Taken together, these in vitro and in vivo findings indicate that the increased mobilisation of mitochondria from the neuronal cell body to the axon by targeting of PGC1α pathway and over-expression of Miro1 enhances ARMD in wild type neurons and protects acutely demyelinated axons from degeneration. The gene discussed is PPARGC1A; the disease is age-related macular degeneration.