Mammalian dendritic regrowth: a new perspective on neural repair

Abstract

This scientific commentary refers to ‘Insulin signalling promotes dendrite and synapse regeneration and restores circuit function after axonal injury’, by Agostinone et al. (doi:10.1093/brain/awy142).

Figure 1

Little is known about adult mammalian dendrite regeneration. Along with somata and axons, dendrites degenerate in CNS injuries (including optic nerve transection) and diseases (including glaucoma). Despite the obvious importance of dendrites to CNS function, and the interdependence (arrows) between neuronal compartments for both degeneration and regeneration/protection/replacement, much more research has been directed toward axon regeneration and soma replacement/protection. A simplified measure of this disparity is the relative number of publications found on PubMed (search terms in parentheses, asterisk represents wildcard), which reveals that for every one dendrite regeneration paper, there are ∼15 publications on axon regeneration and 50 for neuron survival. In this issue of Brain, Agostinone et al. identify a role for insulin/mTOR signalling in dendrite regeneration. Note common targets, including mTOR, as well as unique targets, and possible antagonism of dendrite growth on axon growth (bar-headed line). This simplified diagram does not include data from non-mammalian or developmental models and is not exhaustive. Axon and dendrite protection strategies likely require very early clinical intervention and are therefore noted but not emphasized here.