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(DZNE) in der Helmholtz-Gemeinschaft"}],"content-domain":{"domain":["link.springer.com"],"crossmark-restriction":false},"short-container-title":["J Neurol"],"published-print":{"date-parts":[[2024,12]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec>\n                <jats:title>Background<\/jats:title>\n                <jats:p>The proteins contactin (CNTN) 1\u20136 are synaptic proteins for which there is evidence that they are dysregulated in neurodegenerative dementias. Less is known about CNTN changes and differences in cerebrospinal fluid (CSF) of dementias, which can provide important information about alterations of the CNTN network and be of value for differential diagnosis.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Methods<\/jats:title>\n                <jats:p>We developed a mass spectrometry-based multiple reaction monitoring (MRM) method to simultaneously determine all six CNTNs in CSF samples using stable isotope-labeled standard peptides. The analytical performance of the method was evaluated for peptide stability, dilution linearity and precision. CNTNs were measured in 82 CSF samples from patients with Alzheimer\u2019s disease (AD, <jats:italic>n<\/jats:italic>\u2009=\u200919), behavioural variant frontotemporal dementia (bvFTD, <jats:italic>n<\/jats:italic>\u2009=\u200918), Parkinson\u2019s disease dementia\/dementia with Lewy bodies (PDD\/DLB, <jats:italic>n<\/jats:italic>\u2009=\u200918) and non-neurodegenerative controls (<jats:italic>n<\/jats:italic>\u2009=\u200927) and compared with core AD biomarkers.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Results<\/jats:title>\n                <jats:p>The MRM analysis revealed down-regulation of CNTN2 (fold change (FC)\u2009=\u20090.77), CNTN4 (FC\u2009=\u20090.75) and CNTN5 (FC\u2009=\u20090.67) in bvFTD and CNTN3 (FC\u2009=\u20090.72), CNTN4 (FC\u2009=\u20090.75) and CNTN5 (FC\u2009=\u20090.73) in PDD\/DLB compared to AD. CNTN levels strongly correlated with each other in controls (<jats:italic>r<\/jats:italic>\u2009=\u20090.73), bvFTD (<jats:italic>r<\/jats:italic>\u2009=\u20090.86) and PDD\/DLB (<jats:italic>r<\/jats:italic>\u2009=\u20090.70), but the correlation was significantly lower in AD (<jats:italic>r<\/jats:italic>\u2009=\u20090.41). CNTNs in AD did not show correlation even with core AD biomarkers. Combined use of CNTN1-6 levels increased diagnostic performance of AD core biomarkers.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Conclusions<\/jats:title>\n                <jats:p>Our data show CNTNs differentially altered in dementias and indicate CNTN homeostasis being selectively dysregulated in AD. The combined use of CNTNs with AD core biomarkers might help to improve differential diagnosis.<\/jats:p>\n              <\/jats:sec>","DOI":"10.1007\/s00415-024-12694-6","type":"journal-article","created":{"date-parts":[[2024,9,25]],"date-time":"2024-09-25T03:33:48Z","timestamp":1727235228000},"page":"7516-7524","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["Contactin proteins in cerebrospinal fluid show different alterations in dementias"],"prefix":"10.1007","volume":"271","author":[{"given":"Besnik","family":"Muqaku","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sarah","family":"Anderl-Straub","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Leonie","family":"Werner","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Magdalena","family":"Nagl","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Markus","family":"Otto","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Charlotte E.","family":"Teunissen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7652-7023","authenticated-orcid":false,"given":"Patrick","family":"Oeckl","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2024,9,25]]},"reference":[{"key":"12694_CR1","doi-asserted-by":"publisher","first-page":"505","DOI":"10.1016\/S0140-6736(15)01124-1","volume":"388","author":"P Scheltens","year":"2016","unstructured":"Scheltens P, Blennow K, Breteler MM, de Strooper B, Frisoni GB, Salloway S, Van der Flier WM (2016) Alzheimer\u2019s disease. 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PO and MO received support from the Cure Alzheimer Fund. MO received research support from German Federal Ministry of Education and Research (FTLDc 01GI1007A), the EU Joint Programme-Neurodegenerative Diseases networks Genfi-Prox (01ED2008A), the EU (MOODMARKER 01EW2008), the German Research Foundation\/DFG (SFB1279), the foundation of the state Baden-W\u00fcrttemberg (D.3830), Boehringer Ingelheim Ulm University BioCenter (D.5009), and the Thierry Latran Foundation.","order":2,"name":"Ethics","group":{"name":"EthicsHeading","label":"Conflicts of interest"}},{"value":"The Ethics Committee of Ulm University approved the study (approval no. 20\/10).","order":3,"name":"Ethics","group":{"name":"EthicsHeading","label":"Ethical approval"}},{"value":"All patients gave written informed consent to be included in the study.","order":4,"name":"Ethics","group":{"name":"EthicsHeading","label":"Consent to participate"}}]}}