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Academic literature on the topic 'ApoE-'

Author: Grafiati
Published: 4 June 2021
Last updated: 10 March 2023

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Journal articles on the topic "ApoE-":

1

Begcevic Brkovic, Ilijana, Benedikt Zöhrer, Markus Scholz, Madlen Reinicke, Julia Dittrich, Surab Kamalsada, Ronny Baber, et al. "Simultaneous Mass Spectrometry-Based Apolipoprotein Profiling and Apolipoprotein E Phenotyping in Patients with ASCVD and Mild Cognitive Impairment." Nutrients 14, no. 12 (June 15, 2022): 2474. http://dx.doi.org/10.3390/nu14122474.

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Apolipoprotein E (apoE) occurs on the majority of plasma lipoproteins and plays a major role in the lipid metabolism in the periphery and in the central nervous system. ApoE is a polymorphic protein with three common isoforms, apoE2, apoE3 and apoE4, derived from respective alleles ε2, ε3 and ε4. The aim of this study was to develop a sample pretreatment protocol combined with rapid mass spectrometry (MS)-based assay for simultaneous apolipoprotein profiling and apoE phenotype identification. This assay was validated in 481 samples from patients with stable atherosclerotic cardiovascular disease (ASCVD) and applied to study association with mild cognitive impairment (MCI) in the LIFE Adult study, including overall 690 study subjects. Simultaneous quantification of 8–12 major apolipoproteins including apoA-I, apoB-100 and apoE could be performed within 6.5 min. Phenotyping determined with the developed MS assay had good agreement with the genotyping by real-time fluorescence PCR (97.5%). ApoE2 isoform was associated with the highest total apoE concentration compared to apoE3 and apoE4 (p < 0.001). In the subgroup of diabetic atherosclerotic cardiovascular disease (ASCVD) patients, apoE2 isoform was related to higher apoC-I levels (apoE2 vs. apoE3, p < 0.05), while in the subgroup of ASCVD patients under statin therapy apoE2 was related to lower apoB-100 levels (apoE2 vs. apoE3/apoE4, p < 0.05). A significant difference in apoE concentration observed between mild cognitive impairment (MCI) subjects and controls was confirmed for each apoE phenotype. In conclusion, this study provides evidence for the successful implementation of an MS-based apoE phenotyping assay, which can be used to assess phenotype effects on plasma lipid and apolipoprotein levels.
2

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.
3

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.
4

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.
5

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.
6

Vecchio, Filomena Lo, Paola Bisceglia, Bruno Pietro Imbimbo, Madia Lozupone, Raffaela Rita Latino, Emanuela Resta, Maurizio Leone, et al. "Are apolipoprotein E fragments a promising new therapeutic target for Alzheimer’s disease?" Therapeutic Advances in Chronic Disease 13 (January 2022): 204062232210816. http://dx.doi.org/10.1177/20406223221081605.

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Human apolipoprotein E (ApoE) is a 299-amino acid secreted glycoprotein that binds cholesterol and phospholipids. ApoE exists as three common isoforms (ApoE2, ApoE3, and ApoE4) and heterozygous carriers of the ε4 allele of the gene encoding ApoE ( APOE) have a fourfold greater risk of developing Alzheimer’s disease (AD). The enzymes thrombin, cathepsin D, α-chymotrypsin-like serine protease, and high-temperature requirement serine protease A1 are responsible for ApoE proteolytic processing resulting in bioactive C-terminal-truncated fragments that vary depending on ApoE isoforms, brain region, aging, and neural injury. The objectives of the present narrative review were to describe ApoE processing, discussing current hypotheses about the potential role of various ApoE fragments in AD pathophysiology, and reviewing the current development status of different anti-ApoE drugs. The exact mechanism by which APOE gene variants increase/decrease AD risk and the role of ApoE fragments in the deposition are not fully understood, but APOE is known to directly affect tau-mediated neurodegeneration. ApoE fragments co-localize with neurofibrillary tangles and amyloid β (Aβ) plaques, and may cause neurodegeneration. Among anti-ApoE approaches, a fascinating strategy may be to therapeutically overexpress ApoE2 in APOE ε4/ε4 carriers through vector administration or liposomal delivery systems. Another approach involves reducing ApoE4 expression by intracerebroventricular antisense oligonucleotides that significantly decreased Aβ pathology in transgenic mice. Differences in the proteolytic processing of distinct ApoE isoforms and the use of ApoE fragments as mimetic peptides in AD treatment are also under investigation. Treatment with peptides that mimic the structural and biological properties of native ApoE may reduce Aβ deposition, tau hyperphosphorylation, and glial activation in mouse models of Aβ pathology. Alternative strategies involve the use of ApoE4 structure correctors, passive immunization to target a certain form of ApoE, conversion of the ApoE4 aminoacid sequence into that of ApoE3 or ApoE2, and inhibition of the ApoE-Aβ interaction.
7

