Gerontology & Geriatric Research

Investigating the Chronic Effects of a Single Low-intensity Blast Exposure on Phosphoproteome

Alexis Gordon^* Department of Clinical Gerontology and Geriatric Rehabilitation, Cairo University, Giza Governorate 12613, Egypt
^*Correspondence: Alexis Gordon, Department of Clinical Gerontology and Geriatric Rehabilitation, Cairo University, Giza Governorate 12613, Egypt, Email:

Received: 01-Feb-2024, Manuscript No. jggr-24-25270; Editor assigned: 02-Feb-2024, Pre QC No. P-25270; Reviewed: 16-Feb-2024, QC No. Q-25270; Revised: 22-Feb-2024, Manuscript No. R-25270; Published: 29-Feb-2024, DOI: 10.35248/2167-7182.2024.13.713

Introduction

Blast-induced traumatic brain injury is a significant concern in military and civilian populations exposed to explosive blasts. While the acute effects of blast exposure on the brain have been extensively studied, the chronic repercussions, particularly at the molecular level, remain less understood. This article explores the emerging research on the chronic effects of a single low-intensity blast exposure on the phosphoproteome, shedding light on the intricate molecular mechanisms underlying long-term neurological consequences.

Blast-induced traumatic brain injury poses a critical health challenge globally, affecting military personnel, first responders, and civilians exposed to explosive events. While the acute manifestations of bTBI are well-documented, including cognitive impairments, memory deficits, and motor dysfunction, understanding the long-term molecular alterations following blast exposure remains a frontier in neurotrauma research. Recent studies have begun to unravel the chronic effects of blast exposure on the phosphoproteome, providing insights into the persistent molecular changes underlying neurological dysfunction [1-3].

Description

Blast-induced alterations in phosphoproteome signaling pathways have been observed weeks to months post-exposure, suggesting persistent dysregulation of cellular signaling cascades. Dysregulation of key phosphorylation events within intracellular signaling pathways, such as MAPK/ERK and PI3K/AKT, may contribute to long-term synaptic dysfunction and neuronal degeneration. Chronic changes in the phosphoproteome are associated with alterations in neuronal plasticity and synaptic function, leading to long-lasting deficits in learning and memory. Dysregulated phosphorylation of synaptic proteins, including NMDA and AMPA receptors, impairs synaptic transmission and neuronal connectivity, contributing to cognitive dysfunction.

Prolonged alterations in phosphoproteome signaling are implicated in the sustained inflammatory response and neurodegeneration observed post-bTBI. Aberrant phosphorylation of proteins involved in the regulation of neuroinflammation, such as NF-κB and STAT3, perpetuates neuroinflammatory cascades, exacerbating neuronal damage. Chronic dysregulation of mitochondrial phosphoproteome following blast exposure compromises mitochondrial function and exacerbates oxidative stress. Impaired phosphorylation of mitochondrial proteins involved in electron transport chain complexes and antioxidant defense mechanisms disrupts cellular energy homeostasis and promotes neuronal vulnerability to oxidative damage [4,5].

Advances in phosphoproteomic techniques, such as mass spectrometry-based phosphoproteomics and phospho-specific antibodies, enable comprehensive profiling of phosphorylation dynamics post-blast exposure. Integration of phosphoproteomic data with other omics approaches, including transcriptomics and metabolomics, offers a systems-level understanding of the molecular pathways underlying chronic bTBI. Future studies should focus on elucidating the temporal dynamics of phosphoproteome alterations and their functional consequences on neuronal physiology and behavior using longitudinal experimental designs.

Conclusion

Understanding the chronic effects of a single low-intensity blast exposure on the phosphoproteome provides valuable insights into the molecular mechanisms driving long-term neurological consequences post-bTBI. Targeting dysregulated phosphorylation events and associated signaling pathways may offer novel therapeutic strategies for mitigating the chronic sequelae of blastinduced neurotrauma and improving long-term neurological outcomes in affected individuals.

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