Relevant bibliographies by topics / APOE3

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  2. Dissertations / Theses
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  5. Conference papers

Academic literature on the topic 'APOE3'

Author: Grafiati
Published: 4 June 2021
Last updated: 12 February 2022

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Journal articles on the topic "APOE3"

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Yamauchi, Kazuyoshi, and Yasushi Kawakami. "The redox status of cysteine thiol residues of apolipoprotein E impacts on its lipid interactions." Biological Chemistry 401, no. 5 (April 28, 2020): 617–27. http://dx.doi.org/10.1515/hsz-2019-0414.

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AbstractRedox-mediated modulation of cysteine (Cys) thiols has roles in various pathophysiological functions. We recently found that formation of disulfide-linked complexes of apolipoprotein (apo) E3 prevented apoE3 from irreversible oxidation. In this report, the influence of modification of Cys thiols in apoE2 and apoE3 on interactions with lipids was investigated. The apoE redox status was examined by a band-shift assay using a maleimide compound, and interactions with lipids were evaluated by a kinetic assay using dimyristoyl-sn-glycero-3-phosphocholine (DMPC) and non-denaturing polyacrylamide gel electrophoresis. A reduction in DMPC clearance activity of apoE2 and apoE3 but not apoE4 was observed. Although hydrogen peroxide-induced oxidation decreased the clearance activity of the isoforms, apoE2 showed the greatest residual activity. Both Cys thiol masking and dimerization decreased the activity of apoE2 and apoE3 but not apoE4. In contrast, apoAII preincubation markedly increased the activity (apoE2 > apoE3 > apoE4), in accordance with the formation of apoE-AII and apoAII-E2-AII complexes. ApoAII preincubation also reduced the particle size of apoE-DMPC liposome complexes, especially for apoE2. Redox-mediated modification of Cys thiols of apoE2 or apoE3, especially disulfide bond formation with apoAII, affects lipid metabolism and consequently may be responsible for the diverse isoform specificity of apoE.
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HOFFMANN, MICHAEL M., HUBERT SCHARNAGL, ELEFTHERIA PANAGIOTOU, WERNER T. BANGHARD, HEINRICH WIELAND, and WINFRIED MÄRZ. "Diminished LDL Receptor and High Heparin Binding of Apolipoprotein E2 Sendai Associated with Lipoprotein Glomerulopathy." Journal of the American Society of Nephrology 12, no. 3 (March 2001): 524–30. http://dx.doi.org/10.1681/asn.v123524.

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Abstract. Variants of apolipoprotein E (apoE) have been linked to lipoprotein glomerulopathy, a new glomerular disease characterized by the deposition of lipoproteins in mesangial capillaries. One third of affected patients are heterozygous for apoE2 Sendai (Arg145 Pro). Variants of apoE can also produce type III hyperlipoproteinemia (HLP). Recessive type III HLP is caused by apoE2 (Arg158 Cys), a mutant with diminished low-density lipoprotein (LDL) receptor binding but halfnormal heparin binding. Dominant type III HLP is caused by mutations that markedly alter heparin binding but modestly reduce receptor binding. This study examined whether apoE2 Sendai (Arg145 Pro) was functionally different from type III HLP-producing apoE variants by expressing apoE3, apoE2 (Arg158 Cys), apoE1 (Arg146 Glu), a dominant apoE variant, and apoE2 Sendai (Arg145 Pro) in the baculovirus system. LDL receptor binding was studied using recombinant apoE complexed to phospholipid vesicles and to very lowdensity lipoprotein from a patient with familiar apoE deficiency. Compared with apoE3, receptor-binding activities of apoE2 (Arg158 Cys), apoE1 (Arg146 Glu), and apoE2 Sendai (Arg145 Pro) all were less than 5%. Heparin-binding activities were 53%, 23%, and 66%, respectively, of apoE3. The distribution of apoE2 Sendai among the major plasma lipoprotein fractions was similar to that of apoE3 and apoE2 (Arg158 Cys). ApoE2 Sendai (Arg145 Pro) represents the only known mutation within the heparin-binding domain of apoE (residues 142 through 147), revealing diminished receptor binding and almost normal heparin binding. These unique characteristics of apoE2 Sendai (Arg145 Pro) may relate to the development of lipoprotein glomerulopathy.
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Hudák, Anett, Katalin Jósvay, Ildikó Domonkos, Annamária Letoha, László Szilák, and Tamás Letoha. "The Interplay of Apoes with Syndecans in Influencing Key Cellular Events of Amyloid Pathology." International Journal of Molecular Sciences 22, no. 13 (June 30, 2021): 7070. http://dx.doi.org/10.3390/ijms22137070.

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Apolipoprotein E (ApoE) isoforms exert intricate effects on cellular physiology beyond lipid transport and metabolism. ApoEs influence the onset of Alzheimer’s disease (AD) in an isoform-dependent manner: ApoE4 increases AD risk, while ApoE2 decreases it. Previously we demonstrated that syndecans, a transmembrane proteoglycan family with increased expression in AD, trigger the aggregation and modulate the cellular uptake of amyloid beta (Aβ). Utilizing our previously established syndecan-overexpressing cellular assays, we now explore how the interplay of ApoEs with syndecans contributes to key events, namely uptake and aggregation, in Aβ pathology. The interaction of ApoEs with syndecans indicates isoform-specific characteristics arising beyond the frequently studied ApoE–heparan sulfate interactions. Syndecans, and among them the neuronal syndecan-3, increased the cellular uptake of ApoEs, especially ApoE2 and ApoE3, while ApoEs exerted opposing effects on syndecan-3-mediated Aβ uptake and aggregation. ApoE2 increased the cellular internalization of monomeric Aβ, hence preventing its extracellular aggregation, while ApoE4 decreased it, thus helping the buildup of extracellular plaques. The contrary effects of ApoE2 and ApoE4 remained once Aβ aggregated: while ApoE2 reduced the uptake of Aβ aggregates, ApoE4 facilitated it. Fibrillation studies also revealed ApoE4′s tendency to form fibrillar aggregates. Our results uncover yet unknown details of ApoE cellular biology and deepen our molecular understanding of the ApoE-dependent mechanism of Aβ pathology.
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Li, Meng-Yu, Man-Ki Kwok, and Catherine Mary Schooling. "Investigating Effects of Plasma Apolipoprotein E on Ischemic Heart Disease Using Mendelian Randomization Study." Nutrients 13, no. 7 (June 28, 2021): 2215. http://dx.doi.org/10.3390/nu13072215.

