Mini Review - (2023) Volume 14, Issue 4
Received: 02-Aug-2023, Manuscript No. jmbd-23-111658;
Editor assigned: 04-Aug-2023, Pre QC No. P-111658;
Reviewed: 16-Aug-2023, QC No. Q-111658;
Revised: 21-Aug-2023, Manuscript No. R-111658;
Published:
28-Aug-2023
, DOI: 10.37421/2155-9929.2023.14.591
Citation: Spena, Mario. “Neuro-Enzyme Marker: Unveiling Connections to Autism Spectrum Disorder.” J Mol Biomark Diagn 14 (2023): 591.
Copyright: © 2023 Spena M. This is an open-access article distributed under
the terms of the creative commons attribution license which permits unrestricted
use, distribution and reproduction in any medium, provided the original author and
source are credited
The search for reliable biomarkers to aid in the early detection and understanding of Autism Spectrum Disorder (ASD) has been an ongoing endeavor in the field of neurology and psychiatry. The study delves into the potential significance of Neuron-Specific Enolase (NSE) as a promising biomarker for ASD. This review consolidates recent research findings that highlight NSE's role as a sensitive indicator of neuronal activity and its correlation with ASD-related pathophysiology. Through an exploration of the molecular mechanisms underlying ASD, the paper elucidates the rationale behind NSE's potential involvement in the disorder. Additionally, this review underscores the importance of early ASD diagnosis and intervention, emphasizing NSE's viability as a non-invasive and accessible candidate biomarker. As the field of neurology continues to advance, the integration of NSE as a diagnostic tool could pave the way for improved ASD management and a deeper comprehension of the intricate neurodevelopmental origins of the disorder. However, the paper also acknowledges the need for further research to validate NSE's utility, suggesting avenues for future investigations.
Autism spectrum disorder • Neuron-specific enolase • Neurodevelopmental disorder • Biomarker
Autism Spectrum Disorder (ASD) is a complex neurodevelopmental condition characterized by a range of social, communication, and behavioral challenges. Despite significant advancements in understanding the underlying biology of ASD, early diagnosis and effective intervention remain pressing challenges. The quest for reliable biomarkers that could facilitate early detection, shed light on the disorder's pathophysiology, and guide personalized treatments has garnered considerable attention within the scientific community. Among the candidates, Neuron-Specific Enolase (NSE), an enzyme predominantly expressed in neurons, has emerged as a potential neuro-marker for ASD. This review examines the intricate interplay between NSE and ASD, drawing connections from recent research and proposing avenues for future investigation [1].
Autism Spectrum Disorder (ASD) is a neurodevelopmental condition characterized by persistent challenges in social interaction, communication, and restricted/repetitive behaviors. The etiology of ASD remains multifaceted, encompassing genetic, environmental, and neurobiological factors. Early diagnosis and intervention are crucial for improving outcomes in individuals with ASD. The search for biomarkers that can aid in early identification, elucidate underlying mechanisms, and guide therapeutic strategies has gained significant attention. Neuron-Specific Enolase (NSE), an enzyme primarily expressed in neurons, has emerged as a potential biomarker, offering insights into the neurobiological intricacies of ASD.
Neuron-Specific Enolase (NSE) as a candidate biomarker: NSE is a glycolytic enzyme found predominantly in neurons and neuroendocrine cells. Its release into the bloodstream in response to neuronal injury or damage makes it a compelling candidate for investigating neurological disorders, including ASD. Recent studies have explored the association between NSE levels and ASD, revealing potential correlations that warrant further investigation. NSE's specificity to neurons suggests that alterations in its expression could reflect neurodevelopmental irregularities underlying ASD [2].
Neurobiological mechanisms: The link between NSE and ASD lies in their shared involvement in neuronal metabolism and function. Dysregulated energy metabolism is a hallmark of ASD, with implications for neuronal activity and connectivity. NSE's role in glycolysis positions it at the intersection of energy homeostasis and neuronal health. Dysfunctional energy metabolism and oxidative stress are believed to contribute to ASD pathogenesis. NSE's involvement in these processes raises intriguing questions about its potential role as a mediator or indicator of neurobiological abnormalities in ASD [3].
Clinical implications and early detection: Early diagnosis of ASD is pivotal for initiating tailored interventions that improve outcomes. NSE's accessibility through peripheral blood samples offers a non-invasive means of assessing neuronal health. Elevated NSE levels could potentially serve as an early indicator of neuronal damage or dysfunction, prompting further evaluation and intervention. The integration of NSE measurements into diagnostic protocols could enable clinicians to identify individuals at risk for ASD and implement interventions during critical developmental periods.
Limitations and future directions: While the potential of NSE as a biomarker for ASD is promising, several limitations and challenges need to be addressed. The variability in NSE levels across individuals, age groups, and other factors necessitates rigorous standardization and validation studies. Longitudinal research is required to establish the temporal relationship between NSE alterations and the onset/progression of ASD symptoms. Additionally, investigating the specificity of NSE changes to ASD compared to other neurodevelopmental and neurological disorders is crucial for its clinical utility.
Neuron-Specific Enolase (NSE), an enzyme involved in glycolysis and neuronal energy metabolism, has garnered attention for its potential as a biomarker due to its specificity to neurons and its release into the bloodstream upon neuronal damage or injury. Recent studies have revealed intriguing correlations between NSE levels and ASD. Neurological abnormalities observed in individuals with ASD, such as altered synaptic connectivity and neuronal hyperactivity are accompanied by changes in NSE expression [4,5]. Furthermore, the review delves into the molecular mechanisms that might link NSE to ASD. Dysregulated neuronal metabolism, oxidative stress, and inflammation are proposed pathways that could contribute to altered NSE levels in individuals with ASD. The intricate balance between NSE's role in energy metabolism and its impact on neuronal function adds complexity to its potential role in ASD pathogenesis. The review also emphasizes the practical implications of NSE as a potential biomarker for ASD. Early detection of ASD is crucial for timely intervention, as it allows for the implementation of tailored therapeutic strategies during the critical developmental window. NSE's accessibility through blood tests provides a non-invasive means of assessing neuronal health, potentially enabling clinicians to identify at-risk individuals and initiate interventions to mitigate the severity of ASD symptoms [6].
In conclusion, "Neuro-Enzyme Marker: Unveiling Connections to Autism Spectrum Disorder (ASD)" sheds light on the intricate relationship between Neuron-Specific Enolase (NSE) and ASD. While our understanding of ASD's etiology and pathophysiology continues to evolve, NSE stands out as a promising neuro-marker that could contribute to the early detection, comprehension, and management of ASD. However, it is imperative to recognize that the field is still in its infancy, and further research is needed to validate NSE's utility as a reliable biomarker. Continued investigations exploring the link between NSE, neuronal health, and ASD pathogenesis are necessary to unravel the full potential of this marker. Ultimately, the integration of NSE into the diagnostic toolkit could mark a significant stride towards enhancing the lives of individuals affected by ASD through earlier interventions and a deeper understanding of the disorder's neurobiological underpinnings.
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There are no conflicts of interest by author.
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