https://ogma.newcastle.edu.au/vital/access/ /manager/Index en-au 5 https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:34053 Wed 04 Sep 2019 09:39:49 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:628 Thu 25 Jul 2013 09:10:22 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:469 Thu 25 Jul 2013 09:09:54 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:36726 ɛ4/ɛ3> ɛ3/ɛ3> ɛ2/ɛ3> ɛ2/ɛ2). The greatest variation in lipids was related to the ɛ2 isoform, where various lysophosphatidylcholines and all phosphatidylethanolamine (PE) subclasses were elevated relative to ɛ3/ɛ3 and ɛ4 carriers. APOE ɛ4 carriers had reduced phosphatidylinositol relative to ɛ3/ɛ3 and ɛ2 carriers. Logistic regression revealed that ɛ2 carriers were at least 4 times higher odds of being in the highest tertile of PE lipid level relative to ɛ3/ɛ3. The elevation in PE and other phospholipids in ɛ2 carriers may indicate the protective effect of ɛ2 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.]]> Thu 02 Jul 2020 09:10:42 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:49966 Mon 06 May 2024 15:45:12 AEST ]]>