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Artículos de revistas sobre el tema "ApoE-/- mouse"

Autor: Grafiati

Publicado: 4 de junio de 2021

Última modificación: 25 de julio de 2025

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1

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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2

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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3

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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4

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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5

Watson, Yassin, Brenae Nelson, Jamie Hernandez Kluesner, et al. "Aggregate Trends of Apolipoprotein E on Cognition in Transgenic Alzheimer’s Disease Mice." Journal of Alzheimer's Disease 83, no. 1 (2021): 435–50. http://dx.doi.org/10.3233/jad-210492.

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Background: Apolipoprotein E (APOE) genotypes typically increase risk of amyloid-β deposition and onset of clinical Alzheimer’s disease (AD). However, cognitive assessments in APOE transgenic AD mice have resulted in discord. Objective: Analysis of 31 peer-reviewed AD APOE mouse publications (n = 3,045 mice) uncovered aggregate trends between age, APOE genotype, gender, modulatory treatments, and cognition. Methods: T-tests with Bonferroni correction (significance = p < 0.002) compared age-normalized Morris water maze (MWM) escape latencies in wild type (WT), APOE2 knock-in (KI2), APOE3 kno

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6

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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7

Allphin, Alex J., Ali Mahzarnia, Darin P. Clark, et al. "Advanced photon counting CT imaging pipeline for cardiac phenotyping of apolipoprotein E mouse models." PLOS ONE 18, no. 10 (2023): e0291733. http://dx.doi.org/10.1371/journal.pone.0291733.

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Background Cardiovascular disease (CVD) is associated with the apolipoprotein E (APOE) gene and lipid metabolism. This study aimed to develop an imaging-based pipeline to comprehensively assess cardiac structure and function in mouse models expressing different APOE genotypes using photon-counting computed tomography (PCCT). Methods 123 mice grouped based on APOE genotype (APOE2, APOE3, APOE4, APOE knockout (KO)), gender, human NOS2 factor, and diet (control or high fat) were used in this study. The pipeline included PCCT imaging on a custom-built system with contrast-enhanced in vivo imaging

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8

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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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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Tang, Yanan. "APOE-ε4 genes may accelerate the activation of the latent form of HSV-1 which would lead to a faster progression of AD". BIO Web of Conferences 72 (2023): 01006. http://dx.doi.org/10.1051/bioconf/20237201006.

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This study investigates the impact of APOE alleles and latent Herpes Simplex Type 1 virus (HSV-1) activation on Alzheimer’s disease (AD) progression using the 5xFAD mouse model. APOE ε4 is recognized as a substantial genetic risk factor for sporadic AD, while HSV-1 has been linked to AD pathogenesis through inflammation and plaque formation. The experimental approach involves the introduction of human neurons carrying latent HSV-1 into 5xFAD mice harboring various APOE alleles (APOE2, APOE3, APOE4), along with stress induction and pharmacological interventions. The study aims to elucidate the

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11

Sung, Jin Hee, Yang Ou та Steven W. Barger. "Amyloid β-Peptide Effects on Glucose Regulation Are Dependent on Apolipoprotein E Genotype". eneuro 10, № 4 (2023): ENEURO.0376–22.2023. http://dx.doi.org/10.1523/eneuro.0376-22.2023.

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AbstractThe apolipoprotein E gene (APOE) confers the greatest genetic risk factor for Alzheimer’s disease (AD), wherein the ε4 allele confers an elevated risk compared with the ε3 allele. Biological mechanisms that differ across these alleles have been explored in mouse models wherein the murineApoegene has undergone targeted replacement with sequences encoding human ApoE3 or ApoE4 (ApoE-TR mice). Such models have indicated that the two variants of ApoE produce differential effects on energy metabolism, including metabolic syndrome. However, glucose regulation has not been compared in ApoE-TR

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Allphin, Alex J., Rohan Nadkarni, Zay Y. Han, et al. "Assessing the cardioprotective effects of exercise in APOE mouse models using deep learning and photon-counting micro-CT." PLOS ONE 20, no. 4 (2025): e0320892. https://doi.org/10.1371/journal.pone.0320892.

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Background The allelic variations of the apolipoprotein E (APOE) gene play a critical role in regulating lipid metabolism and significantly impact cardiovascular disease risk (CVD). This study aimed to evaluate the impact of exercise on cardiac structure and function in mouse models expressing different APOE genotypes using photon-counting computed tomography (PCCT) and deep learning-based segmentation. Methods A total of 140 mice were grouped based on APOE genotype (APOE2, APOE3, APOE4), sex, and exercise regimen. All mice were maintained on a controlled diet to isolate the effects of exercis

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13

Grenon, Martine B., Maria-Tzousi Papavergi, Praveen Bathini, Martin Sadowski, and Cynthia A. Lemere. "Temporal Characterization of the Amyloidogenic APPswe/PS1dE9;hAPOE4 Mouse Model of Alzheimer’s Disease." International Journal of Molecular Sciences 25, no. 11 (2024): 5754. http://dx.doi.org/10.3390/ijms25115754.

