<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Nilsson J</submitter><funding>Swedish Federal Government</funding><funding>Skåne University Hospital</funding><funding>Eivind och Elsa K:son Sylvan Stiftelse</funding><funding>Joint Programme-Neurodegenerative Disease Research</funding><funding>Swedish Research Council</funding><funding>Alzheimer Drug Discovery Foundation</funding><funding>Swedish Brain Foundation</funding><funding>GE Healthcare</funding><funding>University College London Hospitals Biomedical Research Centre</funding><funding>Stiftelsen för Gamla Tjänarinnor</funding><funding>Medical Research Council</funding><funding>Erling-Persson Family Foundation</funding><funding>Hjärnfonden</funding><funding>Horizon 2020</funding><funding>Swedish Government</funding><funding>National Institute for Health and Care Research</funding><funding>Alzheimer's Association</funding><funding>Alzheimerfonden</funding><pagination>2414-2427</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11224614</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>147(7)</volume><pubmed_abstract>Synaptic dysfunction and degeneration is likely the key pathophysiology for the progression of cognitive decline in various dementia disorders. Synaptic status can be monitored by measuring synaptic proteins in CSF. In this study, both known and new synaptic proteins were investigated and compared as potential biomarkers of synaptic dysfunction, particularly in the context of Alzheimer's disease (AD). Seventeen synaptic proteins were quantified in CSF using two different targeted mass spectrometry assays in the prospective Swedish BioFINDER-2 study. The study included 958 individuals, characterized as having mild cognitive impairment (MCI, n = 205), AD dementia (n = 149) and a spectrum of other neurodegenerative diseases (n = 171), in addition to cognitively unimpaired individuals (CU, n =</pubmed_abstract><journal>Brain : a journal of neurology</journal><pubmed_title>Cerebrospinal fluid biomarker panel for synaptic dysfunction in a broad spectrum of neurodegenerative diseases.</pubmed_title><pmcid>PMC11224614</pmcid><funding_grant_id>2020-O000028</funding_grant_id><funding_grant_id>2022-01018</funding_grant_id><funding_grant_id>UKDRI-1003</funding_grant_id><funding_grant_id>AF-980907</funding_grant_id><funding_grant_id>FO2022-0204</funding_grant_id><pubmed_authors>Palmqvist S</pubmed_authors><pubmed_authors>Janelidze S</pubmed_authors><pubmed_authors>Nilsson J</pubmed_authors><pubmed_authors>Hansson O</pubmed_authors><pubmed_authors>Zetterberg H</pubmed_authors><pubmed_authors>Pichet Binette A</pubmed_authors><pubmed_authors>Spotorno N</pubmed_authors><pubmed_authors>Brinkmalm A</pubmed_authors><pubmed_authors>Stomrud E</pubmed_authors><pubmed_authors>Ashton NJ</pubmed_authors><pubmed_authors>Brum WS</pubmed_authors><pubmed_authors>Blennow K</pubmed_authors><pubmed_authors>Gobom J</pubmed_authors></additional><is_claimable>false</is_claimable><name>Cerebrospinal fluid biomarker panel for synaptic dysfunction in a broad spectrum of neurodegenerative diseases.</name><description>Synaptic dysfunction and degeneration is likely the key pathophysiology for the progression of cognitive decline in various dementia disorders. Synaptic status can be monitored by measuring synaptic proteins in CSF. In this study, both known and new synaptic proteins were investigated and compared as potential biomarkers of synaptic dysfunction, particularly in the context of Alzheimer's disease (AD). Seventeen synaptic proteins were quantified in CSF using two different targeted mass spectrometry assays in the prospective Swedish BioFINDER-2 study. The study included 958 individuals, characterized as having mild cognitive impairment (MCI, n = 205), AD dementia (n = 149) and a spectrum of other neurodegenerative diseases (n = 171), in addition to cognitively unimpaired individuals (CU, n =</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Jul</publication><modification>2026-06-03T21:55:43.434Z</modification><creation>2025-04-04T19:23:27.025Z</creation></dates><accession>S-EPMC11224614</accession><cross_references><pubmed>38325331</pubmed><doi>10.1093/brain/awae032</doi></cross_references></HashMap>