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@ARTICLE{Maass:285457,
      author       = {Maass, Fabian and Thomas, Carolina and Kurvits, Lille and
                      Hermann, Peter and Schmitz, Matthias and Bähr, Mathias and
                      Stadelmann, Christine and Zechel, Sabrina and Canaslan,
                      Sezgi and Zerr, Inga},
      title        = {{A}lterations in cerebrospinal fluid levels of myelin- and
                      oligodendrocyte-related proteins in sporadic
                      {C}reutzfeldt–{J}akob disease},
      journal      = {Acta Neuropathologica Communications},
      volume       = {14},
      number       = {1},
      issn         = {2051-5960},
      address      = {London},
      publisher    = {Biomed Central},
      reportid     = {DZNE-2026-00239},
      pages        = {51},
      year         = {2026},
      abstract     = {Recent evidence suggests glial dysfunction, particularly
                      involving oligodendrocytes and myelin, as an important part
                      of the primary disease mechanism of sporadic
                      Creutzfeldt–Jakob disease. To the best of our knowledge,
                      cerebrospinal fluid (CSF) biomarkers reflecting
                      oligodendrocyte or myelin damage have not yet been
                      systematically investigated in this context. CSF samples
                      from patients with sporadic Creutzfeldt–Jakob disease
                      (CJD), Alzheimer's disease (AD) and non-neurodegenerative
                      controls (n = 18, respectively) were included in the study,
                      and levels of myelin basic protein (MBP), neural/glial
                      antigen 2 (NG2) and cyclic nucleotide 3′-phosphodiesterase
                      (CNPase) were quantified. Additionally, p25-positive cells
                      were quantified in autopsy tissue from the frontal and
                      parietal cortical regions of five patients with CJD and four
                      controls. In the primary cohort, MBP quantification revealed
                      significantly higher CSF levels in CJD compared to AD (p =
                      0.004) and controls (p = 0.0001) and this difference
                      remained significant after adjustment for age and
                      neurofilament light chain (NfL), indicating that MBP
                      elevations cannot be explained solely by neuroaxonal
                      degeneration. Significant differences were also found for
                      CNPase in CJD compared to AD (p = 0.0011) and controls (p =
                      0.0004). There were no differences in NG2 levels (p > 0.05)
                      among the groups. However, no significant differences were
                      observed in the total number of p25-positive mature
                      oligodendrocytes between CJD and controls in cortical brain
                      tissue (p > 0.05). Additionally, MBP and NfL were quantified
                      in a second cohort of 28 CJD and 20 biomarker-defined AD
                      patients. In this cohort, characterized by more advanced AD
                      pathology, MBP strongly covaried with NfL and no longer
                      differed between diagnostic groups, suggesting a greater
                      influence of neuroaxonal injury on MBP levels in advanced
                      disease stages. In conclusion, in CJD, MBP elevations appear
                      to be only partly related to neuroaxonal degeneration and
                      may reflect disease-related myelin involvement.The online
                      version contains supplementary material available at
                      10.1186/s40478-026-02247-5.},
      keywords     = {Biomarker (Other) / CNPase (Other) / Cerebrospinal fluid
                      (Other) / Creutzfeldt–Jakob disease (Other) / Myelin basic
                      protein (Other) / NG2 (Other)},
      cin          = {AG Zerr / Clinical Dementia Research (Göttingen)},
      ddc          = {610},
      cid          = {I:(DE-2719)1440011-1 / I:(DE-2719)1440015},
      pnm          = {353 - Clinical and Health Care Research (POF4-353)},
      pid          = {G:(DE-HGF)POF4-353},
      typ          = {PUB:(DE-HGF)16},
      doi          = {10.1186/s40478-026-02247-5},
      url          = {https://pub.dzne.de/record/285457},
}