Licci Maria and Oettinghaus Björn
Pharmacological inhibition of dynamin-related protein 1 (Drp1), the major promoter of mitochondrial fission in mammals, has emerged as a promising therapeutic target for the treatment of neuronal injury. However, genetic studies have shown that inhibition of Drp1 during development leads to defects, particularly in neuronal differentiation. To circumvent this neurodevelopmental defect, a number of recent studies have genetically deleted Drp1 in different neuronal subpopulations of adult cells. This has provided new insights into the importance of mitochondrial fission in differentiated neurons and highlighted potentially serious side effects of this new therapeutic strategy.