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Although commonly associated with the primary 4\u2010repeat\u2010tauopathy of corticobasal degeneration, clinicopathological correlation is poor, and a significant proportion is due to Alzheimer's disease (AD). Synaptic loss is a pathological feature of many clinical and preclinical tauopathies. We therefore measured the degree of synaptic loss in patients with CBS and tested whether synaptic loss differed according to \u03b2\u2010amyloid status.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Twenty\u2010five people with CBS, and 32 age\u2010\/sex\u2010\/education\u2010matched healthy controls participated. Regional synaptic density was estimated by [\n                      <jats:sup>11<\/jats:sup>\n                      C]UCB\u2010J non\u2010displaceable binding potential (BP\n                      <jats:sub>ND<\/jats:sub>\n                      ), AD\u2010tau pathology by [\n                      <jats:sup>18<\/jats:sup>\n                      F]AV\u20101451 BP\n                      <jats:sub>ND<\/jats:sub>\n                      , and gray matter volume by T1\u2010weighted magnetic resonance imaging. Participants with CBS had \u03b2\u2010amyloid imaging with\n                      <jats:sup>11<\/jats:sup>\n                      C\u2010labeled Pittsburgh Compound\u2010B ([\n                      <jats:sup>11<\/jats:sup>\n                      C]PiB) positron emission tomography. Symptom severity was assessed with the progressive supranuclear palsy\u2010rating\u2010scale, the cortical basal ganglia functional scale, and the revised Addenbrooke's Cognitive Examination. Regional differences in BP\n                      <jats:sub>ND<\/jats:sub>\n                      and gray matter volume between groups were assessed by ANOVA.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Compared to controls, patients with CBS had higher [\n                      <jats:sup>18<\/jats:sup>\n                      F]AV\u20101451 uptake, gray matter volume loss, and reduced synaptic density. Synaptic loss was more severe and widespread in the \u03b2\u2010amyloid negative group. Asymmetry of synaptic loss was in line with the clinically most affected side.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Discussion<\/jats:title>\n                    <jats:p>\n                      Distinct patterns of [\n                      <jats:sup>11<\/jats:sup>\n                      C]UCB\u2010J and [\n                      <jats:sup>18<\/jats:sup>\n                      F]AV\u20101451 binding and gray matter volume loss, indicate differences in the pathogenic mechanisms of CBS according to whether it is associated with the presence of Alzheimer's disease or not. This highlights the potential for different therapeutic strategies in CBSs. \u00a9 2024 The Authors.\n                      <jats:italic>Movement Disorders<\/jats:italic>\n                      published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/mds.29814","type":"journal-article","created":{"date-parts":[[2024,4,26]],"date-time":"2024-04-26T23:38:40Z","timestamp":1714174720000},"page":"1166-1178","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":6,"title":["Differential Synaptic Loss in \u03b2\u2010Amyloid Positive Versus \u03b2\u2010Amyloid Negative Corticobasal Syndrome"],"prefix":"10.1002","volume":"39","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3813-0882","authenticated-orcid":false,"given":"Negin","family":"Holland","sequence":"first","affiliation":[{"name":"Department of Clinical Neurosciences University of Cambridge, Cambridge Biomedical Campus  Cambridge United Kingdom"},{"name":"Cambridge University Hospitals NHS Foundation Trust  Cambridge United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"George","family":"Savulich","sequence":"additional","affiliation":[{"name":"Department of Psychiatry University of Cambridge, Cambridge Biomedical Campus  Cambridge United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"P. 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