A study the Alzforum has previously described to our audience formally appeared in Cell on December 12. In the paper, first author Beth Stevens in Ben Barres's laboratory at Stanford University in Palo Alto, California, collaborated with Kristina Micheva in Steven Smith's lab, also at Stanford, as well as with physicists at the University of California in Santa Cruz and others. The team report their discovery that the classical complement cascade, long known for its established role in removing infected cells and cellular debris, also functions to eliminate excess synapses during embryonic and postnatal brain development. In particular, the scientists report that astrocytes trigger the production of C1q, the upstream protein starting the complement cascade. Once the physiological period of synapse pruning is over, C1q expression ceases. This research is noteworthy not only for its broadening of the basic biology of the complement cascade, but also because C1q is known to become re-expressed in Alzheimer's, amyotrophic lateral sclerosis, and glaucoma, three neurodegenerative processes marked by synapse loss and reactive astrocytes.—Gabrielle Strobel.

Reference:
Stevens B, Allen NJ, Vazquez LE, Howell GR, Christopherson KS, Nouri N, Micheva KD, Mehalow AK, Huberman AD, Stafford B, Sher A, Litke AM, Lambris JD, Smith SJ, John SWM, Barres BA. The Classical Complement Cascade Mediates CNS Synapse Elimination. Cell. 2007. Abstract

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References

Paper Citations

  1. . The classical complement cascade mediates CNS synapse elimination. Cell. 2007 Dec 14;131(6):1164-78. PubMed.

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Papers

  1. . The classical complement cascade mediates CNS synapse elimination. Cell. 2007 Dec 14;131(6):1164-78. PubMed.

Primary Papers

  1. . The classical complement cascade mediates CNS synapse elimination. Cell. 2007 Dec 14;131(6):1164-78. PubMed.