Archives of General Internal Medicine

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Short Communication - Archives of General Internal Medicine (2023) Volume 7, Issue 4

Prognostic Epigenetic Markers for Neurotrauma Outcomes.

Shehbaz Khan*

Department of Neurology, University of London, London, UK

*Corresponding Author:
Shehbaz Khan
Department of Neurology
London, UK
China
E-mail: shehbaz455@hotmail.com

Received:29-Jul-2023, Manuscript No. AAAGIM-23-109494; Editor assigned:03-Aug-2023, PreQC No. AAAGIM-23-109494 (PQ); Reviewed:17-Aug-2023, QC No. AAAGIM-23-109494; Revised:22-Aug-2023, Manuscript No. AAAGIM-23-109494 (R); Published:30-Aug-2023, DOI:10.35841/ aaaa-7.4.187

Citation: Khan S. Prognostic Epigenetic Markers for Neurotrauma Outcomes. Arch Gen Intern Med. 2023;7(4):190

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Introduction

Neurotrauma, which includes traumatic brain injury (TBI) and spinal cord injury (SCI), is still a major worldwide health concern, impacting millions of people each year and causing significant morbidity and mortality. Because the severity and course of recovery can vary greatly even among individuals with comparable injuries, the complex nature of neurotrauma provides particular obstacles in forecasting patient outcomes. This variation highlights the crucial need for more precise and personalised prognostic tools to guide treatment decisions and improve patient care. The topic of epigenetics has developed as a promising path of research in recent years, offering information on the molecular mechanisms that govern gene expression and cellular function. Epigenetic alterations like as DNA methylation, histone modifications, and non-coding RNA expression are important in controlling gene function without changing the underlying DNA sequence. They are dynamic and receptive to both inner and external inputs, which makes them appealing candidates for affecting the fate of neurotraumatic injuries[1].

The purpose of this review is to look into the potential of epigenetic markers as prognostic indicators for neurotrauma outcomes. We will examine how epigenetic modifications influence cellular responses, neuroinflammation, neuroplasticity, and recovery trajectories in the setting of TBI and SCI, as well as the present state of knowledge. We may foresee a future in which clinicians can better predict patient recovery and adjust treatment regimens based on the identification and comprehension of certain epigenetic markers associated with favourable or poor outcomes[2].

The incorporation of epigenetic knowledge into clinical practise has enormous promise for neurotrauma patient care. The translation of epigenetic markers into prognostic biomarkers is becoming more feasible with the advent of non-invasive technologies for epigenetic profiling and developments in computer tools for data processing. Furthermore, tailored therapies focused at modifying epigenetic alterations have the tantalising promise of improving patient outcomes through neuroregeneration, neuroinflammation reduction, and neuroplasticity enhancement. However, difficulties are ahead. To validate and refine the utility of epigenetic markers as prognostic tools, more large-scale studies and longitudinal research are required. To guarantee responsible and equitable adoption in clinical practise, ethical questions surrounding the use of epigenetic knowledge must also be properly addressed[3].

Epigenetics refers to heritable changes in gene expression that do not involve alterations in the DNA sequence itself. Instead, epigenetic modifications, such as DNA methylation, histone modifications, and non-coding RNA expression, regulate gene activity and play a critical role in various physiological and pathological processes. In the context of neurotrauma, epigenetic mechanisms can influence the response of the nervous system to injury and significantly impact patient outcomes. DNA methylation involves the addition of a methyl group to the cytosine bases in DNA, typically occurring at CpG dinucleotides. Hypermethylation of specific gene promoters can lead to gene silencing, while hypomethylation can result in gene activation. In neurotrauma, alterations in DNA methylation patterns have been observed in various brain regions following traumatic brain injury. Specific genes involved in neuroinflammation, synaptic plasticity, and axonal regeneration have been found to undergo epigenetic changes that influence the recovery process. Histone modifications, such as acetylation, methylation, phosphorylation, and ubiquitination, affect the accessibility of DNA to transcriptional machinery, thereby influencing gene expression. In neurotrauma, changes in histone acetylation and methylation have been linked to altered gene expression patterns associated with neuroinflammation and neuroplasticity. Targeting histone-modifying enzymes has shown promise in preclinical studies as a means to promote recovery after neurotrauma. Non-coding RNAs, including microRNAs (miRNAs) and long non-coding RNAs (lncRNAs), are critical regulators of gene expression. MiRNAs bind to target mRNAs, leading to their degradation or translational inhibition, while lncRNAs can influence gene expression through various mechanisms. In neurotrauma, dysregulation of specific miRNAs has been associated with processes such as neuronal apoptosis, neuroinflammation, and neuroregeneration, highlighting their potential as prognostic markers for outcomes. Epigenetic modifications play a significant role in modulating the neuroinflammatory response following neurotrauma. Dysregulated epigenetic regulation of pro-inflammatory genes can lead to an exacerbated inflammatory response, contributing to secondary brain damage and impaired recovery. Conversely, epigenetic changes that promote an anti-inflammatory environment may facilitate neuroprotection and repair[4].

Epigenetic mechanisms also influence neuronal plasticity and regeneration after neurotrauma. Epigenetic modifications can control the expression of genes involved in axonal growth, synaptogenesis, and synaptic plasticity, affecting the potential for neural repair and functional recovery. The identification of specific epigenetic markers associated with neurotrauma outcomes has the potential for translation into clinical practice. These markers could be used as prognostic indicators to assess the severity of injury and predict recovery trajectories in individual patients. Additionally, epigenetic therapies, such as drugs targeting epigenetic modifiers, may be explored to modulate gene expression and promote neuroregeneration. Despite the promising potential of epigenetic markers for neurotrauma outcomes, several challenges need to be addressed. Large-scale, longitudinal studies are required to validate the prognostic utility of specific epigenetic signatures. Additionally, ethical considerations surrounding the use of epigenetic information, such as privacy concerns and potential stigmatization, must be carefully addressed to ensure responsible implementation in clinical settings[5].

References

  1. Wagner AK, McCullough EH, Niyonkuru C, et al. Acute serum hormone levels: characterization and prognosis after severe traumatic brain injury. J Neurotrauma. 2011;28(6):871-88.
  2. Indexed at, Google Scholar,Cross Ref

  3. Korley FK, Diaz-Arrastia R, Wu AH, et al. TRACK-TBI investigators including, Okonkwo DO, Valadka AB. Circulating brain-derived neurotrophic factor has diagnostic and prognostic value in traumatic brain injury. J Neurotrauma. 2016;33(2):215-25.
  4. Indexed at, Google Scholar,Cross Ref

  5. Hakiki B, Donnini I, Romoli AM, et al. Neurophysiological, and Genetic Predictors of Recovery in Patients With Severe Acquired Brain Injuries (PRABI): A Study Protocol for a Longitudinal Observational Study. Front Neurol. 2022;13:711312.
  6. Indexed at, Google Scholar, Cross Ref

  7. Zhang BY, Chang PY, Zhu QS, et al. Decoding epigenetic codes: new frontiers in exploring recovery from spinal cord injury. Neural Regen Res. 2020;15(9):1613.
  8. Indexed at, Google Scholar, Cross Ref

  9. Saatman KE, Duhaime AC, Bullock R, et al. Classification of traumatic brain injury for targeted therapies. J Neurotrauma. 2008;25(7):719-38.
  10. Indexed at, Google Scholar, Cross Ref

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