Kurano, Makoto, Kazuhisa Tsukamoto, Eri Sakai, Masumi Hara, and Yutaka Yatomi. "Isoform-Dependent Effects of Apolipoprotein E on Sphingolipid Metabolism in Neural Cells." Journal of Alzheimer's Disease 85, no. 4 (February 15, 2022): 1529–44. http://dx.doi.org/10.3233/jad-215205.

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Background: Sphingosine 1-phosphate (S1P) and ceramides have been implicated in the development of Alzheimer’s disease. Apolipoprotein E (ApoE) isoforms are also involved in the development of Alzheimer’s disease. Objective: We aimed at elucidating the potential association of the ApoE isoforms with sphingolipid metabolism in the central nervous system. Methods: We investigated the modulations of apolipoprotein M (apoM), a carrier of S1P, S1P, and ceramides in Apoeshl mice, which spontaneously lack apoE, and U251 cells and SH-SY5Y cells infected with adenovirus vectors encoding for apoE2, apoE3, and apoE4. Results: In the brains of Apoeshl mice, the levels of apoM were lower, while those of ceramides were higher. In U251 cells, cellular apoM and S1P levels were the highest in the cells overexpressing apoE2 among the apoE isoforms. The cellular and medium contents of ceramides decreased in the order of the cells overexpressing apoE3 > apoE2 and increased in the cells overexpressing apoE4. In SH-SY5Y cells, apoM mRNA and medium S1P levels were also the highest in the cells overexpressing apoE2. The cellular contents of ceramides decreased in the order of the cells overexpressing apoE3 > apoE2 = apoE4 and those in medium decreased in the order of the cells overexpressing apoE3 > apoE2, while increased in the cells overexpressing apoE4. Conclusion: The modulation of apoM and S1P might partly explain the protective effects of apoE2 against Alzheimer’s disease, and the modulation of ceramides might be one of the mechanisms explaining the association of apoE4 with the development of Alzheimer’s disease.
8

Chung, Won-Suk, Philip B. Verghese, Chandrani Chakraborty, Julia Joung, Bradley T. Hyman, Jason D. Ulrich, David M. Holtzman, and Ben A. Barres. "Novel allele-dependent role for APOE in controlling the rate of synapse pruning by astrocytes." Proceedings of the National Academy of Sciences 113, no. 36 (August 24, 2016): 10186–91. http://dx.doi.org/10.1073/pnas.1609896113.