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Background: Observationally plasma apolipoprotein E (apoE) is positively associated with ischemic heart disease (IHD). A Mendelian randomization (MR) study suggesting apoE is unrelated to cardiovascular mortality did not consider specific isoforms. We used MR to obtain estimates of plasma apoE2, apoE3 and apoE4 on IHD, low-density lipoprotein (LDL) and high-density lipoprotein (HDL) cholesterol, triglycerides and apolipoprotein B (apoB). Methods: We obtained independent genetic instruments from proteome genome-wide association studies (GWAS) and applied them to large outcome GWAS. We used univariable MR to assess the role of each isoform and multivariable MR to assess direct effects. Results: In univariable MR, apoE4 was positively associated with IHD (odds ratio (OR) 1.05, 95% confidence interval (CI) 1.01 to 1.09), but apoE2 and apoE3 were less clearly associated. Using multivariable MR an association of apoE2 with IHD (OR 1.16, 95% CI 0.98 to 1.38) could not be excluded, and associations of apoE3 and apoE4 with IHD were not obvious. In univariable MR, apoE2 and apoE4 were positively associated with apoB, and a positive association of apoE2 with LDL cholesterol could not be excluded. Using multivariable MR apoE2 was positively associated with LDL cholesterol, and associations with apoB could not be excluded. After adjusting for apoB, no direct effects of apoE isoforms on IHD were evident. Conclusions: Plasma apoE2 and apoE4 may play a role in lipid modulation and IHD. Whether apoE could be a potential therapeutic target requires further clarification when larger genetic studies of apoE isoforms are available.
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Santos-Ferreira, Cátia, Rui Baptista, Manuel Oliveira-Santos, Regina Costa, José Pereira Moura, and Lino Gonçalves. "Apolipoprotein E2 Genotype Is Associated with a 2-Fold Increase in the Incidence of Type 2 Diabetes Mellitus: Results from a Long-Term Observational Study." Journal of Lipids 2019 (August 7, 2019): 1–8. http://dx.doi.org/10.1155/2019/1698610.

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Background. The apolipoprotein E (APOE) polymorphisms are associated with cardiovascular (CV) disease, but its interaction with type 2 diabetes mellitus (T2DM) long-term incidence is unknown. We investigated the association between APOE genotype and long-term (i) CV events and (ii) T2DM incidence in a Southern European primary prevention cohort. Methods. We assessed individual APOE genotypes in a total of 436 patients followed at a lipid clinic, with a 15-year median follow-up time. We collected data on major CV events (CV death, myocardial infarction, and stroke) and T2DM development. Results. No differences were found regarding major CV event incidence among the different APOE genotypes. However, after excluding 39 patients with a prior history of T2DM, APOE2 carriers displayed a higher incidence of T2DM during follow-up (42.2%) than APOE3 (27.1%) and APOE4 (28.7%) carriers. The age-, sex-, triglycerides-, and statin usage-adjusted OR for T2DM incidence in APOE2 carriers was 1.8 (95%CI 1.1-2.9, p=0.03), compared with wild-type APOE3. To address the role of statins as a confounder, we analyzed T2DM incidence in statin-treated patients. Statin-treated APOE2 carriers also had a higher T2DM incidence (57.9%), in comparison with APOE3 homozygotes (31.6%) and APOE4 carriers (32.5%). After adjustment for confounding, APOE2 carriers on statins displayed a similar twofold increase in T2DM risk compared to APOE3 homozygotes (OR 2.1, 95%CI 1.1-4.0, p=0.03). Conclusion. Our findings suggest a twofold increase in T2DM incidence in APOE2 carriers. This may prompt for a specific glucose dysmetabolism follow-up that might be tailored on the APOE genotype.
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Sheng, Huaxin, Daniel T. Laskowitz, Ellen Bennett, Donald E. Schmechel, Robert D. Bart, Ann M. Saunders, Robert D. Pearlstein, Allen D. Roses, and David S. Warner. "Apolipoprotein E Isoform-Specific Differences in Outcome from Focal Ischemia in Transgenic Mice." Journal of Cerebral Blood Flow & Metabolism 18, no. 4 (April 1998): 361–66. http://dx.doi.org/10.1097/00004647-199804000-00003.

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Apolipoprotein E (apoE), a 34-kD glycosylated lipid-binding protein, is expressed as three common isoforms in humans (E2, E3, or E4). Clinical evidence suggests that the apoE genotype (APOE) may be a risk factor for poor outcome after acute central nervous system injury. This was examined further in transgenic mice constructed with the human APOE3 or APOE4 gene under the control of human promoter and tissue expression elements. Presence of human apoE3 and apoE4 proteins in brains of human APOE homozygous transgenic mice was confirmed by Western blotting. APOE3 (n = 12) and APOE4 (n = 10) mice underwent 60 minutes of middle cerebral artery occlusion. After 24-hour recovery, infarct size was measured. Infarct volumes (mean ± standard deviation) were smaller in the APOE3 group (cortex: APOE3 = 18 ± 4 mm3; APOE4 = 30 ± 11 mm3, P = 0.04; subcortex: APOE3 = 12 ± 4 mm3; APOE4 = 18 ± 4 mm3, P = 0.003). Hemiparesis was less severe in APOE3 mice ( P = 0.02). These data indicate that human isoform-specific effects of apoE are relevant to acute pathomechanisms of focal ischemic brain damage when examined in the mouse. APOE transgenic mice may provide an appropriate model to examine the mechanistic basis for the differential effects of human apoE isoforms in acute central nervous system injury.
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Pohlkamp, Theresa. "Apolipoprotein E: Cholesterol metabolism and Alzheimer’s pathology." Neuroforum 26, no. 1 (February 25, 2020): 25–30. http://dx.doi.org/10.1515/nf-2019-0030.

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AbstractAge is the greatest risk factor for Alzheimer’s disease (AD). Today, due to an increase in global life expectancy, AD-related deaths are ranked as the sixth most common cause of death. The allele isoform ɛ4 of apolipoprotein E (ApoE4) is the most important genetic risk factor for AD. Three ApoE isoforms are common in humans: ApoE2, ApoE3, and ApoE4. ApoE3 is the most frequent isoform and considered neutral with regards to AD, whereas the isoform ApoE2 is protective. Thus it is important to understand how ApoE isoforms affect amyloid-β (Aβ) and tau toxicity, the key drivers of AD pathology. Aβ and tau accumulate to form the hallmarks of AD, plaques and neurofibrillary tangles, respectively. ApoE, primarily expressed by astrocytes, is the major lipid transporter in the brain. In this review I summarize some important historic and scientific aspects of our progress in understanding the role of the cholesterol transporter ApoE in the brain, and how the isoform ApoE4 contributes to AD pathology.
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BENTLEY, Nicholas M., Mary Jo LaDU, Chandrika RAJAN, Godfrey S. GETZ, and Catherine A. REARDON. "Apolipoprotein E structural requirements for the formation of SDS-stable complexes with β-amyloid-(1–40): the role of salt bridges." Biochemical Journal 366, no. 1 (August 15, 2002): 273–79. http://dx.doi.org/10.1042/bj20020207.

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Of the three major isoforms of human apolipoprotein E (apoE), apoE4 is a risk factor for the development of Alzheimer's disease. Among possible neurologically relevant differences in the properties of apoE3 and apoE4 is the fact that apoE3 forms an SDS-stable complex with β-amyloid-(1–40) (Aβ40) with greater avidity than does apoE4. This interaction may sequester potentially toxic species of Aβ or facilitate clearance. To understand more about this difference, we examined whether differences in salt bridges between apoE domains influence the capacity of apoE isoforms to form complexes with Aβ. In apoE3 there is a salt bridge between Arg-61 and Asp-65, while in apoE4 there are salt bridges between Arg-61 and Glu-255, and Arg-112 and Glu-109. Mutation of position 112, which is Cys in apoE3 and Arg in apoE4, to Ala or Lys abolished complex formation, while mutant apoE with Ser at this position retained the capacity to form complex. Substituting Ala for Glu-109 had no effect on the ability of either apoE4 or apoE3 to form complexes. On the other hand, substitution of Thr for Arg-61 in apoE3 abolished, and truncation of apoE3 at position 201 substantially lowered, but did not abolish, complex formation. Neither of these mutations within apoE4 had any affect on its complex formation with Aβ. These results suggest that the nature of the cysteine residue in apoE3 and interactions between the N-terminal and C-terminal domains of human apoE are important for the ability of apoE3 to form an SDS-stable complex with Aβ40.
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Cambruzzi, Eduardo, and Karla Lais Pêgas. "Pathogenesis, histopathologic findings and treatment modalities of lipoprotein glomerulopathy: A review." Brazilian Journal of Nephrology 41, no. 3 (September 2019): 393–99. http://dx.doi.org/10.1590/2175-8239-jbn-2018-0148.

