In a paper appearing in this week's Early Edition, researchers at Johns Hopkins University School of Medicine and at the University of California, Irvine, show that deletion of Lhx2 in aging mice induces constitutive reactive gliosis, which then reduces "rates of ongoing apoptosis and compromised both rod and cone photoreceptor function." The Hopkins-Irvine team adds that these animals also "showed a dramatically reduced ability to induce expression of secreted neuroprotective factors and displayed enhanced rates of apoptosis in light-damage assays." Overall, the researchers say their study