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The strongest genetic risk factor influencing susceptibility to late-onset Alzheimer’s disease (AD) is apolipoprotein E (APOE) genotype. APOE has three common isoforms in humans, E2, E3, and E4. The presence of two copies of the E4 allele increases risk by ∼12-fold whereas E2 allele is associated with an ∼twofold decreased risk for AD. These data put APOE central to AD pathophysiology, but it is not yet clear how APOE alleles modify AD risk. Recently we found that astrocytes, a major central nervous system cell type that produces APOE, are highly phagocytic and participate in normal synapse pruning and turnover. Here, we report a novel role for APOE in controlling the phagocytic capacity of astrocytes that is highly dependent on APOE isoform. APOE2 enhances the rate of phagocytosis of synapses by astrocytes, whereas APO4 decreases it. We also found that the amount of C1q protein accumulation in hippocampus, which may represent the accumulation of senescent synapses with enhanced vulnerability to complement-mediated degeneration, is highly dependent on APOE alleles: C1q accumulation was significantly reduced in APOE2 knock-in (KI) animals and was significantly increased in APOE4 KI animals compared with APOE3 KI animals. These studies reveal a novel allele-dependent role for APOE in regulating the rate of synapse pruning by astrocytes. They also suggest the hypothesis that AD susceptibility of APOE4 may originate in part from defective phagocytic capacity of astrocytes which accelerates the rate of accumulation of C1q-coated senescent synapses, enhancing synaptic vulnerability to classical-complement-cascade mediated neurodegeneration.
9

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.
10

Iannucci, Jaclyn, Abhik Sen, and Paula Grammas. "Isoform-Specific Effects of Apolipoprotein E on Markers of Inflammation and Toxicity in Brain Glia and Neuronal Cells In Vitro." Current Issues in Molecular Biology 43, no. 1 (May 27, 2021): 215–25. http://dx.doi.org/10.3390/cimb43010018.

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Mutations to the cholesterol transport protein apolipoprotein E (ApoE) have been identified as a major risk factor for the development of sporadic or late-onset Alzheimer’s disease (AD), with the e4 allele representing an increased risk and the rare e2 allele having a reduced risk compared to the primary e3 form. The reasons behind the change in risk are not entirely understood, though ApoE4 has been connected to inflammation and toxicity in both the brain and the periphery. The goal of this study was to better understand how the ApoE isoforms (ApoE2/3/4) confer differential AD-related risk by assessing cell-specific ApoE-related neuroinflammatory and neurotoxic effects. We compared the effects of ApoE isoforms in vitro on human astrocytes, a human immortalized microglia cell line (HMC3), and the human neuroblastoma cell line SH-SY5Y. Cells were treated for 24 h with or without recombinant ApoE2, ApoE3, or ApoE4 (20 nM) and inflammation and toxicity markers assessed. Our results indicated the expression of inflammatory cytokines IL-1β, TNFα, and IL-6 in human astrocytes was increased in response to all ApoE isoforms, with ApoE4 evoking the highest level of cytokine expression. In response to ApoE2 or ApoE3, microglial cells showed reduced levels of microglial activation markers TREM2 and Clec7a, while ApoE4 induced increased levels of both markers. ApoE2 promoted neuron survival through increased BDNF release from astrocytes. In addition, ApoE2 promoted, while ApoE4 reduced, neuronal viability. Overall, these results suggest that ApoE4 acts on cells in the brain to promote inflammation and neuronal injury and that the deleterious effects of ApoE4 on these cells may, in part, contribute to its role as a risk factor for AD.
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Dissertations / Theses on the topic "ApoE-":

1

Dinkel, Regina Elke. "In-vivo Metabolismus der VLDL-Apolipoproteine ApoB, ApoCIII und ApoE." Diss., lmu, 2002. http://nbn-resolving.de/urn:nbn:de:bvb:19-3562.

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2

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.
3

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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4

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.
Betula
5

Hua, Jennifer. "Rôle des récepteurs P2X4 dans la dégradation d’ApoE : implication dans la maladie d’Alzheimer." Thesis, Montpellier, 2019. http://www.theses.fr/2019MONTT021/document.