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Abstract Lipoprotein glomerulopathy (LPG) is an uncommon cause of nephrotic syndrome and/or kidney failure. At microscopy, LPG is characterized by the presence of lipoprotein thrombi in dilated glomerular capillaries due to different ApoE mutations. ApoE gene is located on chromosome 19q13.2, and can be identified in almost all serum lipoproteins. ApoE works as a protective factor in atherosclerosis due its interaction with receptor-mediated lipoprotein clearance and cholesterol receptor. Most common polymorphisms include ApoE2/2, ApoE3/2, ApoE3/3, ApoE4/2, ApoE4/3, and ApoE4/4. All age-groups can be affected by LPG, with a discrete male predominance. Compromised patients typically reveal dyslipidemia, type III hyperlipoproteinemia, and proteinuria. LPG treatment includes fenofibrate, antilipidemic drugs, steroids, LDL aphaeresis, plasma exchange, antiplatelet drugs, anticoagulants, urokinase, and renal transplantation. Recurrence in kidney graft suggests a pathogenic component(s) of extraglomerular humoral complex resulting from abnormal lipoprotein metabolism and presumably associated to ApoE.
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Alata, Wael, Yue Ye, Isabelle St-Amour, Milène Vandal, and Frédéric Calon. "Human Apolipoprotein E ε4 Expression Impairs Cerebral Vascularization and Blood—Brain Barrier Function in Mice." Journal of Cerebral Blood Flow & Metabolism 35, no. 1 (October 22, 2014): 86–94. http://dx.doi.org/10.1038/jcbfm.2014.172.

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Human apolipoprotein E ( APOE) exists in three isoforms ε2, ε3, and ε4, of which APOE4 is the main genetic risk factor of Alzheimer's disease (AD). As cerebrovascular defects are associated with AD, we tested whether APOE genotype has an impact on the integrity and function of the blood—brain barrier (BBB) in human APOE-targeted replacement mice. Using the quantitative in situ brain perfusion technique, we first found lower (13.0% and 17.0%) brain transport coefficient (Clup) of [3H]-diazepam in APOE4 mice at 4 and 12 months, compared with APOE2 and APOE3 mice, reflecting a decrease in cerebral vascularization. Accordingly, results from immunohistofluorescence experiments revealed a structurally reduced cerebral vascularization (26% and 38%) and thinner basement membranes (30% and 35%) in 12-month-old APOE4 mice compared with APOE2 and APOE3 mice, suggesting vascular atrophy. In addition, APOE4 mice displayed a 29% reduction in [3H]-d-glucose transport through the BBB compared with APOE2 mice without significant changes in the expression of its transporter GLUT1 in brain capillaries. However, an increase of 41.3% of receptor for advanced glycation end products (RAGE) was found in brain capillaries of 12-month-old APOE4 mice. In conclusion, profound divergences were observed between APOE genotypes at the cerebrovascular interface, suggesting that APOE4-induced BBB anomalies may contribute to AD development.
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Dissertations / Theses on the topic "APOE3"

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Reverté, Soler Ingrid. "Neurobehavioural effects associated with postnatal exposure to decabromodiphenyl ether in apoe2, apoe3 and apoe4 transgenic mice." Doctoral thesis, Universitat Rovira i Virgili, 2012. http://hdl.handle.net/10803/76782.

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El Decabromodifenil èter (BDE-209) és un retardant de la flama àmpliament utilitzat i font de preocupació a causa de la toxicitat mostrada per altres Difenil Èters Polibromats (PBDEs). La presència de PBDEs en la llet materna fa preocupant la seva exposició durant el desenvolupament. Pensem que l’exposició primerenca a BDE-209 pot produir efectes a llarg termini i interactuar amb factors genètics, com el genotip de l’ApolipoproteinaE. Ratolins portadors de les diferents isoformeshumanes de l’ApoE foren tractats amb una dosi oral aguda de 0, 10 o 30 mg / kg de BDE-209 en el dia postnatal 10 i van ser avaluats per neurocomportament durant el desenvolupament, a l'edat adulta i la vellesa. L’exposició a BDE-209 indueix un retard en el desenvolupament físic i neuromotor i en la compactació de la mielina en els ratolins ApoE2, disminueix els nivells de tiroxina lliure en les femelles adultes i disminueix l'activitat en ratolins ApoE4. Els efectes més consistents durant tota la vida s'observen en ratolins ApoE3 i consisteixen en problemes d'aprenentatge als 4 mesos, i problemes d'aprenentatge i memòria i un augment de l'ansietat als 12 mesos.
Decabromodiphenyl Ether (BDE-209) is a flame retardant widely used and source of concern because ofthe toxicity showed by other Polibrominateddiphenyl ethers (PBDEs). The presenceof PBDEs in human’s breast milkmakes worrying its exposure during development. We hypothesised that an early exposure to BDE-209 can induce long-term impairments and interact with genetic factors, such as ApolipoproteinE genotype. Mice carrying the different Human ApoE isoforms treated with an acute oral dose of 0, 10 or 30 mg/kg of BDE-209 on postnatal day 10 were assessed for neurobehaviourduring development, in young adulthood and old age. BDE-209 exposure inducesadelay in physic and neuromotordevelopment and in myelin compaction in ApoE2 mice, decreases the levels of free thyroxin in adult femalesand decreases activity in ApoE4 mice. The most consistent effects across the lifespan are observed in ApoE3 mice and consist of impaired learning at 4 months, and impaired learning and memory and increased anxiety at 12 months.
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Donovan, Alexandra. "Comparative Biophysical Analysis of APOE3 and APOE4| A Mechanistic Investigation." Thesis, California State University, Long Beach, 2017. http://pqdtopen.proquest.com/#viewpdf?dispub=10606132.

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Apolipoprotein E is an exchangeable apolipoprotein whose isoforms are associated with various disease risk profiles. Individuals bearing the APOE ϵ4 allele are at increased risk for developing Alzheimer’s disease compared to those bearing the APOE ϵ3 allele. The two isoforms differ in amino acid at position 112: apoE3 bears a Cys while apoE4 bears an Arg. It is hypothesized that the Cys to Arg substitution in apoE4 causes a decrease in stability in comparison to apoE3, which is exaggerated at endosomal pH <6.0. In our study, changes in secondary structure were monitored using circular dichroism at pH 7.4 and pH 3.5. Chemical denaturation indicated that both apoE3 and apoE4 retained their helical secondary structure at the lower pH, with a biphasic and monophasic guanidine HCl denaturation profile, respectively. Tertiary structure was monitored at both pH’s through fluorescence spectral characteristics and mobility of a fluorescent probe attached to each of the 7 major amphipathic α-helices of apoE3 and apoE4. The data showed decreases in fluorescence emission (FE), changes in fluorescence polarization (FP), and fluctuations in probe mobility, which were interpreted as likely formation of a molten globule. Formation of a molten globule appeared to occur during denaturation primarily for apoE4, and thermodynamic parameters of apoE4 showed a lower stability than apoE3, with a larger effect of pH. Taken together, our results suggest that the acidic pH in the endosomal compartments could interact with the native structure of apoE4 to generate a molten globule state that is able to bind endosomal membranes, other proteins, or itself. This study offers mechanistic insight into the impact of the single residue difference between apoE3 and apoE4 with regard to folding/unfolding behavior, and with regard to its physiological and pathological implications.

