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However, a minority of clinically diagnosed PD patients are negative for \u03b1Syn.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>METHODS<\/jats:title>\n                    <jats:p>\n                      The \u03b1Syn\u2010SAA was performed in cerebrospinal fluid (CSF) of individuals with PD (\n                      <jats:italic>n<\/jats:italic>\n                      \u00a0=\u00a093), multiple system atrophy (MSA,\n                      <jats:italic>n<\/jats:italic>\n                      \u00a0=\u00a026), progressive supranuclear palsy (PSP,\n                      <jats:italic>n<\/jats:italic>\n                      \u00a0=\u00a018), corticobasal syndrome (\n                      <jats:italic>n<\/jats:italic>\n                      \u00a0=\u00a03), and healthy controls (\n                      <jats:italic>n<\/jats:italic>\n                      \u00a0=\u00a029).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>RESULTS<\/jats:title>\n                    <jats:p>\n                      The \u03b1Syn\u2010SAA detected \u03b1Syn in 90% of PD and 81% of MSA patients, while exhibiting high specificity (97%). SAA\u2013 PD patients had a distinct phenotype compared to SAA+ PD, including a marked postural instability\/gait disorder (\n                      <jats:italic>P\u00a0<\/jats:italic>\n                      =\u00a00.002), impaired episodic memory, and lower CSF amyloid beta\n                      <jats:sub>42<\/jats:sub>\n                      (\n                      <jats:italic>P\u00a0<\/jats:italic>\n                      =\u00a00.03). SAA+ PSP also displayed distinctive traits.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>DISCUSSION<\/jats:title>\n                    <jats:p>A negative \u03b1Syn\u2010SAA in PD is associated with a distinct phenotype and pathological findings suggesting that these patients may have a motor subtype of\u00a0Alzheimer's disease. This could influence future clinical trials.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Highlights<\/jats:title>\n                    <jats:p>\n                      <jats:list list-type=\"bullet\">\n                        <jats:list-item>\n                          <jats:p>The \u03b1\u2010synuclein seed amplification assay (\u03b1Syn\u2010SAA) is a robust assay.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>\u03b1Syn\u2010SAA\u2013negative Parkinson's disease shows a distinct motor\u2013cognitive phenotype.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>Autopsy showed Alzheimer's disease (AD) pathology in parkinsonian diseases.<\/jats:p>\n                        <\/jats:list-item>\n                        <jats:list-item>\n                          <jats:p>AD stands as a major clinical confounder for the diagnosis of movement disorders.<\/jats:p>\n                        <\/jats:list-item>\n                      <\/jats:list>\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/alz.70284","type":"journal-article","created":{"date-parts":[[2025,5,19]],"date-time":"2025-05-19T08:16:55Z","timestamp":1747642615000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Alzheimer's disease traits in Parkinson's disease without \u03b1\u2010synuclein seeding"],"prefix":"10.1002","volume":"21","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-1512-6699","authenticated-orcid":false,"given":"B\u00e1rbara","family":"Fernandes Gomes","sequence":"first","affiliation":[{"name":"Department of Psychiatry and Neurochemistry Institute of Neuroscience and Physiology the Sahlgrenska Academy at the University of Gothenburg  M\u00f6lndal Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Carly M.","family":"Farris","sequence":"additional","affiliation":[{"name":"R&amp;D Unit, Amprion Inc.  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