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Preclinical studies suggest that \u03b1Syn can exacerbate tau aggregation, implying that \u03b1Syn co-pathology may specifically contribute to the A\u03b2-induced aggregation of tau that drives neurodegeneration and cognitive decline in AD. To investigate this, we combined a novel CSF-based seed-amplification assay (SAA) to determine \u03b1Syn positivity with amyloid- and tau-PET neuroimaging in a large cohort ranging from cognitively normal individuals to those with dementia, examining whether \u03b1Syn co-pathology accelerates A\u03b2-driven tau accumulation and cognitive decline.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      In 284 A\u03b2-positive and 308 A\u03b2-negative subjects, we employed amyloid-PET, Flortaucipir tau-PET, and a CSF-based \u03b1Syn seed-amplification assay (SAA) to detect in vivo \u03b1Syn aggregation. CSF p-tau\n                      <jats:sub>181<\/jats:sub>\n                      measures were available for 384 subjects to assess earliest tau abnormalities. A subset of 155 A\u03b2-positive and 135 A\u03b2-negative subjects underwent longitudinal tau-PET over approximately 2.5 years. Using linear regression models, we analyzed whether \u03b1Syn SAA positivity was linked to stronger A\u03b2-related increases in baseline fluid and PET tau biomarkers, faster A\u03b2-driven tau-PET increase, and more rapid cognitive decline.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      \u03b1Syn SAA positivity was more common in A\u03b2\u2009+\u2009vs. A\u03b2- subjects and increased with clinical severity (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.001). Most importantly, \u03b1Syn positivity was also associated with greater amyloid-associated CSF p-tau\n                      <jats:sub>181<\/jats:sub>\n                      increases (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.005) and higher tau-PET levels in AD-typical brain regions (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.006). Longitudinal analyses confirmed further that \u03b1Syn positivity was associated with faster amyloid-related tau accumulation (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.029) and accelerated amyloid-related cognitive decline, potentially driven driven by stronger tau pathology.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Our findings suggest that \u03b1Syn co-pathology, detectable via CSF-based SAAs, is more prevalent in advanced AD and contributes to the development of aggregated tau pathology thereby driving faster cognitive decline. This highlights that a-Syn co-pathology may specifically accelerate amyloid-driven tau pathophysiology in AD, underscoring the need to consider \u03b1Syn in AD research and treatment strategies.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1186\/s13024-025-00822-3","type":"journal-article","created":{"date-parts":[[2025,3,17]],"date-time":"2025-03-17T20:03:59Z","timestamp":1742241839000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":73,"title":["Alpha synuclein co-pathology is associated with accelerated amyloid-driven tau accumulation in Alzheimer\u2019s disease"],"prefix":"10.1186","volume":"20","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-9736-2283","authenticated-orcid":false,"given":"Nicolai","family":"Franzmeier","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sebastian Niclas","family":"Roemer-Cassiano","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alexander Maximilian","family":"Bernhardt","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Amir","family":"Dehsarvi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anna","family":"Dewenter","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anna","family":"Steward","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Davina","family":"Biel","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lukas","family":"Frontzkowski","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zeyu","family":"Zhu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Johannes","family":"Gn\u00f6rich","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Julia","family":"Pescoller","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fabian","family":"Wagner","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fabian","family":"Hirsch","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hannah","family":"de Bruin","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rik","family":"Ossenkoppele","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Carla","family":"Palleis","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Felix","family":"Str\u00fcbing","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael","family":"Sch\u00f6ll","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Johannes","family":"Levin","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Matthias","family":"Brendel","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"G\u00fcnter U.","family":"H\u00f6glinger","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2025,3,18]]},"reference":[{"key":"822_CR1","doi-asserted-by":"publisher","first-page":"173","DOI":"10.1007\/s13311-021-01146-y","volume":"19","author":"JA Trejo-Lopez","year":"2022","unstructured":"Trejo-Lopez JA, Yachnis AT, Prokop S. 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