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Cieslak, Stephen Gerard. "The Effects of L-Cysteine on Alzheimer's Disease Pathology in APOE2, APOE3, and APOE4 Homozygous Mice." BYU ScholarsArchive, 2016. https://scholarsarchive.byu.edu/etd/6585.

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The APOE gene is of profound importance regarding the onset of Alzheimer's disease (AD). From the small physical differences among the protein products of the isoforms of this gene arises a profound difference in their physiologies. For example, the APOE2 isoform confers resistance to AD, the APOE3 isoform confers neutral susceptibility to AD, and the APOE4 isoform confers proneness to AD. L-cysteine is an amino acid that has several anti-AD properties, among which are its ability to sequester iron and form glutathione – a powerful antioxidant – and therefore may be a promising potential dietary supplement for ameliorating AD pathology. In our experiment, we fed Mus musculus (mice) homozygous for APOE2, APOE3, and APOE4 either a control diet or a diet high in L-cysteine. Using Western blotting analysis, we quantified Amyloid β (Aβ), hyper-phosphorylated Tau (HP-Tau), and the three APOE proteins that we extracted from post-mortem brains of APOE2, APOE3, and APOE4 homozygous mice of 3-, 6-, 9-, and 12-month ages. We calculated a three-way ANOVA on a sample of 86 mice to examine the effect of age, genotype, and diet on protein quantities. We found that administration of L-cysteine trends towards lowering levels of Aβ in each cohort, but this effect is statistically insignificant. On the other hand, L-cysteine caused a significant decrease in APOE production with regard to diet [F(1,62) = 6.17, p=0.02], indicating that less APOE is produced due to the decrease in Aβ burden. Furthermore, administration of L-cysteine revealed no significant impact on or trends regarding HP-Tau deposition between diet types for each cohort. However, we observed that L-cysteine appeared to nullify the increasing trend in HP-Tau deposition between APOE2 and APOE4 cohorts. Thus, L-cysteine may be weakly affecting HP-Tau deposition via its ability to somewhat reduce Aβ burden and consequently prevent the shutdown of the proteosomes responsible for the degradation and clearance of HP-Tau. Taken together, these data suggest that L-cysteine should be considered as an intervention for AD pathology.
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Bour, Alexandra. "Implication d'un dérivé sécrété du précurseur de la protéine β-amyloi͏̈de (sAPP695) et de différentes isoformes de l'apolipoprotéine E humaine (apoE3 et apoE4 ) dans les processus mnésiques chez la Souris." Université Louis Pasteur (Strasbourg) (1971-2008), 2004. https://publication-theses.unistra.fr/public/theses_doctorat/2004/BOUR_Alexandra_2004.pdf.

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Une perturbation du métabolisme du précurseur de la protéine beta-amyloi͏̈de (APP) est associée à la maladie d'Alzheimer (MA) et à l'apparition de troubles mnésiques liés à l'âge. Cette perturbation semble affecter le niveau cérébral de son dérivé soluble, le sAPP, qui possède des propriétés promnésiantes. D'autre part, l'allèle epsilon 4, mais pas l'allèle epsilon 3, du gène de l'apolipoprotéine E (apoE) est un facteur de risque génétique de la MA et des troubles mnésiques liés à l'âge. En outre, l'apoE semble influencer le métabolisme de l'APP. Les effets d'une administration intracérébroventriculaire de sAPP exogène à des souris lors de tâches de reconnaissance d'objet ou spatiale et d'apprentissage opérant indiquent qu'il favorise les mécanismes très précoces de formation de la mémoire. De plus, le blocage des sAPP endogènes par des anticorps affecte les performances mnésiques, ce qui confirme leur rôle dans les processus de consolidation de la mémoire. Parallèlement à cette étude, nous avons mis en évidence une influence néfaste du système de ventilation des salles d'hébergement affectant les performances mnésiques des souris. Les performances de souris transgéniques apoE3 et apoE4 (respectivement porteuses homozygotes de l'allèle humain epsilon 3 et epsilon 4) " âgées " (14-15 mois), ont été évaluées dans des tâches de reconnaissance spatiale et de mémoire spatiale dans la piscine de Morris, ainsi que des tâches d'évitement actif et passif. Les souris apoE4 femelles, en particulier, présentent de faibles performances de mémoire et apparaissent donc comme un bon modèle d'étude des troubles mnésiques liés à l'âge. Enfin, l'administration de sAPP a permis de restaurer les performances de mémoire spatiale des souris apoE4 femelles " âgées " dans la piscine de Morris. L'ensemble de ces résultats suggère que la modulation des niveaux de sAPP cérébraux pourrait permettre de traiter les déficits cognitifs liés au vieillissement en général, et à la MA en particulier
An alteration of the beta-amyloid precursor protein (APP) metabolism is associated with Alzheimer's disease (AD) as well as age-related memory impairments. This alteration seems to affect cerebral level of sAPP, a promnestic and soluble form of APP. On the other hand, the epsilon 4 allele, but not the epsilon 3 allele, of apolipoprotéine E (apoE) gene is a genetic risk factor for AD and for age-related memory impairments. Moreover, APP metabolism seems to be influenced by apoE. First, the effects of exogenous sAPP administration in mice were evaluated in object recognition, spatial recognition and bar-press learning tasks. According to the results, sAPP seems to promote early memory processes. The post-training blockade of endogenous sAPPs with specific antibodies induced memory deficits suggesting a central role of sAPPs in memory consolidation mechanisms. Besides this study, we showed the deleterious effect of the new ventilation system of some animal housing rooms on mice memory performance. Then, the memory performance of "aged" (14-15 months) apoE3 and apoE4 transgenic mice (homozygous carriers of the human apoE allele epsilon 3 and epsilon 4, respectively) were evaluated in spatial memory tasks (spatial recognition and Morris water maze) and active and passive avoidance memory tasks. Compared to apoE3 mice, apoE4 mice, especially females, showed more severe memory deficits. Thus, apoE4 female mice appear as a good model for the study of age-related memory deficits. In a last experiment using the Morris water maze task, the administration of sAPP restored a good level of spatial memory performance in "aged" female apoE4 mice. Altogether, our results suggest that the modulation of cerebral sAPP levels must be considered as a potential therapeutic approach in the treatment of age-related memory deficits in general, or those associated with AD in peculiar
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Cambon, Karine. "Influence of ApoE polymorphism on synaptic morphometry during aging in the dentate gyrus of ApoE knockout and human ApoE transgenic mice." Thesis, [n.p.], 2000. http://oro.open.ac.uk/19118/.

