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We assessed the ability of plasma GFAP to detect Alzheimer\u2019s disease (AD) pathology in the form of AD-related amyloid-\u03b2 (A\u03b2) pathology and conversion to AD dementia in a mild cognitive impairment (MCI) cohort.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Method<\/jats:title>\n                    <jats:p>One hundred sixty MCI patients were followed for 4.7\u2009years (average). AD pathology was defined using cerebrospinal fluid (CSF) A\u03b242\/40 and A\u03b242\/total tau\u00a0(T-tau). Plasma GFAP was measured at baseline and follow-up using Simoa technology.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Baseline plasma GFAP could detect abnormal CSF A\u03b242\/40 and CSF A\u03b242\/T-tau with an AUC of 0.79 (95% CI 0.72\u20130.86) and 0.80 (95% CI 0.72\u20130.86), respectively. When also including\n                      <jats:italic>APOE<\/jats:italic>\n                      \u03b54 status as a predictor, the accuracy of the model to detect abnormal CSF A\u03b242\/40 status improved (AUC\u2009=\u20090.86,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.02). Plasma GFAP predicted subsequent conversion to AD dementia with an AUC of 0.84 (95% CI 0.77\u20130.91), which was not significantly improved when adding\n                      <jats:italic>APOE<\/jats:italic>\n                      \u03b54 or age as predictors to the model. Longitudinal GFAP slopes for A\u03b2-positive and MCI who progressed to dementia (AD or other) were significantly steeper than those\u00a0for A\u03b2-negative (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.007) and stable MCI (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.0001), respectively.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Plasma GFAP can detect AD pathology in patients with MCI and predict conversion to AD dementia.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1186\/s13195-021-00804-9","type":"journal-article","created":{"date-parts":[[2021,3,27]],"date-time":"2021-03-27T09:02:21Z","timestamp":1616835741000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":279,"title":["Plasma glial fibrillary acidic protein detects Alzheimer pathology and predicts future conversion to Alzheimer dementia in patients with mild cognitive impairment"],"prefix":"10.1186","volume":"13","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1806-7089","authenticated-orcid":false,"given":"Claudia","family":"Cicognola","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shorena","family":"Janelidze","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joakim","family":"Hertze","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Henrik","family":"Zetterberg","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kaj","family":"Blennow","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Niklas","family":"Mattsson-Carlgren","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Oskar","family":"Hansson","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2021,3,27]]},"reference":[{"key":"804_CR1","volume-title":"Global Dementia Observatory, Global action plan on the public health response to dementia 2017\u20132025","author":"World Health Organization W","year":"2017","unstructured":"World Health Organization W. 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KB has served as a consultant, at advisory boards, or at data monitoring committees for Abcam, Axon, Biogen, JOMDD\/Shimadzu. Julius Clinical, Lilly, MagQu, Novartis, Roche Diagnostics, and Siemens Healthineers, and is a co-founder of Brain Biomarker Solutions in Gothenburg AB (BBS) (outside submitted work). OH has acquired research support (for the institution) from AVID Radiopharmaceuticals, Biogen, Eli Lilly, Eisai, GE Healthcare, Pfizer, and Roche. In the past 2\u2009years, he has received consultancy\/speaker fees from AC Immune, Alzpath, Biogen, Cerveau, and Roche. The other authors declare no conflict of interest.","order":4,"name":"Ethics","group":{"name":"EthicsHeading","label":"Competing interests"}}],"article-number":"68"}}