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Les récepteurs purinergiques P2X4 (P2X4R) sont des récepteurs canaux exprimés par lesneurones et les microglies du système nerveux central et sont impliqués dans de nombreuxprocessus physiologiques et pathologiques. Des études préliminaires, menées au sein dulaboratoire, ont permis de mettre en évidence une interaction entre P2X4R etl’Apolipoprotéine E (ApoE), ainsi qu’une augmentation d’ApoE dans les macrophages et lesmicroglies provenant de souris déficientes pour P2X4R. Basée sur ces observations, lapremière partie de cette thèse a cherché à caractériser les mécanismes impliquant P2X4R danscet effet. ApoE étant un facteur de risque majeur dans la maladie d’Alzheimer, la deuxièmepartie de cette thèse a été consacrée à étudier l’implication de P2X4R dans cette pathologie.Les résultats présentés montrent que P2X4R module l’activité de la cathepsine B, enzymeresponsable de la dégradation lysosomale d’ApoE. L’utilisation de souris APP/PS1 a permisde montrer que l’absence de P2X4R conduit à une amélioration des capacités mnésiques, unediminution de la concentration de peptide Aβ soluble ainsi qu’à une augmentation d’ApoEmicrogliale.Ces résultats indiquent que P2X4R régule la dégradation d’ApoE par un mécanismedépendant de la cathepsine B, et que son invalidation permet d’améliorer les symptômescognitifs de la maladie d’Alzheimer
P2X4 receptors (P2X4R) are purinergic ion channels expressed on neurons and microglia inthe central nervous system. They have been widely studied and have been implicated in manyphysiological and pathological processes. Previous studies conducted in the laboratoryrevealed an interaction between P2X4R and the Apolipoprotein E (ApoE), as well as anincrease in ApoE level in primary macrophages and microglia obtained from mice lackingP2X4R. Based on these results, this thesis aimed to decipher the mechanisms underlyingP2X4R regulation of ApoE levels. In addition, ApoE being a major risk factor forAlzheimer’s disease, part of this work investigated potential implications of P2X4R in thispathology.Results show that P2X4R modulates cathepsin B activity, which in turn promotes ApoElysosomal degradation. APP/PS1 mice lacking P2X4R show an increase in cognitiveperformances, a decrease in soluble Aβ peptide and an increase of microglia ApoE level.These results support that P2X4R modulates ApoE degradation in a cathepsin B-dependantmanner and that its invalidation leads to an improvement in Alzheimer’s pathology
6

Wassef, Hanny. "Synthesis and secretion of apoC-I and apoE by human SW872 liposarcoma cells." Thesis, McGill University, 2004. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=82447.

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Apolipoprotein C-I (apoC-I) plays an important role in the metabolism of plasma triglyceride levels and cholesterol metabolism. Little is known about the regulation of apoC-I production by human adipocytes. Aim. To investigate the effect of different tissue culture conditions on the synthesis and secretion of apoC-I and apoE in human SW872 liposarcoma cells and to study the effects of apoC-I overexpression in these same cells. Methods. SW872 cells were grown in DMEM/F-12 (3:1, v/v). QPCR was used to quantify mRNA synthesis. ELISAs were used to quantify intracellular and extracellular proteins. Colorimetric reaction kits were used to analyze intracellular cholesterol and triglyceride concentrations. Results . Maturation experiments revealed that after 17 days in culture, SW872 cells contained significantly more cholesterol (100%) and triglyceride (3-fold). Cell maturation was associated with significantly higher levels of apoE mRNA (+200%) but not apoC-I mRNA (-50%). The cells secreted more apoC-I (+110%) and apoE (+340%). Cellular apoC-I increased 620% and apoE increased 1540%. Treatment of cells during maturation with insulin (0, 10 or 1000 nM) significantly reduced the secretion of apoC-I and apoE (-14% and -56%, respectively) and intracellular apoC-I and apoE (-10% and -12%, respectively. Overexpression of apoC-I in SW872 cells resulted in increased cell number (+70%) and decreased lipids per cell (-32% triglyceride, -36% cholesterol) as compared to controls. Conclusion. These results suggest that apoC-I and apoE production is differentially regulated at the transcriptional level in adipocytes and that apoC-I and apoE play a role in the maturation of human adipocytes and may have an important role in mediating or regulating cell lipid accumulation. As well, overexpression of apoC-I in SW872 cells impedes cellular lipid accumulation and stimulates cellular proliferation.
7

Sleiman, Lyne. "The Role of cIAP2 in Early and Late Atherosclerosis Lesion Development." Thesis, Université d'Ottawa / University of Ottawa, 2011. http://hdl.handle.net/10393/20226.

