Redox homeostasis: unlocking the bottleneck in glia-to-neuron conversion
Recent discoveries in the field of regeneration research inspire great optimism for future therapies aimed at repairing the injured or diseased human brain. Of particular clinical significance is the approach to promote neurogenesis from endogenous parenchymal cells independent of the use of embryonic or induced pluripotent stem cells. Perhaps the most attractive strategy appears to be direct in vivo cell reprogramming to induce a neuronal fate. However, the initial enthusiasm in the field has been tempered, as quantity and quality of replenished neuronal populations have remained low. An exciting new study by Magdalena Goetz and co-workers (1) published in Cell Stem Cell sheds new light on the problem of cell death at the time of fate conversion and emphasizes the importance of coordinated metabolic reprogramming to increase neurogenesis successfully. In this editorial we summarize these critical new findings and consider them in the context of the adult brain’s potential for plasticity and self-regeneration.