{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T01:23:38Z","timestamp":1790645018233,"version":"4.1.0"},"reference-count":60,"publisher":"Oxford University Press (OUP)","issue":"10","license":[{"start":{"date-parts":[[2024,9,11]],"date-time":"2024-09-11T00:00:00Z","timestamp":1726012800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2024,10,3]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Positive effects of new anti-amyloid-\u03b2 (A\u03b2) monoclonal antibodies in Alzheimer\u2019s disease (AD) have been attributed to brain amyloid reduction. However, most anti-A\u03b2 antibodies also increase the CSF levels of the 42-amino acid isoform (A\u03b242). We evaluated the associations of changes in CSF A\u03b242 and brain A\u03b2-PET with cognitive and clinical end points in randomized trials of anti-A\u03b2 drugs that lowered (\u03b2- and \u03b3-secretase inhibitors) or increased CSF A\u03b242 levels (anti-A\u03b2 monoclonal antibodies) to test the hypothesis that post-treatment increases in CSF A\u03b242 levels are independently associated with cognitive and clinical outcomes.<\/jats:p>\n               <jats:p>From long-term (\u226512\u2005months) randomized placebo-controlled clinical trials of anti-A\u03b2 drugs published until November 2023, we calculated the post-treatment versus baseline difference in ADAS-Cog (cognitive subscale of the Alzheimer\u2019s Disease Assessment Scale) and CDR-SB (Clinical Dementia Rate-Sum of Boxes) and z-standardized changes in CSF A\u03b242 and A\u03b2-PET Centiloids (CL). We estimated the effect size [regression coefficients (RCs) and confidence intervals (CIs)] and the heterogeneity (I2) of the associations between AD biomarkers and cognitive and clinical end points using random-effects meta-regression models.<\/jats:p>\n               <jats:p>We included 25 966 subjects with AD from 24 trials. In random-effects analysis, increases in CSF A\u03b242 were associated with slower decline in ADAS-Cog (RC: \u22120.55; 95% CI: \u22120.89, \u22120.21, P = 0.003, I2 = 61.4%) and CDR-SB (RC: \u22120.16; 95% CI: \u22120.26, \u22120.06, P = 0.002, I2 = 34.5%). Similarly, decreases in A\u03b2\u2013PET were associated with slower decline in ADAS-Cog (RC: 0.69; 95% CI: 0.48, 0.89, P &amp;lt; 0.001, I2 = 0%) and CDR-SB (RC: 0.26; 95% CI: 0.18, 0.33, P &amp;lt; 0.001, I2 = 0%). Sensitivity analyses yielded similar results.<\/jats:p>\n               <jats:p>Higher CSF A\u03b242 levels after exposure to anti-A\u03b2 drugs are independently associated with slowing cognitive impairment and clinical decline. Increases in A\u03b242 may represent a mechanism of potential benefit of anti-A\u03b2 monoclonal antibodies in AD.<\/jats:p>","DOI":"10.1093\/brain\/awae216","type":"journal-article","created":{"date-parts":[[2024,9,11]],"date-time":"2024-09-11T22:28:42Z","timestamp":1726093722000},"page":"3513-3521","source":"Crossref","is-referenced-by-count":33,"title":["Increases in amyloid-\u03b242 slow cognitive and clinical decline in Alzheimer\u2019s disease trials"],"prefix":"10.1093","volume":"147","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6073-7974","authenticated-orcid":false,"given":"Jesus","family":"Abanto","sequence":"first","affiliation":[{"name":"James J. and Joan A. Gardner Family Center for Parkinson\u2019s disease and Movement Disorders, Department of Neurology, University of Cincinnati , Cincinnati, OH 45219 ,","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4574-1761","authenticated-orcid":false,"given":"Alok K","family":"Dwivedi","sequence":"additional","affiliation":[{"name":"Division of Biostatistics & Epidemiology, Department of Molecular and Translational Medicine, Texas Tech University Health Sciences Center El Paso , El Paso, TX 79905 ,","place":["USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0327-7262","authenticated-orcid":false,"given":"Bruno P","family":"Imbimbo","sequence":"additional","affiliation":[{"name":"Research & Development Department, Chiesi Farmaceutici , 43122 Parma ,","place":["Italy"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3389-136X","authenticated-orcid":false,"given":"Alberto J","family":"Espay","sequence":"additional","affiliation":[{"name":"James J. and Joan A. 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