{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,9]],"date-time":"2026-06-09T21:44:28Z","timestamp":1781041468541,"version":"3.54.1"},"reference-count":50,"publisher":"SAGE Publications","issue":"3","license":[{"start":{"date-parts":[[2020,4,23]],"date-time":"2020-04-23T00:00:00Z","timestamp":1587600000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Journal of Alzheimer\u2019s Disease"],"published-print":{"date-parts":[[2020,6,2]]},"abstract":"<jats:sec>\n                    <jats:title>Background:<\/jats:title>\n                    <jats:p>Numerous studies have reported on cerebrospinal fluid (CSF) and blood biomarkers of Alzheimer\u2019s disease (AD); however, to date, none has compared biomarker patterns across the early-onset subtypes, i.e., early onset sporadic AD (EOsAD) and autosomal dominant AD (ADAD), qualitatively and quantitatively.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objective:<\/jats:title>\n                    <jats:p>To compare the fluid biomarker patterns in early-onset subtypes of AD; EOsAD and ADAD.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods:<\/jats:title>\n                    <jats:p>Six scientific databases were searched for peer-reviewed research publications. The total number of individuals used in all the meta-analysis were 2,427, comprised of 1,337 patients and 1,090 controls.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results:<\/jats:title>\n                    <jats:p>\n                      In the subset of EOsAD cases without APP, PSEN1\/ PSEN2 mutations, CSF A\u03b2\n                      <jats:sub>42<\/jats:sub>\n                      and tau levels were higher when compared to the EOsAD group as a whole. Prevalence of the APOE \u025b4 allele was more elevated in EOsAD relative to controls, and not significantly elevated in ADAD cases.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion:<\/jats:title>\n                    <jats:p>Established CSF biomarkers confirmed quantitative differences between variants of EOAD. EOsAD is enriched with APOE \u025b4, but the level is not higher than generally reported in late-onset AD. The results prompt further exploration of the etiopathogenesis of EOsAD, which accounts for \u223c4\u201310% of all AD cases, but the reasons for the early onset remain poorly understood.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3233\/jad-200052","type":"journal-article","created":{"date-parts":[[2020,4,24]],"date-time":"2020-04-24T11:44:02Z","timestamp":1587728642000},"page":"827-843","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":9,"title":["Fluid Biomarkers and\n                    <i>APOE<\/i>\n                    Status of Early Onset Alzheimer\u2019s Disease Variants: A Systematic Review and Meta-Analysis"],"prefix":"10.1177","volume":"75","author":[{"given":"Gurjeet","family":"Kaur","sequence":"first","affiliation":[{"name":"Centre for Healthy Brain Ageing, School of Psychiatry, University of New South Wales, Sydney, NSW, 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