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000285457 1001_ $$0P:(DE-2719)9001334$$aMaass, Fabian$$b0
000285457 245__ $$aAlterations in cerebrospinal fluid levels of myelin- and oligodendrocyte-related proteins in sporadic Creutzfeldt–Jakob disease
000285457 260__ $$aLondon$$bBiomed Central$$c2026
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000285457 520__ $$aRecent 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.
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000285457 650_7 $$2Other$$aBiomarker
000285457 650_7 $$2Other$$aCNPase
000285457 650_7 $$2Other$$aCerebrospinal fluid
000285457 650_7 $$2Other$$aCreutzfeldt–Jakob disease
000285457 650_7 $$2Other$$aMyelin basic protein
000285457 650_7 $$2Other$$aNG2
000285457 7001_ $$aThomas, Carolina$$b1
000285457 7001_ $$aKurvits, Lille$$b2
000285457 7001_ $$aHermann, Peter$$b3
000285457 7001_ $$0P:(DE-2719)9000287$$aSchmitz, Matthias$$b4$$udzne
000285457 7001_ $$0P:(DE-2719)2811350$$aBähr, Mathias$$b5$$udzne
000285457 7001_ $$aStadelmann, Christine$$b6
000285457 7001_ $$aZechel, Sabrina$$b7
000285457 7001_ $$aCanaslan, Sezgi$$b8
000285457 7001_ $$0P:(DE-2719)2000058$$aZerr, Inga$$b9$$eLast author$$udzne
000285457 773__ $$0PERI:(DE-600)2715589-4$$a10.1186/s40478-026-02247-5$$gVol. 14, no. 1, p. 51$$n1$$p51$$tActa Neuropathologica Communications$$v14$$x2051-5960$$y2026
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