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Synaptic dysfunction is an early feature in bvFTD and identification of specific biomarkers might improve its diagnostic accuracy. Our goal was to understand the differential diagnostic potential of cerebrospinal fluid (CSF) synaptic biomarkers in bvFTD versus PPD and their specificity towards bvFTD compared with Alzheimer\u2019s disease (AD) and controls. Additionally, we explored the association of CSF synaptic biomarkers with social cognition, cognitive performance, and disease severity in these clinical groups.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Methods<\/jats:title>\n                <jats:p>Participants with probable bvFTD (<jats:italic>n<\/jats:italic> = 57), PPD (<jats:italic>n<\/jats:italic> = 71), AD (<jats:italic>n<\/jats:italic> = 60), and cognitively normal controls (<jats:italic>n<\/jats:italic> = 39) with available CSF, cognitive tests, and disease severity as frontotemporal lobar degeneration-modified clinical dementia rating scale (FTLD-CDR) were included. In a subset of bvFTD and PPD cases, Ekman 60 faces test scores for social cognition were available. CSF synaptosomal-associated protein 25 (SNAP25), neurogranin (Ng), neuronal pentraxin 2 (NPTX2), and glutamate receptor 4 (GluR4) were measured, along with neurofilament light (NfL), and compared between groups using analysis of covariance (ANCOVA) and logistic regression. Diagnostic accuracy was assessed using ROC analyses, and biomarker panels were selected using Wald\u2019s backward selection. Correlations with cognitive measures were performed using Pearson\u2019s partial correlation analysis.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Results<\/jats:title>\n                <jats:p>NPTX2 concentrations were lower in the bvFTD group compared with PPD (<jats:italic>p<\/jats:italic> &lt; 0.001) and controls (<jats:italic>p<\/jats:italic> = 0.003) but not compared with AD. Concentrations of SNAP25 (<jats:italic>p<\/jats:italic> &lt; 0.001) and Ng (<jats:italic>p<\/jats:italic> &lt; 0.001) were elevated in patients with AD versus those with bvFTD and controls. The modeled panel for differential diagnosis of bvFTD versus PPD consisted of NfL and NPTX2 (AUC = 0.96, CI: 0.93\u20130.99, <jats:italic>p<\/jats:italic> &lt; 0.001). In bvFTD versus AD, the modeled panel consisted of NfL, SNAP25, Ng, and GluR4 (AUC = 0.86, CI: 0.79\u20130.92, <jats:italic>p<\/jats:italic> &lt; 0.001). In bvFTD, lower NPTX2 (Pearson\u2019s <jats:italic>r<\/jats:italic> = 0.29, <jats:italic>p<\/jats:italic> = 0.036) and GluR4 (Pearson\u2019s <jats:italic>r<\/jats:italic> = 0.34, <jats:italic>p<\/jats:italic> = 0.014) concentrations were weakly associated with worse performance of total cognitive score. Lower GluR4 concentrations were also associated with worse MMSE scores (Pearson\u2019s <jats:italic>r<\/jats:italic> = 0.41, <jats:italic>p<\/jats:italic> = 0.002) as well as with worse executive functioning (Pearson\u2019s <jats:italic>r<\/jats:italic> = 0.36, <jats:italic>p<\/jats:italic> = 0.011) in bvFTD. There were no associations between synaptic markers and social cognition or disease severity in bvFTD.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Conclusion<\/jats:title>\n                <jats:p>Our findings of involvement of NTPX2 in bvFTD but not PPD contribute towards better understanding of bvFTD disease pathology.<\/jats:p>\n              <\/jats:sec>","DOI":"10.1186\/s13195-024-01409-8","type":"journal-article","created":{"date-parts":[[2024,2,14]],"date-time":"2024-02-14T07:02:20Z","timestamp":1707894140000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":11,"title":["The use of synaptic biomarkers in cerebrospinal fluid to differentiate behavioral variant of frontotemporal dementia from primary psychiatric disorders and Alzheimer\u2019s disease"],"prefix":"10.1186","volume":"16","author":[{"given":"Shreyasee","family":"Das","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marie-Paule E.","family":"van Engelen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Julie","family":"Goossens","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dirk","family":"Jacobs","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bram","family":"Bongers","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jay L. 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The study was approved by the Medical Ethical Committee of Amsterdam University Medical Center. All participants provided informed consent and the study has been carried out by the Declaration of Helsinki.","order":2,"name":"Ethics","group":{"name":"EthicsHeading","label":"Ethics approval and consent to participate"}},{"value":"Not applicable.","order":3,"name":"Ethics","group":{"name":"EthicsHeading","label":"Consent for publication"}},{"value":"S.D., and J.G., are employees of ADx NeuroSciences, Gent, Belgium. E.V. is the co-founder of ADx NeuroSciences. D.J. is a former employee of ADx NeuroSciences, Gent, Belgium, and is recently retired. C.E.T. has a collaboration contract with ADx NeuroSciences, Quanterix, and Eli Lilly, and has performed contract research or received grants from AC-Immune, Axon Neurosciences, Bioconnect, Bioorchestra, Brainstorm Therapeutics, Celgene, EIP Pharma, Eisai, Grifols, Novo Nordisk, PeopleBio, Roche, Toyama, and Vivoryon. 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