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Cellular Inhibitor of Apoptosis 2 (cIAP2) belongs to the IAP family, a group of endogenous proteins that inhibit apoptosis. However, the physiological role of cIAP2 remains poorly defined. Knock-out (KO) and wild type (WT) mice were used to examine the effect of cIAP2 protein on the progression of atherosclerosis in apoE -/- mice. Following the high-fat diet period of 4 and 12 wks, tissues were harvested and analysis focused on the aortic root, the aortic arch, the descending aorta, and the blood. Ex vivo results show a significant decrease in aortic arch lesion area in KO vs. WT in both study groups. Results also show a decrease in aortic root lesion size in KO vs. WT in both study groups. These results support that cIAP2 is an important survival factor for lesion-associated macrophages, since loss of cIAP2 expression in this mouse model reduced atherosclerotic lesion development.
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D'EUGENIO, Ottavio. "VALUTAZIONE DI FATTORI DI RISCHIO GENETICI SU BASE POLIMORFICA NELLA MALATTIA DI ALZHEIMER." Doctoral thesis, La Sapienza, 2006. http://hdl.handle.net/11573/917163.

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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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Books on the topic "ApoE-":

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McDonald, Pamela. 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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McPherran, Mark L., ed. Plato's 'Republic'. Cambridge: Cambridge University Press, 2010. http://dx.doi.org/10.1017/cbo9780511763090.

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Bobonich, Christopher, ed. Plato's 'Laws'. Cambridge: Cambridge University Press, 2010. http://dx.doi.org/10.1017/cbo9780511781483.

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Kanta, Chandra. Apne-Apne Konark. [s.l.]: [s.n.], 1995.

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Ajneya. Apne apne ajnabee. New Delhi: Bhartiya Jnanpith Parkashan, 1998.

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Singh, Bhagwan. Apne apne Ram. Delhi: Manaka, 1992.

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Hashmi, Jamila. Apne Apne Rang. New Delhi: Star, 1990.

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Goyal, Ajay. Apne apne dukh. Hapur: Shirshak, 1987.

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Denis, Lara, ed. Kant's 'Metaphysics of Morals'. Cambridge: Cambridge University Press, 2010. http://dx.doi.org/10.1017/cbo9780511763250.

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Melamed, Yitzhak Y., and Michael A. Rosenthal, eds. Spinoza's 'Theological-Political Treatise'. Cambridge: Cambridge University Press, 2010. http://dx.doi.org/10.1017/cbo9780511781339.

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Book chapters on the topic "ApoE-":

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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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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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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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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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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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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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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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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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Conference papers on the topic "ApoE-":

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Grah, Vitor Matias, Guilherme Sampaio Silva, Karla Viana Rezende, Ayrton Senna do Brasil Amaral Alves, Maria Inês Vaz de Oliveira, Maria Paula Banhara Rodrigues, and Juliana Carollyne Amorim. "The relationship between apolipoprotein e4 and bloodbrain barrier dysfunction in Alzheimer Disease." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.091.

