Epigenetic mechanisms of neuroplasticity and the implications for stroke recovery

- There is a defined period after stroke during which mechanisms of neuroplasticity contribute to recovery
- Neurogenesis, axon sprouting and growth, and synaptic remodeling are important components of neuroplasticity after stroke
- DNA methylation status, histone modifications, and microRNAs can influence mechanisms of neuroplasticity
- Further investigation is necessary to understand the role of epigenetic mechanisms in stroke recovery

Ischemic stroke is a devastating brain injury and an important cause of neurologic disability worldwide and across the lifespan. Despite the physical, social, and economic burdens of this disease there is only a single approved medicine for the treatment of acute stroke, and its use is unfortunately limited to the small fraction of patients presenting within the narrow therapeutic window. Following stroke, there is a period of plasticity involving cell genesis, axon growth, and synaptic modulation that is essential to spontaneous recovery. Treatments focusing on neuroprotection and enhancing recovery have been the focus of intense preclinical studies, but translation of these treatments into clinical use has been disappointing thus far. The important role of epigenetic mechanisms in disease states is becoming increasingly apparent, including in ischemic stroke. These regulators of gene expression are poised to be critical mediators of recovery following stroke. In this review we discuss evidence for the role of epigenetics in neuroplasticity and the implications for stroke recovery.