Current Neurobiology Open Access

Targeting Epigenetic Modifications for Neuroprotection in Stroke and Traumatic Brain Injury

Min Choi^* Department of Neurobiology, Shanghai Jiao Tong University, China
^*Correspondence: Min Choi, Department of Neurobiology, Shanghai Jiao Tong University, China, Email:

Received: 02-Sep-2024, Manuscript No. jcnb-24-21680; Editor assigned: 04-Sep-2024, Pre QC No. jcnb-24-21680 (PQ); Reviewed: 18-Sep-2024, QC No. jcnb-24-21680; Revised: 23-Sep-2024, Manuscript No. jcnb-24-21680 (R); Published: 30-Sep-2024, DOI: 10.21767/JCNB-24.3.30

Introduction

Stroke and Traumatic Brain Injury (TBI) are leading causes of morbidity and mortality worldwide. Both conditions result in significant neuronal loss and functional impairments, leading to long-term disabilities. Current therapeutic approaches primarily focus on acute management and rehabilitation, often with limited effectiveness in preventing neuronal damage or promoting recovery. However, emerging research suggests that targeting epigenetic modifications may provide novel strategies for neuroprotection and recovery in stroke and TBI patients. This article explores the role of epigenetics in neuronal response to injury and the potential therapeutic implications. These modifications can be influenced by environmental factors and can impact cellular functions significantly. The most common types of epigenetic modifications include DNA methylation, histone modification, and non-coding RNA regulation. In the context of neurobiology, these modifications play a critical role in regulating gene expression in response to various stimuli, including injury. Both stroke and TBI lead to complex biochemical and cellular responses in the brain. Following injury, a cascade of inflammatory responses, oxidative stress, and metabolic dysregulation occurs, resulting in neuronal death and dysfunction. Research has shown that these injury-induced changes are associated with significant alterations in epigenetic regulation.

Description

After a stroke or TBI, changes in DNA methylation patterns can influence the expression of genes involved in neuroinflammation, apoptosis, and neuroprotection. For example, hypermethylation of neuroprotective genes may exacerbate neuronal damage, while demethylation can enhance the expression of proinflammatory mediators. Histone acetylation and methylation also play crucial roles in gene expression regulation following brain injury. Alterations in histone modifications can lead to changes in chromatin structure, influencing the transcriptional activation or repression of genes involved in neuronal survival and repair. Long non-coding RNAs and microRNAs are important regulators of gene expression. Following a stroke or TBI, the expression of specific lncRNAs and miRNAs changes, contributing to the modulation of inflammatory responses and neuronal survival. Epigenetic drugs, such as DNA methyltransferase inhibitors (e.g., azacytidine) and histone deacetylase inhibitors (e.g., valproic acid), can modify epigenetic marks to reactivate silenced neuroprotective genes or suppress harmful inflammatory pathways. Preclinical studies have shown that these agents can promote neuronal survival and functional recovery following stroke and TBI. CRISPR/Cas9 and other gene editing technologies can be employed to selectively modify epigenetic marks at specific genomic locations. This approach enables researchers to investigate the functional impact of individual epigenetic changes and may ultimately lead to targeted therapies that enhance neuroprotection. While targeting epigenetic modifications holds promise for neuroprotection in stroke and TBI, several challenges remain. The complexity of the brain’s epigenetic landscape necessitates a comprehensive understanding of the specific modifications that contribute to injury outcomes. Additionally, the potential for off-target effects and the long-term consequences of modifying epigenetic marks must be carefully considered [1-4].

Conclusion

Targeting epigenetic modifications represents a novel and promising approach to neuroprotection in stroke and traumatic brain injury. By understanding the intricate interplay between epigenetics and neuronal responses to injury, researchers can develop innovative therapeutic strategies that promote neuronal survival and recovery. As our understanding of the epigenetic mechanisms underlying brain injuries advances, it may pave the way for more effective treatments that improve outcomes for patients suffering from stroke and TBI. Future research should focus on identifying specific epigenetic changes associated with different injury types and developing targeted therapies that maximize neuroprotective effects while minimizing adverse outcomes. Furthermore, integrating epigenetic strategies with existing therapeutic approaches may enhance overall treatment efficacy.

Acknowledgement

None.

Conflict Of Interest

The author declares there is no conflict of interest in publishing this article.

References

1. Capizzi A, Woo J, Verduzco-Gutierrez M (2020) Traumatic brain injury: An overview of epidemiology, pathophysiology, and medical management. Med Clin North Am 104(2):213-238.

   [Crossref] [Google Scholar] [PubMed]

2. Sunnerhagen KS, Opheim A, Murphy MA (2019) Onset, time course and prediction of spasticity after stroke or traumatic brain injury. Ann Phys Rehabil Med 62(6):431-434.

   [Crossref] [Google Scholar] [PubMed]

3. Larson CM, Wilcox GL, Fairbanks CA (2019) Defining and managing pain in stroke and traumatic brain injury research. Comp Med 69(6):510-519.

   [Crossref] [Google Scholar] [PubMed]

4. Hamblin MR (2018) Photobiomodulation for traumatic brain injury and stroke. J Neurosci Res 96(4):731-743.

   [Crossref] [Google Scholar] [PubMed]