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Background: Alzheimer disease(AD) is a progressive neurodegenerative dysfunction with a cognitive deficit and amyloid-β(Aβ) accumulation. That said, the apolipoprotein E (ApoE) has 4 variants, with E4 being linked to decreased cerebral blood flow and fragile blood-brain barrier (BBB). In this way, the BBB has an important role in removing substances that are toxic to the brain such as βA protein. Objective: Demonstrate the relationship of ApoE4 and BBB dysfunction in the pathophysiology of AD. Methods: Bibliographic review using the CAPES journals portal, in the last 5 years. Results: After analyzing the studies, it is inferred that in cases of homozygosity for ApoE4 in relation to ApoE3 there is a 15 fold increased chance of developing AD and 3 fold heterozygosity. It is concluded that the mechanism that probably explain is related to the secretion of ApoE by the pericytes that lining brain vessels in the BBB, whilst the subtype E4 exacerbates cyclophilinA, which promotes the activation of metalloproteinase-9, causing junctions rupture between adjacent endothelial cells, promoting the loss of βA homeostasis. Conclusion: It can be inferred, that ApoE has great importance in the regulation of the integrity of BBB’s integrity, is undeniable that such protein has a significant contribution in the pathophysiology of AD, hereupon, it’s urgent that these studies need to be continued to develop new therapies in individuals who express ApoE4.
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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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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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"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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Silva, Letícia Freitas de Castro, Elisa Pinheiro Weber, Gleice Silva Toledo, and Josiane Fonseca Almeida. "New pharmacological strategies for the treatment of alzheimer’s disease." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.097.

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Introduction: Alzheimer’s disease (AD) is seen as the most important dementia, prevalent in the elderly over 60 years old. There is still no cure, and the pharmacological strategies are to delay the symptoms and development of the pathology. The pathophysiological mechanisms are: hyperphosphorylation of the tau protein and aggregation of amyloid-β. Update studies of the tested therapies target the main pathological mechanisms: accumulation of β amyloid (inhibitors and modulators of β-secretase and γ-secretase and active and passive anti-Aβ immunotherapies), tau protein (inhibition of abnormal hyperphosphorylation with GSK-3 inhibitors, passive and active immunotherapies and the use of intrathecal antisense oligonucleotides (ASOs) and correction of the ApoE protein (increase lipidation, correct structure, clearance of non-lipid ApoE and reduction of ApoE expression). Objectives and methodology: To develop a bibliographic review in order to address new drugs in the treatment of Alzheimer’s. Qualitative and descriptive study carried out by literary review with research on PubMed. Results: Several drugs have been tested in clinical trials, however, due to lack of effectiveness, none have been approved. Therefore, it’s important to understand the limitations of the tests developed as flaws in the methodology, insufficient understanding of the mechanisms involved and inclusion of patients in different stages of AD, so that future investigations can overcome these gaps. Conclusion: It’s important to investigate new pathophysiological mechanisms, as well as the factors that trigger AD. Diagnosis is essential, with further studies to identify new biomarkers of the disease that will also have an impact on the conduct of clinical trials.
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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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"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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Tavares-Junior, Jose Wagner, Pedro Braga-Neto, Manoel Sobreira Neto, Danilo Oliveira, Carmem Gomes, Safira Gaspar, Emmanuelle Sobreira, Werbety Lucas Feitosa, Leticia Chaves Cunha, and Raquel Montenegro. "LONG-COVID COGNITIVE IMPAIRMENT: COGNITIVE ASSESSMENT AND APOLIPOPROTEIN E (APOE) GENOTYPING CORRELATION IN A BRAZILIAN COHORT." In XIII Meeting of Researchers on Alzheimer's Disease and Related Disorders. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1980-5764.rpda030.

