Increased Serum NSE and S100B Indicate Neuronal and Glial Alterations in Subjects Under 71 Years With Mild Neurocognitive Disorder/Mild Cognitive Impairment
BackgroundMild 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.MethodsTo link mild NCD to the und...
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Frontiers Media S.A.
2022-07-01
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| Series: | Frontiers in Cellular Neuroscience |
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| Online Access: | https://www.frontiersin.org/articles/10.3389/fncel.2022.788150/full |
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| author | Maryna Polyakova Maryna Polyakova Maryna Polyakova Maryna Polyakova Karsten Mueller Katrin Arelin Katrin Arelin Leonie Lampe Leonie Lampe Francisca S. Rodriguez Francisca S. Rodriguez Tobias Luck Tobias Luck Jürgen Kratzsch Jürgen Kratzsch Karl-Titus Hoffmann Steffi Riedel-Heller Steffi Riedel-Heller Arno Villringer Arno Villringer Arno Villringer Peter Schoenknecht Peter Schoenknecht Peter Schoenknecht Matthias L. Schroeter Matthias L. Schroeter Matthias L. Schroeter |
| author_facet | Maryna Polyakova Maryna Polyakova Maryna Polyakova Maryna Polyakova Karsten Mueller Katrin Arelin Katrin Arelin Leonie Lampe Leonie Lampe Francisca S. Rodriguez Francisca S. Rodriguez Tobias Luck Tobias Luck Jürgen Kratzsch Jürgen Kratzsch Karl-Titus Hoffmann Steffi Riedel-Heller Steffi Riedel-Heller Arno Villringer Arno Villringer Arno Villringer Peter Schoenknecht Peter Schoenknecht Peter Schoenknecht Matthias L. Schroeter Matthias L. Schroeter Matthias L. Schroeter |
| author_sort | Maryna Polyakova |
| collection | DOAJ |
| description | BackgroundMild 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.MethodsTo 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).ResultsSerum 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.ConclusionOur 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. |
| first_indexed | 2024-12-11T02:05:16Z |
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| issn | 1662-5102 |
| language | English |
| last_indexed | 2024-12-11T02:05:16Z |
| publishDate | 2022-07-01 |
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| series | Frontiers in Cellular Neuroscience |
| spelling | doaj.art-5555bf4ecee84ba099fa3876a1fee7d42022-12-22T01:24:24ZengFrontiers Media S.A.Frontiers in Cellular Neuroscience1662-51022022-07-011610.3389/fncel.2022.788150788150Increased Serum NSE and S100B Indicate Neuronal and Glial Alterations in Subjects Under 71 Years With Mild Neurocognitive Disorder/Mild Cognitive ImpairmentMaryna Polyakova0Maryna Polyakova1Maryna Polyakova2Maryna Polyakova3Karsten Mueller4Katrin Arelin5Katrin Arelin6Leonie Lampe7Leonie Lampe8Francisca S. Rodriguez9Francisca S. Rodriguez10Tobias Luck11Tobias Luck12Jürgen Kratzsch13Jürgen Kratzsch14Karl-Titus Hoffmann15Steffi Riedel-Heller16Steffi Riedel-Heller17Arno Villringer18Arno Villringer19Arno Villringer20Peter Schoenknecht21Peter Schoenknecht22Peter Schoenknecht23Matthias L. Schroeter24Matthias L. Schroeter25Matthias L. Schroeter26Max Planck Institute for Human Cognitive and Brain Sciences, Leipzig, GermanyClinic for Cognitive Neurology, University of Leipzig, Leipzig, GermanyLIFE–Leipzig Research Center for Civilization Diseases, Leipzig University, Leipzig, GermanyUniversity Clinic for Psychiatry and Psychotherapy, Leipzig University, Leipzig, GermanyMax Planck Institute for Human Cognitive and Brain Sciences, Leipzig, GermanyMax Planck Institute for Human Cognitive and Brain Sciences, Leipzig, GermanyLIFE–Leipzig Research Center for Civilization Diseases, Leipzig University, Leipzig, GermanyMax Planck Institute for Human Cognitive and Brain Sciences, Leipzig, GermanyLIFE–Leipzig Research Center for Civilization Diseases, Leipzig University, Leipzig, GermanyLIFE–Leipzig Research Center for Civilization Diseases, Leipzig University, Leipzig, GermanyResearch Group Psychosocial Epidemiology and Public Health, German Center for Neurodegenerative Diseases (DZNE), Greifswald, GermanyLIFE–Leipzig Research Center for Civilization Diseases, Leipzig University, Leipzig, GermanyFaculty of Applied Social Sciences, University of Applied Sciences Erfurt, Erfurt, GermanyLIFE–Leipzig Research Center for Civilization Diseases, Leipzig University, Leipzig, GermanyInstitute of Laboratory Medicine, Clinical Chemistry and Molecular Diagnostics, Leipzig University, Leipzig, GermanyInstitute of Neuroradiology, University Clinic, Leipzig, GermanyLIFE–Leipzig Research Center for Civilization Diseases, Leipzig University, Leipzig, GermanyInstitute of Social Medicine, Occupational Health and Public Health (ISAP), Leipzig University, Leipzig, GermanyMax Planck Institute for Human Cognitive and Brain Sciences, Leipzig, GermanyLIFE–Leipzig Research Center for Civilization Diseases, Leipzig University, Leipzig, GermanyInstitute of Neuroradiology, University Clinic, Leipzig, GermanyLIFE–Leipzig Research Center for Civilization Diseases, Leipzig University, Leipzig, GermanyUniversity Clinic for Psychiatry and Psychotherapy, Leipzig University, Leipzig, Germany0Department of Psychiatry and Psychotherapy, University Affiliated Hospital Arnsdorf, Technical University of Dresden, Dresden, GermanyMax Planck Institute for Human Cognitive and Brain Sciences, Leipzig, GermanyClinic for Cognitive Neurology, University of Leipzig, Leipzig, GermanyLIFE–Leipzig Research Center for Civilization Diseases, Leipzig University, Leipzig, GermanyBackgroundMild 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.MethodsTo 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).ResultsSerum 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.ConclusionOur 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.https://www.frontiersin.org/articles/10.3389/fncel.2022.788150/fullmild cognitive impairmentwhite matter hyperintensitiesS100Bneuron-specific enolaseNSEBrain-Derived Neurotrophic Factor |
| spellingShingle | Maryna Polyakova Maryna Polyakova Maryna Polyakova Maryna Polyakova Karsten Mueller Katrin Arelin Katrin Arelin Leonie Lampe Leonie Lampe Francisca S. Rodriguez Francisca S. Rodriguez Tobias Luck Tobias Luck Jürgen Kratzsch Jürgen Kratzsch Karl-Titus Hoffmann Steffi Riedel-Heller Steffi Riedel-Heller Arno Villringer Arno Villringer Arno Villringer Peter Schoenknecht Peter Schoenknecht Peter Schoenknecht Matthias L. Schroeter Matthias L. Schroeter Matthias L. Schroeter Increased Serum NSE and S100B Indicate Neuronal and Glial Alterations in Subjects Under 71 Years With Mild Neurocognitive Disorder/Mild Cognitive Impairment Frontiers in Cellular Neuroscience mild cognitive impairment white matter hyperintensities S100B neuron-specific enolase NSE Brain-Derived Neurotrophic Factor |
| title | Increased Serum NSE and S100B Indicate Neuronal and Glial Alterations in Subjects Under 71 Years With Mild Neurocognitive Disorder/Mild Cognitive Impairment |
| title_full | Increased Serum NSE and S100B Indicate Neuronal and Glial Alterations in Subjects Under 71 Years With Mild Neurocognitive Disorder/Mild Cognitive Impairment |
| title_fullStr | Increased Serum NSE and S100B Indicate Neuronal and Glial Alterations in Subjects Under 71 Years With Mild Neurocognitive Disorder/Mild Cognitive Impairment |
| title_full_unstemmed | Increased Serum NSE and S100B Indicate Neuronal and Glial Alterations in Subjects Under 71 Years With Mild Neurocognitive Disorder/Mild Cognitive Impairment |
| title_short | Increased Serum NSE and S100B Indicate Neuronal and Glial Alterations in Subjects Under 71 Years With Mild Neurocognitive Disorder/Mild Cognitive Impairment |
| title_sort | increased serum nse and s100b indicate neuronal and glial alterations in subjects under 71 years with mild neurocognitive disorder mild cognitive impairment |
| topic | mild cognitive impairment white matter hyperintensities S100B neuron-specific enolase NSE Brain-Derived Neurotrophic Factor |
| url | https://www.frontiersin.org/articles/10.3389/fncel.2022.788150/full |
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