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Pandeirada, Ana Raquel Gonçalves. "Association between common lipid metabolism genes polymorphisms and sporadic colorectal adenocarcinoma risk." Master's thesis, Universidade de Aveiro, 2015. http://hdl.handle.net/10773/16151.

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Mestrado em Biomedicina Molecular
Lipids can modulate the risk of developing sporadic colorectal adenocarcinoma (SCA), since alterations into lipid metabolism and transport pathways influence directly cholesterol and lipids absorption by colonic cells and indirectly reactive oxygen species (ROS) synthesis in rectum cells due to lipid accumulation. Lipid metabolism is regulated by several proteins APOA1, APOB, APOC3, APOE, CETP, NPY, PON1 and PPARG that could influence both metabolism and transport processes. Is been reported that several common single-nucleotide polymorphisms (SNPs) in these genes could influence their function and/or expression, changing lipid metabolism balance. Thus, genetic changes in those genes can influence SCA development, once the majority of them were never studied in this disease. Furthermore, there are contradictory results between some studied polymorphisms and SCA risk. Thus, the aim of this study was to explore and describe lipid metabolism-associated genes common polymorphisms (APOA1 -75 G>A; APOB R3500Q; APOC3 C3175G, APOC3 T3206G; APOE Cys112/158Arg; CETP G279A, CETP R451Q; NPY Leu7Pro; PON1 Q192R; PPARG Pro12Ala) status among SCA, and their relationship with SCA risk. Genotyping of common lipid metabolism genes polymorphisms (APOA1 75 G>A; APOB R3500Q; APOC3 C3175G, APOC3 T3206G; APOE Cys112/158Arg; CETP G279A, CETP R451Q; NPY Leu7Pro; PON1 Q192R; PPARG Pro12Ala) were done by PCR-SSP techniques, from formalin-fixed and paraffin-embedded biopsies of 100 healthy individuals and 68 SCA subjects. Mutant genotypes of APOA1 -75AA (32% vs 12%; p=0.001; OR=3.51; 95% CI 1.59-7.72); APOB 3500AA (7% vs 0%; p=0.01); APOC3 3175GG (19% vs 2%; p=0.0002; OR=11.58; 95% CI 2.52-53.22), APOC3 3206GG (19% vs 0%; p<0.0001); CETP 279AA (12% vs 1%; p=0.003; OR=13.20; 95% CI 1.61-108.17), CETP 451AA (16% vs 0%; p<0.0001); NPY 7CC (15% vs 0%; p<0.0001); PPARG 12GG (10% vs 0%; p=0.001); and heterozygote genotype PON1 192AG (56% vs 22%; p<0.0001; OR=4.49; 95% CI 2.298.80) were found associated with SCA prevalence. While, APOE E4/E4 (0% vs 8%; p=0.02) mutant haplotype seemed to have a protective effect on SCA. Moreover, it also been founded differences between APOB 3500GA, APOC3 3206TG, CETP 279AA genotypes and PPARG 12Ala allele prevalence and tissue localization (colon vs rectum). These findings suggest a positive association between most of common lipid metabolism genes polymorphisms studied and SCA prevalence. Dysregulation of APOA1, APOB, APOC3, CETP, NPY, PON1 and PPARG genes could be associated with lower cholesterol plasma levels and increase ROS among colon and rectum mucosa. Furthermore, these results also support the hypothesis that CRC is related with intestinal lipid absorption decrease and secondary bile acids production increase. Moreover, the polymorphisms studied may play an important role as biomarkers to SCA susceptibility.
Os lípidos podem modular o risco de desenvolver Adenocarcinoma Colorectal Esporádico (ACE), uma vez que alterações nas vias do metabolismo e do transporte lipídico podem influenciar diretamente a absorção do colesterol e dos lípidos pelas células do cólon e indiretamente a síntese de espécies reativas de oxigénio (ERO) no reto, devido à acumulação de lípidos. O metabolismo lipídico é regulado por várias proteínas (APOA1, APOB, APOC3, APOE, CETP, NPY, PON1, PPARG) que podem influenciar o metabolismo e o transporte de lípidos. Tem sido reportados nestes genes, vários polimorfismos comuns (SNP) que podem alterar a sua função e/ ou a expressão, causando um desequilíbrio no metabolismo dos lípidos. Estas alterações genéticas podem influenciar o desenvolvimento de ACE, no entanto a maioria dos polimorfismos nunca foram estudados nesta patologia. Além disso, existem resultados contraditórios entre alguns dos polimorfismos e o risco de ACE. Deste modo, o objetivo deste estudo foi explorar e descrever o efeito dos polimorfismos comuns de genes associados ao metabolismo lipídico (APOA1 -75 G>A; APOB R3500Q; APOC3 C3175G, APOC3 T3206G; APOE Cys112/158Arg; CETP G279A, CETP R451Q; NPY Leu7Pro; PON1 Q192R; PPARG Pro12Ala) no ACE e a sua relação com o risco de desenvolver ACE. A genotipagem dos polimorfismos comuns de genes associados ao metabolismo lipídico (APOA1 -75 G>A; APOB R3500Q; APOC3 C3175G, APOC3 T3206G; APOE Cys112/158Arg; CETP G279A, CETP R451Q; NPY Leu7Pro; PON1 Q192R; PPARG Pro12Ala) foi efetuada pela técnica de PCR-SSP, a partir de biópsias incluídas em parafina e fixadas em formol de 100 indivíduos saudáveis e de 68 indivíduos com ACE. Os genótipos mutantes APOA1 -75AA (32% vs 12%; p=0.001; OR=3.51; 95% CI 1.59-7.72); APOB 3500AA (7% vs 0%; p=0.01); APOC3 3175GG (19% vs 2%; p=0.0002; OR=11.58; 95% CI 2.52-53.22), APOC3 3206GG (19% vs 0%; p<0.0001); CETP 279AA (12% vs 1%; p=0.003; OR=13.20; 95% CI 1.61-108.17), CETP 451AA (16% vs 0%; p<0.0001); NPY 7CC (15% vs 0%; p<0.0001); PPARG 12GG (10% vs 0%; p=0.001); e o genótipo heterozigótico PON1 192AG (56% vs 22%; p<0.0001; OR=4.49; 95% CI 2.29-8.80) demonstraram estar associados à prevalência de ACE. Enquanto, o haplótipo mutante APOE E4/E4 (0% vs 8%; p=0.02) mostrou ter um efeito protetor no ACE. Adicionalmente, também foram encontradas diferenças entre a prevalência e a localização tumoral (cólon ou reto) para os genótipos APOB 3500GA, APOC3 3206TG, CETP 279AA e para o alelo PPARG 12Ala. Estes resultados sugerem uma associação positiva entre a maioria dos polimorfismos genéticos comuns estudados envolvidos no metabolismo lipídico e a prevalência de ACE. A desregulação dos genes APOA1, APOB, APOC3, CETP, NPY, PON1, PPARG poderá estar associada com a diminuição dos níveis plasmáticos de colesterol e o aumento de ERO na mucosa do colon e do reto. Para além disso, estes resultados também suportam a hipótese de que o CCR esta relacionado com a diminuição da absorção intestinal e com o aumento da produção de ácidos biliares secundários. Adicionalmente, os polimorfismos estudados podem desempenhar um importante papel como biomarcadores de suscetibilidade para ACE.
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Evans, Vanessa. "Intramuscular gene transfer of apolipoprotein E (ApoE) to reverse hyperlipidaemia and atherosclerosis in ApoE-deficient mice." Thesis, University College London (University of London), 2007. http://discovery.ucl.ac.uk/1444704/.

