{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,28]],"date-time":"2026-04-28T17:04:42Z","timestamp":1777395882679,"version":"3.51.4"},"reference-count":61,"publisher":"SAGE Publications","issue":"3","license":[{"start":{"date-parts":[[2019,10,17]],"date-time":"2019-10-17T00:00:00Z","timestamp":1571270400000},"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":[[2019,11,26]]},"abstract":"<jats:p>\u00a0Apolipoprotein E ( APOE) genotype is an established genetic risk factor for sporadic Alzheimer\u2019s disease (AD) but the extent to which APOE genotype influences the plasma lipidome is unknown, even though lipids are potential diagnostic or prognostic biomarkers for AD. We quantified plasma lipids using untargeted liquid chromatography coupled mass spectrometry in a total of 152 non-demented participants aged 65\u2013100 years carrying at least one \u025b2 or \u025b4 allele ( \u025b2\/ \u025b2 or \u025b2\/ \u025b3, n\u200a=\u200a38: \u025b4\/ \u025b3 or \u025b4\/ \u025b4, n\u200a=\u200a38), who were roughly matched to an \u025b3\/ \u025b3 control by age, sex, and lipid-lowering medication ( n\u200a=\u200a76). Low density lipoprotein cholesterol levels were genotype dependent ( \u025b4\/ \u025b4&gt; \u025b4\/ \u025b3&gt; \u025b3\/ \u025b3&gt; \u025b2\/ \u025b3&gt; \u025b2\/ \u025b2). The greatest variation in lipids was related to the \u025b2 isoform, where various lysophosphatidylcholines and all phosphatidylethanolamine (PE) subclasses were elevated relative to \u025b3\/ \u025b3 and \u025b4 carriers. APOE \u025b4 carriers had reduced phosphatidylinositol relative to \u025b3\/ \u025b3 and \u025b2 carriers. Logistic regression revealed that \u025b2 carriers were at least 4 times higher odds of being in the highest tertile of PE lipid level relative to \u025b3\/ \u025b3. The elevation in PE and other phospholipids in \u025b2 carriers may indicate the protective effect of \u025b2 is linked to these phospholipids. Additionally, high baseline PE in cognitively normal participants predicted protection against cognitive decline six years later. Our data suggest substantial modulation of plasma lipids by APOE genotype and therefore indicates possible lipid targets and pathomechanisms involved in AD risk.<\/jats:p>","DOI":"10.3233\/jad-190524","type":"journal-article","created":{"date-parts":[[2019,10,18]],"date-time":"2019-10-18T11:01:26Z","timestamp":1571396486000},"page":"703-716","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":15,"title":["<i>APOE<\/i>\n                    Genotype Differentially Modulates Plasma Lipids in Healthy Older Individuals, with Relevance to Brain Health"],"prefix":"10.1177","volume":"72","author":[{"given":"Matthew Wai Kin","family":"Wong","sequence":"first","affiliation":[{"name":"Centre for Healthy Brain Ageing, School of Psychiatry, Faculty of Medicine, University of New South Wales, Sydney, 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