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. 2022 Jul 14:16:788150.
doi: 10.3389/fncel.2022.788150. eCollection 2022.

Increased Serum NSE and S100B Indicate Neuronal and Glial Alterations in Subjects Under 71 Years With Mild Neurocognitive Disorder/Mild Cognitive Impairment

Maryna Polyakova  1   2   3   4 , Karsten Mueller  1 , Katrin Arelin  1   3 , Leonie Lampe  1   3 , Francisca S Rodriguez  3   5 , Tobias Luck  3   6 , Jürgen Kratzsch  3   7 , Karl-Titus Hoffmann  8 , Steffi Riedel-Heller  3   9 , Arno Villringer  1   3   8 , Peter Schoenknecht  3   4   10 , Matthias L Schroeter  1   2   3
Affiliations

Increased Serum NSE and S100B Indicate Neuronal and Glial Alterations in Subjects Under 71 Years With Mild Neurocognitive Disorder/Mild Cognitive Impairment

Maryna Polyakova et al. Front Cell Neurosci. .

Abstract

Background: Mild cognitive impairment (MCI) is considered a pre-stage of different dementia syndromes. Despite diagnostic criteria refined by DSM-5 and a new term for MCI - "mild neurocognitive disorder" (mild NCD) - this diagnosis is still based on clinical criteria.

Methods: To link mild NCD to the underlying pathophysiology we assessed the degree of white matter hyperintensities (WMH) in the brain and peripheral biomarkers for neuronal integrity (neuron-specific enolase, NSE), plasticity (brain-derived neurotrophic factor, BDNF), and glial function (S100B) in 158 community-dwelling subjects with mild NCD and 82 healthy controls. All participants (63-79 years old) were selected from the Leipzig-population-based study of adults (LIFE).

Results: Serum S100B levels were increased in mild NCD in comparison to controls (p = 0.007). Serum NSE levels were also increased but remained non-significant after Bonferroni-Holm correction (p = 0.04). Furthermore, age by group interaction was significant for S100B. In an age-stratified sub-analysis, NSE and S100B were higher in younger subjects with mild NCD below 71 years of age. Some effects were inconsistent after controlling for potentially confounding factors. The discriminatory power of the two biomarkers NSE and S100B was insufficient to establish a pathologic threshold for mild NCD. In subjects with mild NCD, WMH load correlated with serum NSE levels (r = 0.20, p = 0.01), independently of age.

Conclusion: Our findings might indicate the presence of neuronal (NSE) and glial (S100B) injury in mild NCD. Future studies need to investigate whether younger subjects with mild NCD with increased biomarker levels are at risk of developing major NCD.

Keywords: BDNF; Brain-Derived Neurotrophic Factor; NSE; S100B; mild cognitive impairment; neuron-specific enolase; white matter hyperintensities.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
Group comparisons – S100B and neuron-specific enolase are increased in mild neurocognitive disorder. Furthermore, results of correlation between fluid biomarkers and age are shown. (A) Serum NSE levels in mild NCD vs. healthy controls; (B) Serum S100B levels in mild NSE vs. healthy controls; (C) Serum BDNF levels in mild NCD vs. healthy controls; (D) Correlation between serum NSE and age in mild NCD and HC; (E) Correlation between serum S100B and age in mild NCD and healthy controls; (F) Correlation between serum BDNF and age in mild NCD and healthy controls, BDNF Brain-Derived Neurotrophic Factor; NCD neurocognitive disorder; HC healthy controls; NSE neuron-specific enolase. * p < 0.05; ** p < 0.01.
Figure 2
Figure 2
Correlation between WMH and serum NSE in the younger mild NCD subgroup.
Figure 3
Figure 3
Receiver operating characteristic curves for serum S100B and NSE in the younger subgroup, i.e., participants with mild neurocognitive disorder vs. healthy controls. AUC area under the curve, NSE neuron-specific enolase.
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