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Plasma ApoE has multiple atheroprotective actions, including clearance of cholesterol-rich remnant lipoproteins, and is an attractive gene therapy candidate to treat atherosclerosis. Here, I focus on the single intramuscular injection of an ApoE-expressing vector, non-viral DNA (plasmid) or adeno-associated virus (AAV), as a safe and effective treatment to alleviate hypercholesterolaemia and atherosclerosis in ApoE-deficient (ApoE" ") mice. Firstly, I constructed expression plasmids harbouring human ApoE3 cDNA, driven by two muscle-specific (CK6 and C512) and one ubiquitous (CAG) promoter. The CAG-driven plasmid was injected into tibialis anterior muscles, pre-treated with hyaluronidase, of young ApoE"'" mice and, provided the injection site was electropulsed, gave strong local expression of ApoE3 protein at 1 week (13.38 7.46jig ApoE3 per muscle). This amount was much greater than the CK6- and C512-driven plasmids (0.61 0.38 and 0.45 0.38/ig, respectively), but in all mice plasma ApoE3 levels were below the detection limit (<15ng/ml) and did not ameliorate the hyperlipidaemia. Next, I generated both single-stranded (ss) and self- complementary (sc) AAV2/7 vectors. At 1, 2 and 4 weeks, ApoE was readily measured in the plasma of ApoE'" mice injected with the ssAAV2/7.CAG vector, reaching levels of 1.4/ig/ml, whereas plasma ApoE was again undetected after administration of the CAG-driven plasmid . By contrast, both ssAAV2/7 and scAAV2/7 vectors driven by the muscle-specific promoters performed poorly and ApoE could not be detected in plasma. Therefore, for my final experiment I pseudotyped the ssAAV2.CAG.ApoE3 vector with the robust serotypes 8 and 9, and directly compared their efficiency with ssAAV2/7.CAG.ApoE3 in ApoE"" mice. After 1 week plasma ApoE had reached 2ug/ml in ssAAV2/7 and ssAAV2/8-treated animals, and persisted at l-2ug/ml throughout the 13 week study, whereas the ssAAV2/9 vector was less effective and gave only 0.5ug ApoE/ml. Disappointingly, however, these concentrations of plasma ApoE were still insufficient to have hypolipidaemic effects or to inhibit plaque development in the brachiocephalic artery. In conclusion, although electropulsation enhanced plasmid-mediated transgene expression from skeletal muscle, rAAV was a more efficient gene transfer vector and modest additional optimisation should provide therapeutic levels of ApoE3 in plasma.
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Rantsi, P. (Petra). "Apoe 4-alleelien rooli saamelaisväestön muistisairauksissa." University of Oulu, 2017. http://urn.fi/URN:NBN:fi:oulu-201711083079.

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Alzheimerin tauti (AT) on yleisin etenevä muistisairaus. Eteneviin muistisairauksiin luetaan myös aivoverenkiertosairauden muistisairaus, Lewyn kappale- patologiaan liittyvät aivoja rappeuttavat sairaudet ja otsa-ohimolohkorappeumat. Elimistön rasva- aineenvaihduntaan liittyvän apolipoproteiini E4- (ApoE4) alleelin on todettu olevan sydän- ja verisuonisairauksien, kuten myös AT:n myöhemmällä iällä alkavan muodon geneettinen riskitekijä. ApoE4-alleelin yhteyttä muihin eteneviin muistisairauksiin ei ole osoitettu. Vaikka ApoE4:n roolia muistisairauksien ja etenkin AT:n riskitekijänä on tutkittu maailmalla runsaasti eri väestöissä, ApoE4-alleelin roolia saamelaisten muistisairauksissa ei ole aiemmin tutkittu. Yksittäisen aiemman tutkimuksen perusteella Suomen saamelaisista 5%:lla on E2-, 64%:lla E3- ja 31%:lla E4- alleeli. Tutkimuksen tavoitteena oli selvittää ApoE4- alleelin esiintyminen Suomen Lapin saamelaisväestön muistisairauspotilailla. Tutkimukseen osallistui yhteensä 50 saamelaista potilasta, joilla oli todettu muistihäiriö tai muistisairauden diagnoosi. Laskimoverinäytteet ApoE-fenotyypitystä varten ja kyselykaavakkeiden tiedot kerättiin saamea puhuvan sairaanhoitajan avulla. ApoE4- alleeli esiintyi yhteensä 78%:lla potilaista (n=39). Apolipoproteiini E-fenotyyppiä E3/E3 kantoi 22% (n=11) potilaista, E3/E4 62% (n=31), E4/E4 14% (n=7) ja E2/E4 2 % (n=1) tutkittavista. Verrokkeja tutkimuksessa ei ollut, mutta tuloksia verrattiin aiempaan tietoon ApoE-alleelien esiintyvyyteen sekä saamelaisilla että maailmanlaajuisesti AT:a sairastavilla. Yhteenvetona voidaan todeta, että ApoE4 on tärkeä riskigeeni muistisairauksille myös saamelaisväestössä. Lisäksi huomionarvoista on, että ApoE4-alleelin esiintyminen saamelaisväestön muistipotilailla on korkein, mitä on kuvattu missään aiemmassa muistipotilaiden ja AT-tutkimuksissa.
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Carvalho, Liliana Patrícia Rodrigues de. "Genetic profiling of ApoE in dementia." Master's thesis, Universidade de Aveiro, 2012. http://hdl.handle.net/10773/10720.

