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However, the A\u03b2 levels necessary for tau to spread in the neocortex is still unclear.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Methods<\/jats:title>\n                <jats:p>Four hundred sixty-six participants underwent tau imaging with [18F]MK6420 and A\u03b2 imaging with [<jats:sup>18<\/jats:sup>F]NAV4694. A\u03b2 scans were quantified on the Centiloid (CL) scale with a cut-off of 25 CL for abnormal levels of A\u03b2 (A+). Tau scans were quantified in three regions of interest (ROI) (mesial temporal (Me); temporoparietal neocortex (Te); and rest of neocortex (R)) and four mesial temporal region (entorhinal cortex, amygdala, hippocampus, and parahippocampus). Regional tau thresholds were established as the 95%ile of the cognitively unimpaired A- subjects. The prevalence of abnormal tau levels (T+) along the Centiloid continuum was determined.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Results<\/jats:title>\n                <jats:p>The plots of prevalence of T+ show earlier and greater increase along the Centiloid continuum in the medial temporal area compared to neocortex. Prevalence of T+ was low but associated with A\u03b2 level between 10 and 40 CL reaching 23% in Me, 15% in Te, and 11% in R. Between 40 and 70 CL, the prevalence of T+ subjects per CL increased fourfold faster and at 70 CL was 64% in Me, 51% in Te, and 37% in R. In cognitively unimpaired, there were no T+ in R below 50 CL. The highest prevalence of T+\u00a0were found in the entorhinal cortex, reaching 40% at 40 CL and 80% at 60 CL.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Conclusion<\/jats:title>\n                <jats:p>Outside the entorhinal cortex, abnormal levels of cortical tau on PET are rarely found with A\u03b2 below 40 CL. Above 40 CL prevalence of T+ accelerates in all areas. Moderate A\u03b2 levels are required before abnormal neocortical tau becomes detectable.<\/jats:p>\n              <\/jats:sec>","DOI":"10.1007\/s00259-021-05191-9","type":"journal-article","created":{"date-parts":[[2021,1,26]],"date-time":"2021-01-26T03:02:44Z","timestamp":1611630164000},"page":"2225-2232","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":79,"title":["Relationship between amyloid and tau levels and its impact on tau spreading"],"prefix":"10.1007","volume":"48","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8051-0558","authenticated-orcid":false,"given":"Vincent","family":"Dor\u00e9","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Natasha","family":"Krishnadas","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pierrick","family":"Bourgeat","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kun","family":"Huang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shenpeng","family":"Li","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Samantha","family":"Burnham","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Colin L.","family":"Masters","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jurgen","family":"Fripp","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Victor L.","family":"Villemagne","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Christopher C.","family":"Rowe","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2021,1,26]]},"reference":[{"key":"5191_CR1","doi-asserted-by":"publisher","first-page":"351","DOI":"10.1016\/S0197-4580(97)00056-0","volume":"18","author":"H Braak","year":"1997","unstructured":"Braak H, Braak E. 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Rowe has received research grants from NHMRC, Enigma Australia, Biogen, Eisai, and Abbvie. He is on the scientific advisory board for Cerveau Technologies and Biogen Australia. Victor Villemagne is and has been a consultant or paid speaker at sponsored conference sessions for Eli Lilly, Life Molecular Imaging, GE Healthcare, Abbvie, Lundbeck, Shanghai Green Valley Pharmaceutical Co. Ltd., and Hoffmann La Roche. All the other authors declare that they have no conflict of interest.","order":2,"name":"Ethics","group":{"name":"EthicsHeading","label":"Conflict of interest"}},{"value":"This study was approved by the Austin Health Human Research ethics Committee (HREC\/18\/Austin\/201).","order":3,"name":"Ethics","group":{"name":"EthicsHeading","label":"Ethics approval and<!--Emphasis Type='Bold' removed-->consent to participate"}},{"value":"Given the retrospective nature of the study and the use of anonymized patient data, requirements for informed consent were waived.","order":4,"name":"Ethics","group":{"name":"EthicsHeading","label":"Consent for publication"}},{"value":"The datasets used and\/or analysed during the current study are available from the corresponding author on reasonable request.","order":5,"name":"Ethics","group":{"name":"EthicsHeading","label":"Code availability"}}]}}