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Artículos de revistas sobre el tema "ApoE-"

Autor: Grafiati

Publicado: 4 de junio de 2021

Última modificación: 25 de julio de 2025

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1

Begcevic Brkovic, Ilijana, Benedikt Zöhrer, Markus Scholz, et al. "Simultaneous Mass Spectrometry-Based Apolipoprotein Profiling and Apolipoprotein E Phenotyping in Patients with ASCVD and Mild Cognitive Impairment." Nutrients 14, no. 12 (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 disea

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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 (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 univ

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3

Budny, Vanessa, Yannic Knöpfli, Debora Meier, et al. "APOE4 Increases Energy Metabolism in APOE-Isogenic iPSC-Derived Neurons." Cells 13, no. 14 (2024): 1207. http://dx.doi.org/10.3390/cells13141207.

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The apolipoprotein E4 (APOE4) allele represents the major genetic risk factor for Alzheimer’s disease (AD). In contrast, APOE2 is known to lower the AD risk, while APOE3 is defined as risk neutral. APOE plays a prominent role in the bioenergetic homeostasis of the brain, and early-stage metabolic changes have been detected in the brains of AD patients. Although APOE is primarily expressed by astrocytes in the brain, neurons have also been shown as source for APOE. However, the distinct roles of the three APOE isoforms in neuronal energy homeostasis remain poorly understood. In this study, we g

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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 (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 polyacryla

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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 (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 red

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6

Vecchio, Filomena Lo, Paola Bisceglia, Bruno Pietro Imbimbo, 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,

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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 (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, apoE

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8

Chung, Won-Suk, Philip B. Verghese, Chandrani Chakraborty, et al. "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 (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 pr

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9

Pohlkamp, Theresa. "Apolipoprotein E: Cholesterol metabolism and Alzheimer’s pathology." Neuroforum 26, no. 1 (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 pathol

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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 (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

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11

Civeira-Marín, María, Ana Cenarro, Victoria Marco-Benedí, et al. "APOE Genotypes Modulate Inflammation Independently of Their Effect on Lipid Metabolism." International Journal of Molecular Sciences 23, no. 21 (2022): 12947. http://dx.doi.org/10.3390/ijms232112947.

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The association between APOE genotypes and cardiovascular disease (CVD) is partially mediated by LDL-cholesterol concentration but persists after adjusting for lipid levels and other cardiovascular risk factors. Data from the Aragon Workers Health Study (AWHS) (n = 4159) and the Lipid Unit at the Hospital Universitario Miguel Servet (HUMS) (n = 3705) were used to investigate the relationship between C-reactive protein (CRP) levels and APOE genotype. Lipoprotein particle and GlycA concentrations were analyzed in a subsample from AWHS. APOE genotyping was carried out by the Sanger method in both

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12

Zuniga, Nathan R., Noah E. Earls, Ariel E. A. Denos, et al. "Quantitative and Kinetic Proteomics Reveal ApoE Isoform-dependent Proteostasis Adaptations in Mouse Brain." PLOS Computational Biology 20, no. 12 (2024): e1012407. https://doi.org/10.1371/journal.pcbi.1012407.

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Apolipoprotein E (ApoE) polymorphisms modify the risk of Alzheimer’s disease with ApoE4 strongly increasing and ApoE2 modestly decreasing risk relative to the control ApoE3. To investigate how ApoE isoforms alter risk, we measured changes in proteome homeostasis in transgenic mice expressing a human ApoE gene (isoform 2, 3, or 4). The regulation of each protein’s homeostasis is observed by measuring turnover rate and abundance for that protein. We identified 4849 proteins and tested for ApoE isoform-dependent changes in the homeostatic regulation of ~2700 ontologies. In the brain, we found tha

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13

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

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14

Villeneuve, Sylvia, Diane Brisson, and Daniel Gaudet. "Influence of Abdominal Obesity on the Lipid-Lipoprotein Profile in Apoprotein E2/4 Carriers: The Effect of an Apparent Duality." Journal of Lipids 2015 (2015): 1–10. http://dx.doi.org/10.1155/2015/742408.

