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We developed a computational model in which neuronal activity and amyloid-\u03b2 (A\u03b2) modulate tau transport, hypothesizing that this mechanism explains entorhinal vulnerability to early tau pathology.<\/jats:p>\n                  <jats:p>The model combines structural connectivity with either neuronal activity (measured by FDG PET) or A\u03b2 burden (measured by A\u03b2 PET). We analysed Alzheimer\u2019s Disease Neuroimaging Initiative (ADNI) data comprising 527 FDG PET scans (mean age 71.8 years; 174 cognitively normal, 293 mild cognitive impairment, 60 Alzheimer\u2019s disease) and 1244 A\u03b2 PET scans (mean age 72.4 years; 501 cognitively normal, 588 mild cognitive impairment, 155 Alzheimer\u2019s disease). From these, 253 FDG\u2013tau and 453 A\u03b2\u2013tau PET pairs were used in regression analyses. Key results were replicated in the Harvard Aging Brain Study (HABS; 300 FDG, 348 A\u03b2, 116 FDG\u2013tau and 255 A\u03b2\u2013tau pairs).<\/jats:p>\n                  <jats:p>Both FDG- and A\u03b2-based models consistently identified the entorhinal cortex as a primary tau seeding region in ADNI (FDG: z \u2248 4.6\u20134.9, P &amp;lt; 0.0066; A\u03b2: z \u2248 4.0\u20138.7, P \u2264 0.011) and in HABS (FDG: z = 5.7, P = 0.030; A\u03b2: z = 6.0, P = 0.0018). Simple linear regression showed modest associations between model-derived seeding and empirical entorhinal tau in ADNI (FDG: \u03b2 = 6.7, P = 0.0039; A\u03b2: \u03b2 = 11.3, P &amp;lt; 0.001), which remained significant after adjustment for age, sex, and APOE4 status (FDG: \u03b2 = 7.1, P &amp;lt; 0.001; A\u03b2: \u03b2 = 9.7, P &amp;lt; 0.001). A\u03b2-based associations replicated in HABS (\u03b2 = 3.3, P &amp;lt; 0.001), while FDG-based correlations were not detectable in this predominantly cognitively normal cohort (\u03b2 = \u22120.43, P = 0.80; power = 49%).<\/jats:p>\n                  <jats:p>These findings support a mechanistic role for neuronal activity and A\u03b2 in initiating tau pathology, with the entorhinal cortex consistently emerging as highly vulnerable. Our computational model reliably identifies this region as the epicentre of pathology, supporting the idea that brain-wide patterns of neuronal activity and amyloid burden determine where tau pathology begins.<\/jats:p>","DOI":"10.1093\/brain\/awaf374","type":"journal-article","created":{"date-parts":[[2025,10,5]],"date-time":"2025-10-05T11:42:49Z","timestamp":1759664569000},"page":"1915-1928","source":"Crossref","is-referenced-by-count":4,"title":["Neuronal activity and amyloid-\u03b2 promote tau seeding in the entorhinal cortex in Alzheimer\u2019s disease"],"prefix":"10.1093","volume":"149","author":[{"given":"Christoffer G","family":"Alexandersen","sequence":"first","affiliation":[{"name":"Department of Bioengineering, School of Engineering and Applied Science, University of Pennsylvania , Philadelphia, PA 19104 ,","place":["USA"]},{"name":"Mathematical Institute, University of Oxford , Oxford OX4 6GG ,","place":["UK"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6183-4493","authenticated-orcid":false,"given":"Dani S","family":"Bassett","sequence":"additional","affiliation":[{"name":"Department of Bioengineering, School of Engineering and Applied Science, University of Pennsylvania , Philadelphia, PA 19104 ,","place":["USA"]},{"name":"Department of Electrical & Systems Engineering, School of Engineering and Applied Science, University of Pennsylvania , Philadelphia, PA 19104 ,","place":["USA"]},{"name":"Department of Physics & Astronomy, School of Arts & Sciences, University of Pennsylvania , Philadelphia, PA 19104 ,","place":["USA"]},{"name":"Departments of Neurology & Psychiatry, Perelman School of Medicine, University of Pennsylvania , Philadelphia, PA 19104 ,","place":["USA"]},{"name":"The Neuro, Montreal Neurological Institute, McGill University , Montreal, QC H3A 0G4 ,","place":["Canada"]},{"name":"Santa Fe Institute , Santa Fe, NM 87501 ,","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6436-8483","authenticated-orcid":false,"given":"Alain","family":"Goriely","sequence":"additional","affiliation":[{"name":"Mathematical Institute, University of Oxford , Oxford OX4 6GG ,","place":["UK"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pavanjit","family":"Chaggar","sequence":"additional","affiliation":[{"name":"Mathematical Institute, University of Oxford , Oxford OX4 6GG ,","place":["UK"]},{"name":"Clinical Memory Research, Lund University , Lund 221 00 ,","place":["Sweden"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2025,10,7]]},"reference":[{"key":"2026060316593323000_awaf374-B1","doi-asserted-by":"crossref","first-page":"135","DOI":"10.1016\/j.neurobiolaging.2021.09.017","article-title":"Tau pathology mediates age effects on medial temporal lobe 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