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Background: COVID-19 neurological manifestations were demonstrated during the pandemic, including cognitive impairment. Objectives: To determine the prevalence of cognitive and behavioral complaints (such as dementia, MCI or SCD) in a outpatient sample with recent SARS-COV2 infection. Specific: Evaluate the association of cognitive impairment with the presence of the polymorphism found in the APOE gene and with respiratory disease. Methodology: Observational, longitudinal, prospective clinical study. Inclusion criteria: patients with confirmed Covid-19. Patients are evaluated in an outpatient clinic. They are evaluated through a standardized attendance record, with somatic and cognitive neurological assessment. Cognitive assessment involves the application of cognitive (ACER, MMSE and CDR), functional (Pfeffer) and psychiatric (GDS or Beck) screening instruments, in addition to subsequent extensive neuropsychological assessment. In addition, APOE polymorphism is analysed. Preliminary. Results: To date, 191 patients and 11 controls were evaluated. The average age is 46.5 years, with 65.4% female, 79.16% with 8 or more years of schooling, in addition to 57.5% of the sample with cognitive complaints. Conclusions: The results so far in our study demonstrate that cognitive complaints are frequent in patients even in the chronic phase of the disease.
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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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Eugene, Lius Putri Felicia, Ferry Pergamus Gultom, Yurnadi Hanafi Midoen, Antonius Winoto Suhartono, Triana Marchelina, and Elza Ibrahim Auerkari. "Polymorphism of Apolipoprotein E (APOE) gene in head and neck cancer." In SECOND INTERNATIONAL CONFERENCE OF MATHEMATICS (SICME2019). Author(s), 2019. http://dx.doi.org/10.1063/1.5096758.

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Reports on the topic "ApoE-":

1

Conte, Ianina, Mary Turner, Iris Fineberg, David Clark, Brian Francis, Kath Nuttall, and Lee Storey. Community-based evaluation of &apos;Preferred Place of Care&apos; in the North West of England. National Institute for Health Research, January 2022. http://dx.doi.org/10.3310/nihropenres.1115172.1.

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Webber, Franklin, Partha P. Pal, Michael Atighetchi, Chris Jones, and Paul Rubel. Applications That Participate in Their Own Defense (APOD). Fort Belvoir, VA: Defense Technical Information Center, May 2003. http://dx.doi.org/10.21236/ada415561.

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Boothman, David A. Nuclear apoJ: An X-ray-inducible cell death signal. Final Report. Office of Scientific and Technical Information (OSTI), December 2003. http://dx.doi.org/10.2172/824533.

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Wheeler, Hilary, and Crystal Densmore. Bench-Scale Synthetic Optimization of 1,2-bis(2-aminophenylthio)ethane (APO-Link) Used in the Production of APO-BMI Resin. Office of Scientific and Technical Information (OSTI), July 2007. http://dx.doi.org/10.2172/926448.

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TEXAS INSTRUMENTS INC MCKINNEY TX. APSE(Ada Programming Support Environment) Interactive Monitor. User's Manual Ada (trademark) Version. Fort Belvoir, VA: Defense Technical Information Center, January 1988. http://dx.doi.org/10.21236/ada198151.

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Reser, Patrick M., Matthew W. Lewis, Jarod Clark, Nishant Ahuja, and Lary R. Lenke. Characterization of Shear Properties for APO/MBI Syntactic Foam. Office of Scientific and Technical Information (OSTI), December 2017. http://dx.doi.org/10.2172/1414077.

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Freyre, Jairo, David Remkes, and Jeffrey Ragsdale. Common Ada Programming Support Environment (APSE) Interface Set (CAIS) Implementation Validation Capability (CIVC2). Fort Belvoir, VA: Defense Technical Information Center, June 1992. http://dx.doi.org/10.21236/ada261043.

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Leveling, A. F., and /Fermilab. Radiatio Detector Characterization at APO While Stacking pbars in 1999. Office of Scientific and Technical Information (OSTI), February 2000. http://dx.doi.org/10.2172/984631.

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Connor, James R. Apo-Ferritin as a Therapeutic Treatment for Amyotrophic Lateral Sclerosis. Fort Belvoir, VA: Defense Technical Information Center, September 2012. http://dx.doi.org/10.21236/ada567828.

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Connor, James R. Apo-Ferritin as a Therapeutic Treatment for Amyotrophic Lateral Sclerosis. Fort Belvoir, VA: Defense Technical Information Center, December 2013. http://dx.doi.org/10.21236/ada598852.

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