to be unraveled – for example, what’s happening downstream of VCAM signaling to cause the trouble? You’d figure that it’s leukocyte-related, but there’s a lot to find out (and that may reveal additional ideas for intervention). How do the microglia and hippocampal cells know what’s going on, and by what pathways do they react? All this is well worth study – but another thing that’s well worth study is the effect of VCAM inhibition in the brains of more animal models, and if those bode well, in humans too. Here’s hoping that something comes of it!