Abstract
Autophagy induction is an attractive therapeutic approach to ameliorate aggregate accumulation in many neurodegenerative diseases. In Huntington's disease (HD) in vivo models, a number of genetic and pharmacological mechanisms aimed to induce autophagy have been successfully tested [1], demonstrating the role of autophagy in promoting the elimination of mutant huntingtin (mHTT) aggregates and its neuroprotective effect. In their recent report in Cells, Vernizzi and colleagues [2] presented a totally new mechanism to induce autophagy, promote the elimination of mHTT aggregates, and ultimately achieve neuroprotection. This novel therapy is based on the overexpression of glutamine synthetase 1 (GS1), an enzyme that catalyzes the synthesis of L-glutamine from L-glutamate as part of the glutamate glutamine cycle (GGC), a physiological process between glia and neurons that controls glutamate homeostasis [3].[...].
