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@ARTICLE{Polyakova:165107,
      author       = {Polyakova, Maryna and Mueller, Karsten and Arelin, Katrin
                      and Lampe, Leonie and Rodriguez, Francisca S and Luck,
                      Tobias and Kratzsch, Jürgen and Hoffmann, Karl-Titus and
                      Riedel-Heller, Steffi and Villringer, Arno and Schoenknecht,
                      Peter and Schroeter, Matthias L},
      title        = {{I}ncreased {S}erum {NSE} and {S}100{B} {I}ndicate
                      {N}euronal and {G}lial {A}lterations in {S}ubjects {U}nder
                      71 {Y}ears {W}ith {M}ild {N}eurocognitive {D}isorder/{M}ild
                      {C}ognitive {I}mpairment.},
      journal      = {Frontiers in cellular neuroscience},
      volume       = {16},
      issn         = {1662-5102},
      address      = {Lausanne},
      publisher    = {Frontiers Research Foundation},
      reportid     = {DZNE-2022-01416},
      pages        = {788150},
      year         = {2022},
      abstract     = {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.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).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.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 (Other) / Brain-Derived Neurotrophic Factor (Other) /
                      NSE (Other) / S100B (Other) / mild cognitive impairment
                      (Other) / neuron-specific enolase (Other) / white matter
                      hyperintensities (Other)},
      cin          = {AG Rodriguez-Muela},
      ddc          = {610},
      cid          = {I:(DE-2719)1713001},
      pnm          = {353 - Clinical and Health Care Research (POF4-353)},
      pid          = {G:(DE-HGF)POF4-353},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:35910248},
      pmc          = {pmc:PMC9329528},
      doi          = {10.3389/fncel.2022.788150},
      url          = {https://pub.dzne.de/record/165107},
}