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Still, it remains unclear how BDNF relates to clinicoradiological characteristics particularly at the early stage of the disease where precise prognosis for the further MS course is crucial.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Methods<\/jats:title>\n            <jats:p>BDNF, NfL and GFAP concentrations in serum and CSF were assessed in 106 treatment na\ufeff\u00efve patients with MS (pwMS) as well as 73 patients with other inflammatory\/non-inflammatory neurological or somatoform disorders using a single molecule array HD-1 analyser. PwMS were evaluated for highly active profiles by applying the aggressive disease course criteria proposed by ECTRIMS. Serum\/CSF values were logarithmically transformed and compared across groups using one-way ANOVA, while correlations were calculated using Pearson\u2019s correlations. ROC analysis and AUC comparisons for diagnostic performance of the three biomarkers were computed in an explorative analysis.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Results<\/jats:title>\n            <jats:p>Serum BDNF (sBDNF) concentrations were higher in treatment na\u00efve pwMS with disease onset after the age of 40\u00a0years (<jats:italic>p<\/jats:italic>\u2009=\u20090.029), in pwMS with \u22652 gadolinium-enhancing lesions (<jats:italic>p<\/jats:italic>\u2009=\u20090.009) and with motor, cerebellar, cognitive or sphincter symptoms at onset (<jats:italic>p<\/jats:italic>\u2009=\u20090.036). BDNF correlated positively with NfL (<jats:italic>r<\/jats:italic>\u2009=\u20090.198, <jats:italic>p<\/jats:italic>\u2009=\u20090.014) and GFAP (<jats:italic>r<\/jats:italic>\u2009=\u20090.253, <jats:italic>p<\/jats:italic>\u2009=\u20090.002) in serum, but not in CSF. Neurological patients with an acute inflammatory relapse showed significantly higher sBDNF levels (<jats:italic>p<\/jats:italic>\u2009=\u20090.03) compared to somatoform controls, while patients without acute relapse did not differ from somatoform controls (<jats:italic>p<\/jats:italic>\u2009=\u20090.4). Better diagnostic performance was found for sBDNF than sNfL and sGFAP in differentiating between patients with vs. without 2 or more gadolinium-enhancing lesions (<jats:italic>p<\/jats:italic>\u2009&lt;\u20090.05) and for sBDNF as compared to sNfL for separating patients with disease onset after vs. before age of 40\u00a0years.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusion<\/jats:title>\n            <jats:p>In pwMS, BDNF serum levels differ depending on disease-related characteristics, suggesting that not only inflammatory activity but also remyelination capacities may vary with disease severity. BDNF is increased when other biomarkers of neuroaxonal damage and neurodegeneration, such as NfL and GFAP, are elevated, possibly as a compensatory mechanism, and reflect possibly further pathophysiological aspects in MS beyond NfL and GFAP, probably including an apoptotic role for BDNF in neuroinflammation.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1007\/s00415-024-12875-3","type":"journal-article","created":{"date-parts":[[2025,1,15]],"date-time":"2025-01-15T13:37:15Z","timestamp":1736948235000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["BDNF levels in serum and CSF are associated with clinicoradiological characteristics of aggressive disease in MS patients"],"prefix":"10.1007","volume":"272","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3674-0601","authenticated-orcid":false,"given":"Michelle","family":"Maiworm","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kimberly","family":"Koerbel","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Victoria","family":"Ansch\u00fctz","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jasmin","family":"Jakob","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Martin A.","family":"Schaller-Paule","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jan Hendrik","family":"Sch\u00e4fer","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lucie","family":"Friedauer","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Katharina J.","family":"Wenger","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Maya C.","family":"Hoelter","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Falk","family":"Steffen","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Stefan","family":"Bittner","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Christian","family":"Foerch","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yavor","family":"Yalachkov","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2025,1,15]]},"reference":[{"key":"12875_CR1","doi-asserted-by":"crossref","first-page":"2659","DOI":"10.1093\/hmg\/ddm189","volume":"16","author":"R Zivadinov","year":"2007","unstructured":"Zivadinov R et al (2007) Preservation of gray matter volume in multiple sclerosis patients with the Met allele of the rs6265 (Val66Met) SNP of brain-derived neurotrophic factor. 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CF reports speaker honoraria and honoraria for participating in advisory boards from Alexion, Bristol Myers Squibb, Novartis, Teva, Merck, Sanofi Genzyme and Roche, and received research support from Novartis and Sanofi Genzyme. YY has been supported by travel grants from Novartis and Sanofi Genzyme and has received honoraria for active participation in advisory boards and speaker\/writing honoraria by Bristol Meyers Squibb, Kassen\u00e4rztliche Vereinigung Hessen, Landes\u00e4rztekammer Hessen, Merck, Novartis, RG Gesellschaft f\u00fcr Information und Organisation mbH, Roche, Sanofi Genzyme, TEVA. His research is funded by Novartis. SB received honoraria from Biogen Idec, Bristol Meyer Squibbs, Hexal, Merck Healthcare, Mylan, Novartis, Roche, Sanofi Genzyme and TEVA and his research is supported by the Deutsche Forschungsgemeinschaft (DFG, SFB CRC-TR-128 and CRC-TR-355) and the Hermann and Lilly Schilling Foundation. MM, KK, KW, MSP, MH, FS, JJ, LF, VA report no conflicts of interest.","order":2,"name":"Ethics","group":{"name":"EthicsHeading","label":"Conflicts of interest"}}],"article-number":"147"}}