The amazing astrocyte.
Nature. 2002 May 2;417(6884):29-32.
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I was not surprised by this paper. Though the abstract says, "This role in fate specification was unexpected," we have already indicated (Brannen & Sugaya, 2000) that astrocytes may contribute to cell fate regulation in human neural stem cells in vitro. We have reported a large population of GFAP-positive cells in earlier stages of differentiation under serum-free conditions and gradual increase in betaIII-tubulin-positive cells in later stages. This indicates that astrocytes may produce some factor(s) to induce neuronal differentiation in human neural stem cells in vitro. We also found that dying neurons produce AβPP fragments, which induced glial differentiation in the neural stem cells in the early stage of serum-free differentiation. We are hypothesizing that AβPP fragments produced by neuronal damage induce astrocyte differentiation or activation, and the activated astrocytes (some type of radial glia?) may recruit and differentiate the neural stem cell to replace the damaged neurons. This mechanism could be very important in adult neurogenesis, and the Song et al. paper proves a part of it in an elegant way.
We have to understand not only the bad side of glial activation (inflammation of the brain), but also the beneficial side of glial activity (including regulation of stem cell biology) in relation to AD pathology. In another words, excess suppression of glial activity or AβPP processing may not be a cure for AD.