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Mestrado em Biomedicina Molecular
A demência é uma das principais causas de incapacidade entre os idosos, afetando mais de 36 milhões de pessoas em todo o mundo. É caracterizada pela deterioração progressiva das funções cognitivas, resultando em dificuldades no desempenho das atividades diárias do indivíduo. A idade de aparecimento dos sintomas, bem como a sua taxa de progressão, são variáveis entre a maior parte das demências, sendo estas geralmente caracterizadas por uma natureza progressiva, aumentando de gravidade ao longo do tempo. Entre os tipos mais frequentes de demência encontram-se a Doença de Alzheimer (DA), Demência Vascular, Demência de Corpos de Lewy e Demência Frontotemporal. O diagnóstico diferencial das demências é realizado tipicamente por testes neuro-psicológicos (para a exclusão de outras demências) e por exames imagiológicos. Contudo, muitos dos sintomas clínicos característicos podem sobrepor-se entre os diversos tipos de demência, o que pode constituir um problema devido a falta de especificidade e erros de diagnóstico. A compreensão dos fatores de risco ambientais e genéticos que podem modular o aparecimento e/ou progressão de doenças abre novas perspetivas relativamente à gestão destas neuropatologias. O gene da apolipoproteína E (ApoE) é reconhecido como o maior fator de risco na demência, desempenhando um papel central em particular no desenvolvimento da DA, sendo que os portadores do alelo ε4 são mais suscetíveis para a doença. Além disso, possíveis associações foram também propostas entre este gene e outras doenças neurológicas, sendo no entanto estes dados ainda controversos. Assim, o objetivo principal deste trabalho consistiu em determinar as frequências alélicas e genotípicas do gene ApoE num grupo de estudo piloto de pacientes com demência na região de Aveiro. Este grupo foi subdividido com base no diagnóstico neuroquímico, no qual foram avaliados os níveis de Aβ1-42, Tau-total e fosfo-Tau 181 no líquido cefalorraquidiano dos pacientes. Como resultado, observou-se que o alelo ε3 foi o mais frequente no grupo total, independentemente do tipo de patologia, e que o alelo ε2 foi o menos comum. O alelo ε4 foi de facto mais frequente em pacientes com DA do que em pacientes com outras neuropatologias, o que está de acordo com a relação proposta por outros autores. Adicionalmente, foi possível verificar que a frequência deste alelo nos pacientes com patologia amilóide é semelhante à observada no grupo DA, sugerindo um papel relevante para o ApoE no metabolismo e acumulação cerebral do Aβ. Consequentemente, estes indivíduos podem ter uma maior suscetibilidade para o desenvolvimento de DA no futuro. Deste modo, os nossos dados corroboram a ideia de que o alelo ε4 é um forte fator de risco para a DA e que deve ser considerado como um teste genético relevante que pode contribuir para o diagnóstico clínico da demência.
Dementia is one of the leading causes of disability among the elderly, affecting over 36 million people worldwide. It is characterized by progressive deterioration in cognitive functions that impair the successful performance of daily living activities. Most forms of dementia are progressive in nature, increasing in severity over time, with the rate of symptoms progression and the age at onset differing among the major dementing disorders. The most frequent types of dementia include Alzheimer´s Disease (AD), Vascular Dementia, Dementia of Lewy bodies and Frontotemporal Dementia. Differential diagnosis of dementia is typically done by neuropsychological testing (for exclusion of other dementias) and neuroimaging investigations. However, many of the clinical symptoms typical of dementia may overlap across dementia subtypes, which may constitute a diagnosis problem leading to lack of specificity and misdiagnosis. Understanding the environmental and genetic factors that modulate risks and outcomes of diseases can open new perspectives on the management of these neurological disorders. Apolipoprotein E gene (ApoE) is recognized as the major genetic risk factor in dementia, in particular playing a central role in AD development, being that ApoE allele ε4 carriers are more susceptible to disease. Furthermore, putative associations have also been proposed between this gene and other neurological disorders, nonetheless controversial data have been reported regarding these aspect. Hence, the aim of this work was to determine ApoE genotypic and allelic frequencies in a pilot study group of dementing patients from the catchment area of the “Hospital de São Sebastião” in “Santa Maria da Feira”. This group was subdivided according to their neurochemical-based diagnosis of dementia, in which Aβ1-42, phospho-Tau 181 and total-Tau levels in patients’ cerebrospinal fluid were evaluated. In this study, we could observe that allele ε3 was the most frequent in the total study group, independent of the type of pathology, and that allele ε2 was the less frequent. Allele ε4 was in fact more frequent in AD patients than in other neurological disease patients, in agreement with the proposed link established by other authors. Additionally, we also find that allele ε4 frequency in patients suffering from amyloid pathology is similar to that observed in AD group, suggesting a role for ApoE in Aβ metabolism and brain accumulation. Potentially, these patients have a higher susceptibility to develop AD pathology in the future. Thus, our data supports the idea that ApoE allele ε4 is a strong risk factor for AD development and that it may be considered as a relevant genetic test that may assist in the clinical diagnosis of dementia.
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Lundbäck, Daniel. "Alkoholkonsumtion och episodiskt minne.Kan APOE genen vid olika konsumtionsnivåer ha betydelse?" Thesis, Stockholms universitet, Psykologiska institutionen, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-88448.

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I denna studie undersöktes om relationen mellan alkoholkonsumtion och episodiskt minne skiljer sig beroende på vilken allele av APOE genen en person har. Undersökningsdeltagarna delades upp i fyra grupper, medelålders män, medelålders kvinnor, äldre män och äldre kvinnor. Utbildningsnivå och ålder inom varje åldersgrupp användes som kovariat. APOE delades upp på 4 bärare och icke bärare. Några signifikanta interaktionseffekter mellan alkoholkonsumtion och APOE framkom inte i någon grupp. I gruppen medelåldersmän hittades en signifikant huvudeffekt av alkoholkonsumtion, där de som avstod från alkohol presterade sämre än de med olika nivåer av alkoholkonsumtion. Liknande tendenser syntes i de tre övriga grupperna där undersökningsdeltagare som avstod från alkohol presterade sämst, dock inte signifikant. En anledning till att de som konsumerar alkohol presterar bättre på episodiskt minnestest än de som inte dricker förmodas vara alkoholens positiva effekter på det kardiovaskulära systemet. Ytterligare forskning på området behövs då andra faktorer, så som hur mycket som dricks vid ett enskilt tillfälle, kan vara mer avgörande.
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Books on the topic "APOE3"

1

Hartigan, Anne Le Marquand. Now is a moveable feast: Apoem and drawings. Galway: Salmon, 1991.

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Donaghy, Michael. Machines: Apoem by Michael Donaghy with Artwork by Barbara Tetenbaum. Guildford: Circle Press, 1986.

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The Apoe gene diet: A breakthrough in lowering cholesterol, weight, and the risk of cardiovascular and Alzheimer's disease through knowledge of your body's genes. Santa Rosa, CA: Elite Books, 2007.

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Apolipoprotein E (ApoE) allelic variants: Involvement in type 2 dibetes. Ottawa: National Library of Canada, 2003.

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Allen, Shelley J. Pathophysiology of Alzheimer’s disease. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198779803.003.0002.

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We now know that the onset of the pathological processes leading to Alzheimer’s disease (AD) may be 15–20 years before symptoms appear. This focuses attention on synaptic changes and the early role of tau, and less on the hallmark amyloid plaques (Aβ‎) and neurofibrillary tau tangles. Sensitive biomarkers to allow early screening will be essential. Familial autosomal AD is the result of mutations in one of three genes (APP, PSEN1, or PSEN2), each directly related to increased Aβ‎, and informs pathological mechanisms in common sporadic cases, but are also subject to influence by many risk genes and environmental factors. The essential role of apolipoprotein E in neuronal repair and Aβ‎ clearance provides a therapeutic target but also a challenge in carriers of the risk gene APOE4. Current treatments are symptomatic, derived from neurotransmitter deficits seen; particularly cholinergic, but emerging data suggest alternative targets which may prove more productive.
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Harold, Denise, and Julie Williams. Molecular genetics and biology of dementia. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199644957.003.0008.

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Considerable progress has been made in our understanding of the genetics and molecular biology of dementia. In this chapter we focus predominantly on the most common form of dementia, Alzheimer’s disease (AD), but also discuss vascular dementia and frontotemporal dementia. Genetic mutations have been identified that cause Mendelian subtypes of each disorder, and in recent years genome-wide association studies have greatly aided the identification of risk genes for more common forms of disease. For example, 9 susceptibility genes have been identified in AD in the past 3 years as a result of genome-wide association studies, the first robust risk loci to be identified since APOE in 1993. This progress in genetic research is having a dramatic effect on our understanding of disease pathogenesis, by refining previous ideas and defining new primary disease mechanisms.
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Book chapters on the topic "APOE3"

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Scherrmann, Jean-Michel, Kim Wolff, Christine A. Franco, Marc N. Potenza, Tayfun Uzbay, Lisiane Bizarro, David C. S. Roberts, et al. "APOE." In Encyclopedia of Psychopharmacology, 131. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_4065.