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Background. Apolipoprotein (Apo) E plays a key role in the handling of lipoprotein particles with ApoE2 and ApoE4 frequently having opposite effects compared to ApoE3. Some individuals simultaneously carry both E2 and E4 alleles. The impact of the ApoE2/4 genotype on lipid concentrations and its consequences on health remain poorly documented.Objective. This study compared the lipid profile between ApoE2/4 carriers and other ApoE genotypes in relation to the waist circumference.Methods. Cholesterol, triglyceride (TG), and ApoB concentrations were measured among 2,680 Caucasians. Multivariate l

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15

Alata, Wael, Yue Ye, Isabelle St-Amour, Milène Vandal та Frédéric Calon. "Human Apolipoprotein E ε4 Expression Impairs Cerebral Vascularization and Blood—Brain Barrier Function in Mice". Journal of Cerebral Blood Flow & Metabolism 35, № 1 (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 cerebra

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16

Moraes, Ruan C. M., Jonathan R. Roth, Hailey Mao, et al. "Apolipoprotein E Induces Lipid Accumulation Through Dgat2 That Is Prevented with Time-Restricted Feeding in Drosophila." Genes 15, no. 11 (2024): 1376. http://dx.doi.org/10.3390/genes15111376.

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Background: Apolipoprotein E (ApoE) is the leading genetic risk factor for late-onset Alzheimer’s disease (AD), which is the leading cause of dementia worldwide. Most people have two ApoE-ε3 (ApoE3) alleles, while ApoE-ε2 (ApoE2) is protective from AD, and ApoE-ε4 (ApoE4) confers AD risk. How these alleles modulate AD risk is not clearly defined, and ApoE’s role in lipid metabolism is also not fully known. Lipid droplets increase in AD. However, how ApoE contributes to lipid accumulation in the brain remains unknown. Methods: Here, we use Drosophila to study the effects of ApoE alleles on lipi

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17

Cambruzzi, Eduardo, and Karla Lais Pêgas. "Pathogenesis, histopathologic findings and treatment modalities of lipoprotein glomerulopathy: A review." Brazilian Journal of Nephrology 41, no. 3 (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

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18

Zhang, Ting, Pengyuan Dai, Dong Cheng, et al. "Obesity occurring in apolipoprotein E-knockout mice has mild effects on fertility." REPRODUCTION 147, no. 2 (2014): 141–51. http://dx.doi.org/10.1530/rep-13-0470.

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The Apolipoprotein (Apo) family is implicated in lipid metabolism. There are five types of Apo: Apoa, Apob, Apoc, Apod, and Apoe. Apoe has been demonstrated to play a central role in lipoprotein metabolism and to be essential for efficient receptor-mediated plasma clearance of chylomicron remnants and VLDL remnant particles by the liver. Apoe-deficient (Apoe−/−) mice develop atherosclerotic plaques spontaneously, followed by obesity. In this study, we investigated whether lipid deposition caused by Apoe knockout affects reproduction in female mice. The results demonstrated that Apoe−/− mice we

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19

Liampas, Ioannis, Panagiota Kyriakoulopoulou, Vasileios Siokas та ін. "Apolipoprotein E Gene in α-Synucleinopathies: A Narrative Review". International Journal of Molecular Sciences 25, № 3 (2024): 1795. http://dx.doi.org/10.3390/ijms25031795.

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In this narrative review, we delved into the intricate interplay between Apolipoprotein E (APOE) alleles (typically associated with Alzheimer’s disease—AD) and alpha-synucleinopathies (aS-pathies), involving Parkinson’s disease (PD), Parkinson’s disease dementia (PDD), dementia with Lewy bodies (DLB), and multiple-system atrophy (MSA). First, in-vitro, animal, and human-based data on the exacerbating effect of APOE4 on LB pathology were summarized. We found robust evidence that APOE4 carriage constitutes a risk factor for PDD—APOE2, and APOE3 may not alter the risk of developing PDD. We confir

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20

Gao, Huiling, Wei Zheng, Cheng Li, and He Xu. "Isoform-Specific Effects of Apolipoprotein E on Hydrogen Peroxide-Induced Apoptosis in Human Induced Pluripotent Stem Cell (iPSC)-Derived Cortical Neurons." International Journal of Molecular Sciences 22, no. 21 (2021): 11582. http://dx.doi.org/10.3390/ijms222111582.

