Leveraging neural plasticity for the treatment of amblyopia

Abstract

Amblyopia is a form of visual cortical impairment that arises from abnormal visual experience early in life. Most often, amblyopia is a unilateral visual impairment that can develop as a result of strabismus, anisometropia, or a combination of these conditions that result in discordant binocular experience. Characterized by reduced visual acuity and impaired binocular function, amblyopia places a substantial burden on the developing child. Although frontline treatment with glasses and patching can improve visual acuity, residual amblyopia remains for most children. Newer binocular-based therapies can elicit rapid recovery of visual acuity and may also improve stereoacuity in some children. Nevertheless, for both treatment modalities full recovery is elusive, recurrence of amblyopia is common, and improvements are negligible when treatment is administered at older ages. Insights derived from animal models about the factors that govern neural plasticity have been leveraged to develop innovative treatments for amblyopia. These novel therapies exhibit efficacy to promote recovery, and some are effective even at ages when conventional treatments fail to yield benefit. Approaches for enhancing visual system plasticity and promoting recovery from amblyopia include altering the balance between excitatory and inhibitory mechanisms, reversing the accumulation of proteins that inhibit plasticity, and harnessing the principles of metaplasticity. Although these therapies have exhibited promising results in animal models, their safety and ability to remediate amblyopia need to be evaluated in humans.