Clinical relevance of the quantification of apolipoprotein E in cerebrospinal fluid
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Cited by (92)
Cholesterol metabolism: Towards a therapeutic approach for multiple sclerosis
2023, Neurochemistry InternationalCSF ApoE predicts clinical progression in nondemented APOEε4 carriers
2017, Neurobiology of AgingCitation Excerpt :In addition to mechanisms directly related to pathophysiological processes in the brain, the APOEε4 genotype could also increase risk of dementia due to AD by influencing cardiovascular risk (Caselli and Reiman, 2013; Holtzman et al., 2012; Kester et al., 2010; Mahley and Rall, 2000). If this is the case, plasma ApoE may be a better reflection of this mechanism in vivo than CSF ApoE, because the 2 are not correlated and it is therefore likely that plasma ApoE is derived from a peripheral source (the liver), while CSF ApoE is derived from the brain (Baker-Nigh et al., 2016; Carlsson et al., 1991; Cruchaga et al., 2012; Fagan et al., 2000). Our finding that plasma ApoE did not predict clinical progression while CSF ApoE did, could imply that the activity of ApoE in the brain determines the risk of developing dementia due to AD to a larger extent than its cardiovascular effects.
Redox status of serum apolipoprotein E and its impact on HDL cholesterol levels
2017, Clinical BiochemistryCitation Excerpt :This finding indicated that this method would allow us to determine the number of cysteine residues in the target protein by estimating the extent of mobility shift. The reason for the inconsistency between the apparent and actual molecular weight is that the PEG molecule is hydrated extensively, as demonstrated previously [29,30]. In accordance with the number of cysteine residues, recombinant apoE3 showed a mobility shift equivalent to labeling with one PEG-PC-Mal moiety (PEG-PC-Mal)1, and recombinant apoE4, which possesses no cysteine, showed no mobility shift.
Cholesterol and markers of cholesterol turnover in multiple sclerosis: Relationship with disease outcomes
2016, Multiple Sclerosis and Related DisordersCitation Excerpt :ApoB is a major component of low density lipoprotein (LDL), intermediate density cholesterol (IDL) and very low density cholesterol (VLDL), and composes 95%, 60%, and 30% of their protein content, respectively (Ginsberg, 1998). LDL, IDL, and VLDL and ApoB are synthesized exclusively in the periphery and cannot pass through an intact blood-brain barrier (BBB; Carlsson et al., 1991; Di Paolo and Kim, 2011). ApoA1 and ApoA2 are major components of high-density lipoprotein (HDL), consisting of 70–80% and 10–15% of its protein mass, respectively (Ginsberg, 1998).
Total ApoE and ApoE4 isoform assays in an Alzheimer's disease case-control study by targeted mass spectrometry (n = 669): A pilot assay for methionine-containing proteotypic peptides
2012, Molecular and Cellular ProteomicsCitation Excerpt :The same influencing order is found for brain amyloid β accumulation across cognitively normal individuals as demonstrated by imaging studies (82–85). Thus, a large body of evidence converges on a pivotal role of ApoE in the neurodegeneration process associated with a possible disruption of ApoE levels in the cerebrospinal fluid (7, 86–95). This is reinforced by the recent article by Cramer et al. who demonstrated reduced Aβ plaque area and improved cognitive functions in a mouse model of AD after treatment by bexarotene, an agonist of nuclear receptors that transcriptionally regulates ApoE expression (96).
Roles of extracellular chaperones in amyloidosis
2012, Journal of Molecular BiologyCitation Excerpt :Furthermore, in SAP knockout mice, amyloid deposition is delayed, suggesting that it has a pro-amyloidogenic role in vivo.155 ApoE is a 34-kDa secreted protein that is found in human plasma at approximately 60–120 μg/mL and in CSF at around one-tenth of this concentration.175 In humans, there are three common alleles of the ApoE gene designated ɛ2, ɛ3 and ɛ4, which result in three heterozygous and three homozygous genotypes.176