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Hydrogen peroxide (H2O2)-induced neuronal apoptosis is critical to the pathology of Alzheimer’s disease (AD) as well as other neurodegenerative diseases. The neuroprotective effects of apolipoprotein (ApoE) isoforms against apoptosis and the underlying mechanism remains controversial. Here, we have generated human cortical neurons from iPSCs and induced apoptosis with H2O2. We show that ApoE2 and ApoE3 pretreatments significantly attenuate neuronal apoptosis, whereas ApoE4 has no neuroprotective effect and higher concentrations of ApoE4 even display toxic effect. We further identify that ApoE2

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21

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 (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

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22

Kraft, Lucas, Louise Serpell, and John Atack. "A Biophysical Approach to the Identification of Novel ApoE Chemical Probes." Biomolecules 9, no. 2 (2019): 48. http://dx.doi.org/10.3390/biom9020048.

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Alzheimer’s disease (AD) is the most common type of dementia and, after age, the greatest risk factor for developing AD is the allelic variation of apolipoprotein E (ApoE), with homozygote carriers of the ApoE4 allele having an up to 12-fold greater risk of developing AD than noncarriers. Apolipoprotein E exists as three isoforms that differ in only two amino acid sites, ApoE2 (Cys112/Cys158), ApoE3 (Cys112/Arg158), and ApoE4 (Arg112/Arg158). These amino acid substitutions are assumed to alter ApoE structure and function, and be responsible for the detrimental effects of ApoE4 via a mechanism

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23

Herrmann, Wolfgang, Sigrid Hanf, Jürgen Reißner, Hans Kaffarnik, Sabine Motzny, and Armin Steinmetz. "The Influence of Apolipoprotein E Polymorphism on Plasma Concentrations of Apolipoprotein B and A-I During the First Year of Life." Pediatrics 93, no. 2 (1994): 296–302. http://dx.doi.org/10.1542/peds.93.2.296.

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Apolipoprotein (apo)E polymorphism has been shown to be associated with different serum levels of cholesterol, apoB, and apoE. In clarifying the degree of influence of the apoE isoforms, investigations in an early stage of life are useful. The aim of the study was to investigate the plasma levels of apoB and apoA-I as structural proteins of low and high density lipoproteins, in relation to apoE phenotypes during the first year of life. Conclusions about the relationship between apoE phenotype and the development of the lipoprotein patterns can be drawn. The concentrations of apoB and apoA-I in

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24

Gunzburg, Menachem J., Matthew A. Perugini, and Geoffrey J. Howlett. "Structural Basis for the Recognition and Cross-linking of Amyloid Fibrils by Human Apolipoprotein E." Journal of Biological Chemistry 282, no. 49 (2007): 35831–41. http://dx.doi.org/10.1074/jbc.m706425200.

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Apolipoprotein (apo) E is a well characterized lipid-binding protein in plasma that also exists as a common nonfibrillar component of both cerebral and systemic amyloid deposits. A genetic link between a common isoform of apoE, apoE4, and the incidence of late onset Alzheimer disease has drawn considerable attention to the potential roles of apoE in amyloid-related disease. We examined the interactions of apoE with amyloid fibrils composed of apoC-II and the amyloid-β (Aβ) peptide. Aggregates of apoE with Aβ and apoC-II are found in Alzheimer and atherosclerotic plaques, respectively. Sediment

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Mamun, Abdullah Al, Md Sahab Uddin, Md Fahim Bin Bashar, et al. "Molecular Insight into the Therapeutic Promise of Targeting APOE4 for Alzheimer’s Disease." Oxidative Medicine and Cellular Longevity 2020 (May 15, 2020): 1–16. http://dx.doi.org/10.1155/2020/5086250.

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Alzheimer’s disease (AD) is a progressive neurodegenerative disease that causes chronic cognitive dysfunction. Most of the AD cases are late onset, and the apolipoprotein E (APOE) isoform is a key genetic risk factor. The APOE gene has 3 key alleles in humans including APOE2, APOE3, and APOE4. Among them, APOE4 is the most potent genetic risk factor for late-onset AD (LOAD), while APOE2 has a defensive effect. Research data suggest that APOE4 leads to the pathogenesis of AD through various processes such as accelerated beta-amyloid aggregations that raised neurofibrillary tangle formation, cer

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Sheng, Huaxin, Daniel T. Laskowitz, Ellen Bennett, et al. "Apolipoprotein E Isoform-Specific Differences in Outcome from Focal Ischemia in Transgenic Mice." Journal of Cerebral Blood Flow & Metabolism 18, no. 4 (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

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Hsu, Michelle, Mehek Dedhia, Wim Crusio, and Anna Delprato. "Sex differences in gene expression patterns associated with the APOE4 allele." F1000Research 8 (April 5, 2019): 387. http://dx.doi.org/10.12688/f1000research.18671.1.

