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With new treatments targeting the core biology of Alzheimer\u2019s disease, understanding the timeline of biological changes is crucial as the disease progresses over decades.<\/jats:p>\n                  <jats:p>Longitudinal data from amyloid-beta (A\u03b2) PET and cognitive tests [Mini-Mental State Examination (MMSE) and Alzheimer's Disease Assessment Scale\u2013Cognitive Subscale (ADAS-cog)] from the Alzheimer\u2019s Disease Neuroimaging Initiative (n = 1448) and BioFINDER (n = 2088) were used to stage patients against an estimated continuous disease timeline (predicted time since A\u03b2-PET positivity). The estimated timeline was validated by comparing correlations with unseen biomarkers and cognitive measures against alternative staging approaches. Trajectories for plasma, CSF, MRI and PET biomarkers, measuring A\u03b2, tau and neurodegeneration, were mapped along this Alzheimer\u2019s disease continuum.<\/jats:p>\n                  <jats:p>The proposed staging approach was found to produce stronger correlations with unseen cognitive measures and biomarkers compared to alternative staging methods, including amyloid and tau PET clocks (all pairwise P &amp;lt; 0.05). Findings related to biomarker trajectories were highly consistent across cohorts. The period from A\u03b2-PET positivity to end-stage Alzheimer\u2019s disease dementia (MMSE = 0) was estimated at 20\u201325 years, with a presymptomatic phase of 7\u201311 years. CSF A\u03b242\/A\u03b240 became abnormal about a year before A\u03b2-PET positivity, CSF phosphorylated-tau (p-tau)231, p-tau217 and plasma phosphorylated\/neuritic plaque-tau217 1\u20133 years after, and tau-PET about 8 years after. Neurodegenerative biomarkers, such as hippocampal volume, became clearly abnormal in early dementia stages, 14\u201316 years after A\u03b2-PET positivity.<\/jats:p>\n                  <jats:p>The progression from initial biomarker abnormality to severe Alzheimer\u2019s disease spans two decades. Disease progression modelling elucidates the evolution of AD biomarkers and cognition, highlighting the relative timing of biomarker abnormalities. These models can determine disease stages, aiding in prognosis and the evaluation of disease-modifying treatments.<\/jats:p>","DOI":"10.1093\/brain\/awaf413","type":"journal-article","created":{"date-parts":[[2025,10,30]],"date-time":"2025-10-30T13:18:19Z","timestamp":1761830299000},"page":"1929-1943","source":"Crossref","is-referenced-by-count":17,"title":["Estimating the time course of biomarker changes in Alzheimer\u2019s disease"],"prefix":"10.1093","volume":"149","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-7099-2314","authenticated-orcid":false,"given":"Lars Lau","family":"Raket","sequence":"first","affiliation":[{"name":"Clinical Memory Research Unit, Department of Clinical Sciences in Malm\u00f6, Lund University , Lund 223 62 ,","place":["Sweden"]},{"name":"Eli Lilly and Company , Indianapolis, IN 46285 ,","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alexa 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Malm\u00f6, Lund University , Lund 223 62 ,","place":["Sweden"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3930-4354","authenticated-orcid":false,"given":"Henrik","family":"Zetterberg","sequence":"additional","affiliation":[{"name":"Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the University of Gothenburg , M\u00f6lndal 431 39 ,","place":["Sweden"]},{"name":"Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital , M\u00f6lndal 431 39 ,","place":["Sweden"]},{"name":"Department of Neurodegenerative Disease, UCL Institute of Neurology , London WC1N 3BG ,","place":["UK"]},{"name":"UK Dementia Research Institute at UCL , London NW1 3BT ,","place":["UK"]},{"name":"Hong Kong Center for Neurodegenerative Diseases, Clear Water Bay , Hong Kong 999077 ,","place":["China"]},{"name":"Wisconsin Alzheimer\u2019s Disease Research Center, University of Wisconsin School of Medicine and Public Health, University of Wisconsin-Madison , Madison, WI 53792 ,","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nicholas J","family":"Ashton","sequence":"additional","affiliation":[{"name":"Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the University of Gothenburg , M\u00f6lndal 431 39 ,","place":["Sweden"]},{"name":"Banner Alzheimer\u2019s Institute and University of Arizona , Phoenix, AZ 85006 ,","place":["USA"]},{"name":"Banner Sun Health Research Institute , Sun City, AZ 85351 ,","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kaj","family":"Blennow","sequence":"additional","affiliation":[{"name":"Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, the Sahlgrenska Academy at the University of Gothenburg , M\u00f6lndal 431 39 ,","place":["Sweden"]},{"name":"Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital , M\u00f6lndal 431 39 ,","place":["Sweden"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Erik","family":"Stomrud","sequence":"additional","affiliation":[{"name":"Clinical Memory Research Unit, Department of Clinical Sciences in Malm\u00f6, Lund University , Lund 223 62 ,","place":["Sweden"]},{"name":"Memory Clinic, Sk\u00e5ne University Hospital , Malm\u00f6 211 46 ,","place":["Sweden"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9267-1930","authenticated-orcid":false,"given":"Sebastian","family":"Palmqvist","sequence":"additional","affiliation":[{"name":"Clinical Memory Research Unit, Department of Clinical Sciences in Malm\u00f6, Lund University , Lund 223 62 ,","place":["Sweden"]},{"name":"Memory Clinic, Sk\u00e5ne University Hospital , Malm\u00f6 211 46 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