Evidence map›Paper›PMID 29463007›Full record

ReviewBrain sciences2018

New Insights into the Role of Neuron-Specific Enolase in Neuro-Inflammation, Neurodegeneration, and Neuroprotection.

Azizul Haque, Rachel Polcyn, Denise Matzelle, Naren L Banik

Registry-linked trialOpen access · goldAbstract readReview
In one paragraph

Review in Brain sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05175638 (Macrophage Migration Inhibiting Factor, Enolase and Caspase-3 as Indicators of Neuronal Insult in Newborns of COVID-19 Positive Mothers.), which is not on this map. Cited by 125 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
125citing papers in PubMed, 5 pooled it
9.0field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

NCT05175638 unknown statusnot on this mapstarted 2022, after this paper: background citation

Macrophage Migration Inhibiting Factor, Enolase and Caspase-3 as Indicators of Neuronal Insult in Newborns of COVID-19 Positive Mothers.

TypeobservationalSponsorAssiut UniversityRan2022 to 2022Enrolled50ConditionsCOVID-19 PandemicArmsGene Expression
3 · Its place in the literature

Who cites it

125 citing papers in PubMed, 5 syntheses or guidelines pooled it, 235 citations in OpenAlex.

  1. Pooled it
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  6. Trial
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  9. Article
  10. Human Neurotoxicity of Trichloroethylene: A Biomarker Approach.Journal of applied toxicology : JAT · 2026
    Article
  11. PMiScience · 2026
    Review
  12. Potential of Saliva in Stroke Patients: A Review.International journal of molecular sciences · 2026
    Review
  13. Article
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65 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Azizul HaqueDepartment of Microbiology and Immunology, Medical University of South Carolina, Charleston, SC 29401, USA. haque@musc.edu.
Rachel PolcynDepartment of Microbiology and Immunology, Medical University of South Carolina, Charleston, SC 29401, USA. polcyn@musc.edu.
Denise MatzelleDepartment of Neurosurgery, Medical University of South Carolina, Charleston, SC 29401, USA. baniknl@musc.edu.
Naren L BanikDepartment of Microbiology and Immunology, Medical University of South Carolina, Charleston, SC 29401, USA. matzeldd@musc.edu.
Medical University of South Carolina · USRalph H. Johnson VA Medical Center · US

Funding

Disruption of HLA Class II-Mediated Immune Recognition of B-Cell LymphomasR01CA129560 · NCI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI HAQUE, AZIZUL · 2009 to 2013
$1.5M
Regulation of inflammatory T Cells and Neuroprotection by Calpain Inhibitor in MSI01BX002349 · VA · RALPH H JOHNSON VA MEDICAL CENTER · PI BANIK, NAREN L · 2014 to 2017
–
BLRD VA I01 BX002349NCI NIH HHS R01 CA129560
6 · The paper itself

Abstract

Neurodegeneration is a complex process that leads to irreversible neuronal damage and death in spinal cord injury (SCI) and various neurodegenerative diseases, which are serious, debilitating conditions. Despite exhaustive research, the cause of neuronal damage in these degenerative disorders is not completely understood. Elevation of cell surface α-enolase activates various inflammatory pathways, including the production of pro-inflammatory cytokines, chemokines, and some growth factors that are detrimental to neuronal cells. While α-enolase is present in all neurological tissues, it can also be converted to neuron specific enolase (NSE). NSE is a glycolytic enzyme found in neuronal and neuroendocrine tissues that may play a dual role in promoting both neuroinflammation and neuroprotection in SCI and other neurodegenerative events. Elevated NSE can promote ECM degradation, inflammatory glial cell proliferation, and actin remodeling, thereby affecting migration of activated macrophages and microglia to the injury site and promoting neuronal cell death. Thus, NSE could be a reliable, quantitative, and specific marker of neuronal injury. Depending on the injury, disease, and microenvironment, NSE may also show neurotrophic function as it controls neuronal survival, differentiation, and neurite regeneration via activation of phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K) and mitogen-activated protein kinase (MAPK) signaling pathways. This review discusses possible implications of NSE expression and activity in neuroinflammation, neurodegeneration, and neuroprotection in SCI and various neurodegenerative diseases for prognostic and therapeutic potential.

Indexed as

cathepsin Xdegenerationgliosisneuron specific enolase (NSE)neuroprotectionspinal cord injury (SCI)

Identifiers

PMID29463007
PMCPMC5836052
OpenAlexW2791910913

What OpenQuestion holds

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Registered trials

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.