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Background: The APOE gene encodes apolipoprotein ε (ApoE), a protein that associates with lipids to form lipoproteins that package and traffic cholesterol and lipids through the bloodstream. There are at least three different alleles of the APOE gene: APOE2, APOE3, and APOE4. The APOE4 allele increases an individual's risk for developing late-onset Alzheimer disease (AD) in a dose-dependent manner. Sex differences have been reported for AD susceptibility, age of onset, and symptom progression, with females being more affected than males. Methods: In this study, we use a systems biology approac

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Zhao, Na, Olivia N. Attrebi, Yingxue Ren та ін. "APOE4 exacerbates α-synuclein pathology and related toxicity independent of amyloid". Science Translational Medicine 12, № 529 (2020): eaay1809. http://dx.doi.org/10.1126/scitranslmed.aay1809.

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The apolipoprotein E (APOE) ε4 allele is the strongest genetic risk factor for late-onset Alzheimer’s disease mainly by driving amyloid-β pathology. Recently, APOE4 has also been found to be a genetic risk factor for Lewy body dementia (LBD), which includes dementia with Lewy bodies and Parkinson’s disease dementia. How APOE4 drives risk of LBD and whether it has a direct effect on α-synuclein pathology are not clear. Here, we generated a mouse model of synucleinopathy using an adeno-associated virus gene delivery of α-synuclein in human APOE-targeted replacement mice expressing APOE2, APOE3,

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Marin, Guilherme B., Marli H. Tavella, João F. Guerreiro, Sidney E. B. Santos, and Marco A. Zago. "Absence of the E2 allele of apolipoprotein in Amerindians." Brazilian Journal of Genetics 20, no. 4 (1997): 741–43. http://dx.doi.org/10.1590/s0100-84551997000400029.

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Determination of the ApoE allele distribution in five South American Amerindian tribes revealed absence of the ApoE2 allele, accompanied by high ApoE3 and low ApoE4 allele frequencies for most tribes, a distribution only previously reported for the Inuit Eskimo from Greenland.

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Zhang, Xin, Long Wu, Russell H. Swerdlow, and Liqin Zhao. "Opposing Effects of ApoE2 and ApoE4 on Glycolytic Metabolism in Neuronal Aging Supports a Warburg Neuroprotective Cascade against Alzheimer’s Disease." Cells 12, no. 3 (2023): 410. http://dx.doi.org/10.3390/cells12030410.

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Apolipoprotein E4 (ApoE4) is the most recognized genetic risk factor for late-onset Alzheimer’s disease (LOAD), whereas ApoE2 reduces the risk for LOAD. The underlying mechanisms are unclear but may include effects on brain energy metabolism. Here, we used neuro-2a (N2a) cells that stably express human ApoE isoforms (N2a-hApoE), differentiated N2a-hApoE neuronal cells, and humanized ApoE knock-in mouse models to investigate relationships among ApoE isoforms, glycolytic metabolism, and neuronal health and aging. ApoE2-expressing cells retained robust hexokinase (HK) expression and glycolytic ac

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31

Dunk, Michelle M., and Ira Driscoll. "Total Cholesterol and APOE-Related Risk for Alzheimer’s Disease in the Alzheimer’s Disease Neuroimaging Initiative." Journal of Alzheimer's Disease 85, no. 4 (2022): 1519–28. http://dx.doi.org/10.3233/jad-215091.

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Background: APOE ɛ4 allele confers greatest genetic risk for Alzheimer’s disease (AD), yet mechanisms underlying this risk remain elusive. APOE is involved in lipid metabolism, and literature suggest relationships between high total cholesterol, APOE, and AD. Further investigation is needed to elucidate the potential role of total cholesterol in AD risk. Objective: To investigate the relationship between total cholesterol and APOE-related AD risk in the Alzheimer’s Disease Neuroimaging Initiative. Methods: Participants (N = 1,534) were classified as controls (cognitively normal; N = 404), earl

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Simon, Romain, Marion Girod, Catherine Fonbonne, et al. "Total ApoE and ApoE4 Isoform Assays in an Alzheimer's Disease Case-control Study by Targeted Mass Spectrometry (n = 669): A Pilot Assay for Methionine-containing Proteotypic Peptides." Molecular & Cellular Proteomics 11, no. 11 (2012): 1389–403. http://dx.doi.org/10.1074/mcp.m112.018861.