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Yamamoto, Tokuo. "Receptors for Apoe-Containing Lipoproteins." In Drugs Affecting Lipid Metabolism, 281–83. Dordrecht: Springer Netherlands, 1996. http://dx.doi.org/10.1007/978-94-009-0311-1_34.

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Pradier, L., C. Czech, L. Mercken, S. Moussaoui, M. Reibaud, P. Delaère, and G. Tremp. "App, Apoe, and Presenilin Transgenics." In Advances in Behavioral Biology, 25–30. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-5337-3_5.

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Corzo, L., L. Fernández-Novoa, R. Zas, K. Beyer, J. I. Lao, X. A. Alvarez, and R. Cacabelos. "Influence of the Apoe Genoptype on Serum Apoe Levels in Alzheimer’s Disease Patients." In Advances in Behavioral Biology, 765–71. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-5337-3_109.

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Sullivan, Patrick M. "APOE-Based Models of “Pre-Dementia”." In Neuromethods, 439–47. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-898-0_22.

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Abrams, David B., J. Rick Turner, Linda C. Baumann, Alyssa Karel, Susan E. Collins, Katie Witkiewitz, Terry Fulmer, et al. "Apolipoproteins: APOA-I, APOA-IV, APOE." In Encyclopedia of Behavioral Medicine, 122. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-1005-9_1245.

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Whang, William. "Apolipoproteins: APOA-I, APOA-IV, APOE." In Encyclopedia of Behavioral Medicine, 1. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4614-6439-6_1245-2.

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Whang, William. "Apolipoproteins: APOA-I, APOA-IV, APOE." In Encyclopedia of Behavioral Medicine, 142–43. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-39903-0_1245.

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Yin, Yuemiao, and Zhao Wang. "ApoE and Neurodegenerative Diseases in Aging." In Advances in Experimental Medicine and Biology, 77–92. Singapore: Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-13-1117-8_5.

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Soininen, Hilkka S., and Paavo J. Riekkinen. "Apoe and Memory in Alzheimer’s Disease." In Advances in Behavioral Biology, 13–16. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-5337-3_3.

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Conference papers on the topic "APOE3"

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Vengrenyuk, Yuliya, Theodore J. Kaplan, Luis Cardoso, Gwendalyn J. Randolph, and Sheldon Weinbaum. "Biomechanical Modeling of Atherosclerotic Lesions in ApoE Deficient Mice." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206571.

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Cardiovascular disease remains the principal killer in the western world despite major advances in treatment of its patients [1]. It is generally accepted that sudden rupture of vulnerable plaque followed by thrombus formation underlies most cases of myocardial infarction and is responsible for more than a half of 500,000 coronary heart disease deaths every year. Although histopathological analysis of postmortem specimens have provided important data on histological features of ruptured human plaques, there is an urgent need for good representative animal models of plaque rupture. Over the last decade and a half, genetically engineered mice have been widely used to study the pathogenesis and potential treatment of atherosclerotic lesions, as well as genetic, hormonal and environmental influences on development of atherosclerosis. Though many of the features of plaque development and progression that occur in human plaques are similarly observed in murine plaques, these mouse models have long been regarded as poor models to study plaque rupture because the aortic sinus lesions seldom show any signs of fibrous cap disruption. Several recent studies reported potentially unstable atherosclerotic lesions in older apoE-deficient mice in another anatomic site, the proximal part of the brachiocephalic artery (BCA) [2, 3]. The unusual stability of aortic lesions compared to the BCA lesions in ApoE knockout mice is an unexplained paradox in developing a mouse model of plaque rupture. In this paper, we use histology based finite element analysis to evaluate peak circumferential stresses in aortic and BCA lesions from high fat fed ApoE KO mice.
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"APOE Gene Expression in Patients with Alzheimer’s Disease." In International Conference on Cellular & Molecular Biology and Medical Sciences. Universal Researchers (UAE), 2016. http://dx.doi.org/10.17758/uruae.ae0916409.

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Li, Ziying. "New APOE-related therapeutic options for Alzheimer’s disease." In INTERNATIONAL CONFERENCE ON FRONTIERS OF BIOLOGICAL SCIENCES AND ENGINEERING (FBSE 2018). Author(s), 2019. http://dx.doi.org/10.1063/1.5085515.

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Wang, Ying, John A. Johnson, Abigail Fulp, Michael A. Sutton, and Susan M. Lessner. "Adhesive Strength of Atherosclerotic Plaques Depends on Collagen Content." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80433.

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Atherosclerotic plaque rupture is a major cause of myocardial infarction, coronary thrombosis and stroke. In a previous study, we proposed a new plaque rupture mechanism, plaque separation at the shoulder, and developed a novel quantitative mechanical test to measure the adhesive strength between the atherosclerotic plaque and the underlying vascular wall in mouse models using the local energy release rate, G, as a quantifiable metric for direct comparison of plaque separation strengths (1). We have now investigated structure-function relationships between the local energy release rate and local plaque composition. We hypothesize that adhesive strength varies with plaque composition in mice of different genotypes, and that it correlates with collagen deposition and macrophage content in lesions. Mice which are genetically deficient in matrix metalloproteinase 12 (MMP12), have previously been shown to demonstrate altered lesion composition (2). Therefore, we used apoE knockout (KO) and apoE MMP-12 double knockout (DKO) mice for our experiments and expected to see a difference in local energy release rates between strains.
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Tsao, Sinchai, Niharika Gajawelli, Darryl H. Hwang, Stephen Kriger, Meng Law, Helena Chui, Michael Weiner, and Natasha Lepore. "Mapping of ApoE4 related white matter damage using diffusion MRI." In SPIE Medical Imaging, edited by Maria Y. Law and Tessa S. Cook. SPIE, 2014. http://dx.doi.org/10.1117/12.2043925.

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"Methylation and expression profiles in Apoe vicinity point to specific neighboring interaction of Apoe and TOMM40 genes: implication for the Alzheimer disease." In Bioinformatics of Genome Regulation and Structure/ Systems Biology. institute of cytology and genetics siberian branch of the russian academy of science, Novosibirsk State University, 2020. http://dx.doi.org/10.18699/bgrs/sb-2020-127.

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Mengesha, Birga Anteneh, and Huang Jian. "Genome-wide Association of APOE and FOXO3A for human longevity." In ICBBS 2019: 2019 8th International Conference on Bioinformatics and Biomedical Science. New York, NY, USA: ACM, 2019. http://dx.doi.org/10.1145/3369166.3369169.

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Goryawala, Mohammed, Qi Zhou, Ranjan Duara, David Loewenstein, Mercedes Cabrerizo, Warren Barker, and Malek Adjouadi. "Altered small-world anatomical networks in Apolipoprotein-E4 (ApoE4) carriers using MRI." In 2014 36th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2014. http://dx.doi.org/10.1109/embc.2014.6944122.

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Hameed, Abdul G., Sheila E. Francis, David C. Crossman, and Allan Lawrie. "TRAIL Deficiency Protects Fat-fed ApoE-/- Mice From Pulmonary Arterial Hypertension." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a2283.

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Mauderly, Joe L., Steven Seilkop, Jacob D. McDonald, Amie Lund, and Matthew Campen. "Identification Of Combustion Product Components Causing Vascular Responses In ApoE-/- Mice." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a3233.

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