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Despite progress, more biomarkers, ideally in blood, are needed for effective disease monitoring for AD and other neurodegenerative proteinopathies.<\/jats:p>\n <\/jats:sec>\n \n METHODS<\/jats:title>\n \n We used the Nucleic Acid Linked Immuno\u2010Sandwich Assay (NULISA) central nervous system panel for biomarker quantification in plasma, serum, and cerebrospinal fluid of patients with AD, mild cognitive impairment, Lewy body dementia, progranulin (\n GRN<\/jats:italic>\n ) mutation carriers.\n <\/jats:p>\n <\/jats:sec>\n \n RESULTS<\/jats:title>\n \n NULISA identified phosphorylated tau217 and neurofilament light chain as the most deregulated biomarkers in the AD continuum and\n GRN<\/jats:italic>\n mutation carriers, respectively. Importantly, numerous novel proteomic changes were observed in each disease endophenotype, which included synaptic processing, inflammation, microglial reactivity, TAR DNA\u2010binding protein 43, and \u03b1\u2010synuclein pathology.\n <\/jats:p>\n <\/jats:sec>\n \n DISCUSSION<\/jats:title>\n We underline the potential of next\u2010generation biomarker identification tools to detect novel proteomic features that also incorporate established biomarkers. These findings highlight the importance of continued biomarker discovery to improve treatment decisions and help us better understand the complexities of neurodegenerative disorders.<\/jats:p>\n <\/jats:sec>\n \n Highlights<\/jats:title>\n \n \n \n The, direct, or indirect, measures in blood that complement phosphorylated tau (p\u2010tau)217 for other proteinopathies or disease progression are urgently needed.<\/jats:p>\n <\/jats:list-item>\n \n Significant novel proteomic changes were observed in each disease endophenotype in plasma, serum, and cerebrospinal fluid, which included proteins involved in synaptic processing, inflammation, microglial reactivity, TAR DNA\u2010binding protein 43, and \u03b1\u2010synuclein pathology.<\/jats:p>\n <\/jats:list-item>\n \n Nucleic Acid Linked Immuno\u2010Sandwich Assay continued to unbiasely highlight p\u2010tau217 and neurofilament light chain as the most significantly deregulated blood biomarkers in the Alzheimer's disease continuum and progranulin mutation carriers, respectively.<\/jats:p>\n <\/jats:list-item>\n <\/jats:list>\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1002\/alz.14621","type":"journal-article","created":{"date-parts":[[2025,5,22]],"date-time":"2025-05-22T06:34:10Z","timestamp":1747895650000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":34,"title":["Biomarker discovery in Alzheimer's and neurodegenerative diseases using Nucleic Acid Linked Immuno\u2010Sandwich Assay"],"prefix":"10.1002","volume":"21","author":[{"given":"Nicholas J.","family":"Ashton","sequence":"first","affiliation":[{"name":"Department of Psychiatry and Neurochemistry Institute of Neuroscience & Physiology the Sahlgrenska Academy at the University of Gothenburg M\u00f6lndal Sweden"},{"name":"Banner Alzheimer's Institute and University of Arizona Phoenix Arizona USA"},{"name":"Banner Sun Health Research Institute Sun City Arizona USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andrea L.","family":"Benedet","sequence":"additional","affiliation":[{"name":"Department of Psychiatry and Neurochemistry Institute of Neuroscience & Physiology the Sahlgrenska Academy at the University of Gothenburg M\u00f6lndal Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Guglielmo Di","family":"Molfetta","sequence":"additional","affiliation":[{"name":"Department of Psychiatry and Neurochemistry Institute of Neuroscience & Physiology the Sahlgrenska Academy at the University of Gothenburg M\u00f6lndal Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ilaria","family":"Pola","sequence":"additional","affiliation":[{"name":"Department of Psychiatry and Neurochemistry Institute of Neuroscience & Physiology the Sahlgrenska Academy at the University of Gothenburg M\u00f6lndal 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