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Allelic polymorphism of the apolipoprotein E (ApoE) gene (ApoE ε2, ApoE ε3 and ApoE ε4 alleles) gives rise to three protein isoforms (ApoE2, ApoE3 and ApoE4) that differ by 1 or 2 amino acids. Inheritance of the ApoE ε4 allele is a risk factor for developing Alzheimer's disease (AD). The potential diagnostic value of ApoE protein levels in biological fluids (i.e. cerebrospinal fluid, plasma and serum) for distinguishing between AD patients and healthy elderly subjects is subject to great controversy. Although a recent study reported subnormal total ApoE and ApoE4 levels in the plasma of AD pat

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Richard, Pascale, Isabelle Beucler, Maria Pascual De Zulueta, Nicolas Biteau, Jean-Luc De Gennes, and Albert Iron. "Compound Heterozygote for Both Rare Apolipoprotein E1(Gly127→Asp, Arg158→Cys) and E3(Cys112 → Arg, Arg251 → Gly) Alleles in a Multigeneration Pedigree with Hyperlipoproteinaemia." Clinical Science 93, no. 1 (1997): 89–95. http://dx.doi.org/10.1042/cs0930089.

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1. A French multigeneration pedigree with hyperlipoproteinaemia was investigated for the transmission of the rare apolipoprotein E1(Gly127 → Asp, Arg158 → Cys) variant. The proband, a 46-year-old male carrying the rare apoE1 variant, presented a severe type III hyperlipoproteinaemia like his three brothers and his sister. 2. ApoE phenotyping and genotyping showed a discrepancy in the second allele carried by the proband's wife and two of her children, thus suggesting another apoE gene mutation. Cloning and sequencing of the entire exon 4 demonstrated a point mutation at codon 251, leading to a

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Ozen, Ezgi, Rada G. Mihaylova, Natalie J. Lord, Julie A. Lovegrove, and Kim G. Jackson. "Association between APOE Genotype with Body Composition and Cardiovascular Disease Risk Markers Is Modulated by BMI in Healthy Adults: Findings from the BODYCON Study." International Journal of Molecular Sciences 23, no. 17 (2022): 9766. http://dx.doi.org/10.3390/ijms23179766.

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Body mass index (BMI) has been suggested to play an important role in the relationship between the APOLIPOPROTEIN (APO)E genotype and cardiovascular disease (CVD) risk. Using data from the BODYCON cross-sectional study (n = 360 adults) we assessed the association between body composition and CVD risk markers according to APOE genotype, with examination of the role of BMI. In this study cohort, the APOE2/E3 group had lower fasting blood lipids than APOE4 carriers and APOE3/E3 group (p ≤ 0.01). After stratifying the group according to BMI, APOE4 carriers in the normal BMI subgroup had a higher l

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Ghosh, Shamasree, Shanmugam Tamilselvi, Chloe Williams, et al. "ApoE Isoforms Inhibit Amyloid Aggregation of Proinflammatory Protein S100A9." International Journal of Molecular Sciences 25, no. 4 (2024): 2114. http://dx.doi.org/10.3390/ijms25042114.

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Increasing evidence suggests that the calcium-binding and proinflammatory protein S100A9 is an important player in neuroinflammation-mediated Alzheimer’s disease (AD). The amyloid co-aggregation of S100A9 with amyloid-β (Aβ) is an important hallmark of this pathology. Apolipoprotein E (ApoE) is also known to be one of the important genetic risk factors of AD. ApoE primarily exists in three isoforms, ApoE2 (Cys112/Cys158), ApoE3 (Cys112/Arg158), and ApoE4 (Arg112/Arg158). Even though the difference lies in just two amino acid residues, ApoE isoforms produce differential effects on the neuroinfl

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Sae-Lee, Wisath, Luisa L. Scott, Lotti Brose, et al. "APP-Induced Patterned Neurodegeneration Is Exacerbated by APOE4 in Caenorhabditis elegans." G3: Genes|Genomes|Genetics 10, no. 8 (2020): 2851–61. http://dx.doi.org/10.1534/g3.120.401486.

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Genetic and epidemiological studies have found that variations in the amyloid precursor protein (APP) and the apoliopoprotein E (APOE) genes represent major modifiers of the progressive neurodegeneration in Alzheimer’s disease (AD). An extra copy of or gain-of-function mutations in APP correlate with early onset AD. Compared to the other variants (APOE2 and APOE3), the ε4 allele of APOE (APOE4) hastens and exacerbates early and late onset forms of AD. Convenient in vivo models to study how APP and APOE4 interact at the cellular and molecular level to influence neurodegeneration are lacking. He

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James, Niaya, Oyinkansola Shonde, Nahdia Jones, Verona E. Mulgrave, G. William Rebeck, and Joanne Allard. "Impact of APOE Genotype on Diet-induced Mitochondrial Adaptations in Mouse Skeletal Muscle." Innovation in Aging 5, Supplement_1 (2021): 971. http://dx.doi.org/10.1093/geroni/igab046.3496.

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Abstract Apolipoprotein E (APOE), a component of lipoproteins that facilitates cholesterol transportation, has three variants in the human genome: APOE2, E3, and E4. Prior research found that carriers of APOE4 are more susceptible to developing Alzheimer's disease (AD) and other brain disorders than those who possess other APOE alleles, and that these carriers are also predisposed to mitochondrial impairment– an early characteristic of neuronal dysfunction. Peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1ɑ) is a major biomarker for mitochondrial biogenesis and functi

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BENTLEY, Nicholas M., Mary Jo LaDU, Chandrika RAJAN, Godfrey S. GETZ та 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, № 1 (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.

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Tai, Leon M., Katherine L. Youmans, Lisa Jungbauer, Chunjiang Yu та Mary Jo LaDu. "Introducing HumanAPOEinto AβTransgenic Mouse Models". International Journal of Alzheimer's Disease 2011 (2011): 1–9. http://dx.doi.org/10.4061/2011/810981.

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Apolipoprotein E (apoE) and apoE/amyloid-β(Aβ) transgenic (Tg) mouse models are critical to understanding apoE-isoform effects on Alzheimer's disease risk. Compared to wild type,apoE−/−mice exhibit neuronal deficits, similar to apoE4-Tg compared to apoE3-Tg mice, providing a model for Aβ-independent apoE effects on neurodegeneration. To determine the effects of apoE on Aβ-induced neuropathology,apoE−/−mice were crossed with Aβ-Tg mice, resulting in a significant delay in plaque deposition. Surprisingly, crossing human-apoE-Tg mice withapoE−/−/Aβ-Tg mice further delayed plaque deposition, which

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Alagarsamy, Jeyashree, Anja Jaeschke, and David Y. Hui. "Apolipoprotein E in Cardiometabolic and Neurological Health and Diseases." International Journal of Molecular Sciences 23, no. 17 (2022): 9892. http://dx.doi.org/10.3390/ijms23179892.

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A preponderance of evidence obtained from genetically modified mice and human population studies reveals the association of apolipoprotein E (apoE) deficiency and polymorphisms with pathogenesis of numerous chronic diseases, including atherosclerosis, obesity/diabetes, and Alzheimer’s disease. The human APOE gene is polymorphic with three major alleles, ε2, ε3 and ε4, encoding apoE2, apoE3, and apoE4, respectively. The APOE gene is expressed in many cell types, including hepatocytes, adipocytes, immune cells of the myeloid lineage, vascular smooth muscle cells, and in the brain. ApoE is presen

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Burgos, Javier S., Carlos Ramirez, Isabel Sastre, and Fernando Valdivieso. "Effect of Apolipoprotein E on the Cerebral Load of Latent Herpes Simplex Virus Type 1 DNA." Journal of Virology 80, no. 11 (2006): 5383–87. http://dx.doi.org/10.1128/jvi.00006-06.

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ABSTRACT Herpes simplex virus type 1 (HSV-1) is neurotropic and enters a latent state lasting the lifetime of the host. This pathogen has recently been proposed as a risk factor for Alzheimer's disease (AD) in conjunction with apolipoprotein E4 (ApoE4). In a murine acute infection model, we showed that viral neuroinvasiveness depends directly on the overall ApoE dosage and especially on the presence of isoform ApoE4. If an interaction between ApoE and HSV-1 is involved in AD, it may occur during latency rather than during acute infection. Certainly, ApoE plays an important role in late-onset A

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Ohm, Thomas G., Ulrike Hamker, Angel Cedazo-Minguez та ін. "Apolipoprotein E and ϐA4-amyloid: signals and effects". Biochemical Society Symposia 67 (1 лютого 2001): 121–29. http://dx.doi.org/10.1042/bss0670121.

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In humans, the apolipoprotein E gene (APOE) is polymorphic with the alleles APOE ϵ2, 3 and 4 coding for apolipoproteins (Apo) E2, 3 and 4. Apart from age, the APOE ϵ4 allele represents the most important risk factor in sporadic Alzheimer's disease (AD). Compared to APOE ϵ3 homozygotes, the histopathological onset of tau pathology is found 1-2 decades earlier but progresses with the same speed. ApoE dose-dependently and specifically increases free intraneuronal calcium levels in the order ApoE4 > ApoE3 > ApoE2. This effect is amplified in the presence of ϐA4-peptide. The ApoE effects on c

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Koren-Iton, Amit, Shiran Salomon-Zimri, Alex Smolar, et al. "Central and Peripheral Mechanisms in ApoE4-Driven Diabetic Pathology." International Journal of Molecular Sciences 21, no. 4 (2020): 1289. http://dx.doi.org/10.3390/ijms21041289.

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Apolipoprotein E (APOE) ε4 gene allele and type 2 diabetes mellitus (T2DM) are prime risk factors for Alzheimer’s disease (AD). Despite evidence linking T2DM and apoE4, the mechanism underlying their interaction is yet to be determined. In the present study, we employed a model of APOE-targeted replacement mice and high-fat diet (HFD)-induced insulin resistance to investigate diabetic mechanisms associated with apoE4 pathology and the extent to which they are driven by peripheral and central processes. Results obtained revealed an intriguing pattern, in which under basal conditions, apoE4 mice

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Hsu, Michelle, Mehek Dedhia, Wim E. Crusio, and Anna Delprato. "Sex differences in gene expression patterns associated with the APOE4 allele." F1000Research 8 (July 23, 2019): 387. http://dx.doi.org/10.12688/f1000research.18671.2.

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Background: The APOE gene encodes apolipoprotein ε (ApoE), a protein that associates with lipids to form lipoproteins that package and traffic cholesterol and lipids through the bloodstream. There are at least three different alleles of the APOE gene: APOE2, APOE3, and APOE4. The APOE4 allele increases an individual's risk for developing late-onset Alzheimer disease (AD) in a dose-dependent manner. Sex differences have been reported for AD susceptibility, age of onset, and symptom progression, with females being more affected than males. Methods: In this study, we use a systems biology approac

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TOKUDA, Takahiko, Miguel CALERO, Etsuro MATSUBARA та ін. "Lipidation of apolipoprotein E influences its isoform-specific interaction with Alzheimer's amyloid β peptides". Biochemical Journal 348, № 2 (2000): 359–65. http://dx.doi.org/10.1042/bj3480359.

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The inheritance of the apolipoprotein E (apoE) ϵ4 allele is a prevailing risk factor for sporadic and familial Alzheimer's disease (AD). ApoE isoforms bind directly to Alzheimer's amyloid β (Aβ) peptides both in vitro and in vivo. Recent studies suggest that association of apoE with lipids may modulate its interaction with Aβ. We examined the binding of lipid-associated and delipidated apoE3 and apoE4 isoforms to Aβ utilizing a solid-phase binding assay and estimated the dissociation constants for the interaction of various apoE and Aβ species. Using native apoE isoforms from stably transfecte

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Washington, Patricia M., та Mark P. Burns. "The Effect of the APOE4 Gene on Accumulation of Aβ 40 After Brain Injury Cannot Be Reversed by Increasing apoE4 Protein". Journal of Neuropathology & Experimental Neurology 75, № 8 (2016): 770–78. http://dx.doi.org/10.1093/jnen/nlw049.

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Abstract The apolipoprotein E (apoE) protein is involved in clearance of β-amyloid (Aβ) from the brain; and the APOE4 gene is associated with Aβ plaque formation in humans following traumatic brain injury (TBI). Here, we examined the association between apoE and Aβ 40 after experimental TBI and the effects of APOE alleles on this relationship. We report a biphasic response of soluble apoE protein after TBI with an acute reduction at 1 day postinjury followed by an increase at 7 days postinjury. TBI-induced Aβ 40 levels decreased as soluble apoE levels increased. In APOE4 mice there was a dimin

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Mai, Zhenhua, Wenyan Wei, Haibin Yu, Yongze Chen, Yongxiang Wang, and Yuanlin Ding. "Molecular recognition of the interaction between ApoE and the TREM2 protein." Translational Neuroscience 13, no. 1 (2022): 93–103. http://dx.doi.org/10.1515/tnsci-2022-0218.

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Abstract Alzheimer’s disease (AD) is the most common type of dementia. The ε4 allele of the apolipoprotein E (ApoE) gene is the strongest known genetic risk factor for late-onset AD. Triggering receptor expressed on myeloid cells 2 (TREM2) is another important risk factor affecting the AD process after ApoE. Emerging evidence has identified TREM2 as a putative receptor for ApoE, raising the possibility that interactions between ApoE and TREM2 modulate the pathogenesis of AD. In this study, we performed molecular docking and molecular dynamics (MD) analyses to characterize the ApoE–TREM2 intera

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Yamauchi, Kazuyoshi, Minoru Tozuka, Hiroya Hidaka, Eiko Hidaka, Yoshiyuki Kondo, and Tsutomu Katsuyama. "Characterization of Apolipoprotein E-containing Lipoproteins in Cerebrospinal Fluid: Effect of Phenotype on the Distribution of Apolipoprotein E." Clinical Chemistry 45, no. 9 (1999): 1431–38. http://dx.doi.org/10.1093/clinchem/45.9.1431.

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Abstract Background: Apolipoprotein (apo) E, one of the main apolipoproteins in the central nervous system, may play an important role in lipid metabolism; however, the details of its function are poorly understood. In this study, we characterized apoE-containing lipoproteins in cerebrospinal fluid (CSF) and examined the effect of apoE phenotype on the distribution of apoE among the lipoprotein fractions. Methods: CSF lipoproteins were fractionated by gel filtration and ultracentrifugation, and then characterized by electrophoresis, immunoblot, electron microscopy, and analysis of apoE, total

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Ibrahim, Amnah Raad, Raghad Hassan Hussein, and Athraa Zaidan Hassan. "Alterations of Some Apolipoprotein Levels and ApoE RNA Expression in Iraqi Patients with Chronic Hepatitis B Viral Infection." Medical Journal of Babylon 21, Suppl 2 (2024): S266—S271. http://dx.doi.org/10.4103/mjbl.mjbl_1077_23.

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Abstract Background: The high prevalence of hepatitis B virus (HBV) makes it a significant health concern, especially in Iraq. Clinical studies have found that chronic HBV infection affects the occurrence of cardiovascular disease (CVD) by regulating cholesterol metabolism in liver cells. Objective: This study aimed to determine alterations in some serum lipoproteins (ApoA, ApoB, and apolipoprotein E [ApoE]) and oxidized low-density lipoprotein (OxLDL), as well as ApoE gene expression in Iraqi patients with chronic HBV infection, as potential markers for increased cardiovascular risk. Material

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Trigo, Arturo Nicolás, Marina Muzzio, Marcelo Isidro Figueroa, et al. "Apolipoprotein E Polymorphisms in Andean Population of Jujuy, Argentina." Journal of Alzheimer's Disease Reports 8, no. 1 (2024): 95–99. http://dx.doi.org/10.3233/adr-230061.

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The pleiotropic nature of the apolipoprotein E (APOE) gene is associated with complex diseases in different populations. We analyzed APOE polymorphisms in 76 individuals from Jujuy – Argentina using NGS technology. The observed genotypes align with the expected Hardy–Weinberg equilibrium. APOE3 was the most common allele, followed by APOE4 and APOE2. The allele distribution pattern is consistent with findings in previously studied populations of Native Americans and Asians. The E4 allele’s low frequency, always observed in a heterozygous state, raises questions regarding its relevance in expla

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