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Alzheimer’s disease (AD) is a devastating disorder with a global prevalence estimated at 55 million people. In clinical studies administering certain anti-beta-amyloid (Aβ) antibodies, amyloid-related imaging abnormalities (ARIAs) have emerged as major adverse events. The frequency of these events is higher among apolipoprotein ε4 allele carriers (APOE4) compared to non-carriers. To reflect patients most at risk for vascular complications of anti-Aβ immunotherapy, we selected an APPswe/PS1dE9 transgenic mouse model bearing the human APOE4 gene (APPPS1:E4) and compared it with the same APP/PS1

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Dafnis, Ioannis, Christina Raftopoulou, Christina Mountaki, Evgenia Megalou, Vassilis I. Zannis та Angeliki Chroni. "ApoE isoforms and carboxyl-terminal-truncated apoE4 forms affect neuronal BACE1 levels and Aβ production independently of their cholesterol efflux capacity". Biochemical Journal 475, № 10 (2018): 1839–59. http://dx.doi.org/10.1042/bcj20180068.

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The β-site amyloid precursor protein-cleaving enzyme 1 (BACE1) initiates the production of amyloid-β peptide (Aβ), which is central to the pathogenesis of Alzheimer's disease (AD). Changes in brain cholesterol homeostasis have been suggested to affect Aβ metabolism. Cholesterol homeostasis is maintained in the brain by apolipoprotein E (apoE). The apoE4 isoform constitutes the major risk factor for AD. Here, we investigated the effect of apoE forms on Aβ generation and on BACE1 levels. We also examined the potential involvement in these processes of cholesterol transporters ABCG1 and ABCG4 or

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15

Huang, Yadong. "Roles of apolipoprotein E4 (ApoE4) in the pathogenesis of Alzheimer's disease: lessons from ApoE mouse models." Biochemical Society Transactions 39, no. 4 (2011): 924–32. http://dx.doi.org/10.1042/bst0390924.

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ApoE4 (apolipoprotein E4) is the major known genetic risk factor for AD (Alzheimer's disease). In most clinical studies, apoE4 carriers account for 65–80% of all AD cases, highlighting the importance of apoE4 in AD pathogenesis. Emerging data suggest that apoE4, with its multiple cellular origins and multiple structural and biophysical properties, contributes to AD in multiple ways either independently or in combination with other factors, such as Aβ (amyloid β-peptide) and tau. Many apoE mouse models have been established to study the mechanisms underlying the pathogenic actions of apoE4. The

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Staurenghi, Erica, Valerio Leoni, Marco Lo Iacono, et al. "ApoE3 vs. ApoE4 Astrocytes: A Detailed Analysis Provides New Insights into Differences in Cholesterol Homeostasis." Antioxidants 11, no. 11 (2022): 2168. http://dx.doi.org/10.3390/antiox11112168.

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The strongest genetic risk factor for sporadic Alzheimer’s disease (AD) is the presence of the ε4 allele of the apolipoprotein E (ApoE) gene, the major apolipoprotein involved in brain cholesterol homeostasis. Being astrocytes the main producers of cholesterol and ApoE in the brain, we investigated the impact of the ApoE genotype on astrocyte cholesterol homeostasis. Two mouse astrocytic cell lines expressing the human ApoE3 or ApoE4 isoform were employed. Gas chromatography–mass spectrometry (GC-MS) analysis pointed out that the levels of total cholesterol, cholesterol precursors, and various

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Mhatre-Winters, Isha, Aseel Eid, Yoonhee Han, Kim Tieu, and Jason R. Richardson. "Sex and APOE Genotype Alter the Basal and Induced Inflammatory States of Primary Astrocytes from Humanized Targeted Replacement Mice." ASN Neuro 15 (January 2023): 175909142211445. http://dx.doi.org/10.1177/17590914221144549.

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Apolipoprotein E4 (APOE4) genotype and sex are significant risk factors for Alzheimer's disease (AD), with females demonstrating increased risk modulated by APOE genotype. APOE is predominantly expressed in astrocytes, however, there is a lack of comprehensive assessments of sex differences in astrocytes stratified by APOE genotype. Here, we examined the response of mixed-sex and sex-specific neonatal APOE3 and APOE4 primary mouse astrocytes (PMA) to a cytokine mix of IL1b, TNFa, and IFNg. Pro-inflammatory and anti-inflammatory cytokine profiles were assessed by qRT-PCR and Meso Scale Discover

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Demby, Tamar, G. William Rebeck, Christopher Albanese, Olga C. Rodriguez, Yichien Lee, and Jeanne Mandelblatt. "3367 A Mouse Model of APOE Genotype in Chemotherapy Related Cognitive Impairment." Journal of Clinical and Translational Science 3, s1 (2019): 1. http://dx.doi.org/10.1017/cts.2019.6.

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OBJECTIVES/SPECIFIC AIMS: Chemotherapy-related cognitive impairment (CRCI) affects 15-35% of breast cancer survivors and constitutes a significant challenge for survivor quality of life. Among older breast cancer survivors who received chemotherapy treatment, carriers of at least one ɛ4 allele of the APOE gene, which encodes apolipoprotein E, are at higher risk for developing CRCI than non-carriers. APOE4 is well characterized as the strongest genetic risk factor for Alzheimer’s disease, but how it contributes to CRCI is not yet understood, and no animal models of APOE genotype and CRCI have y

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Zhu, Li, Minghao Zhong, Gregory A. Elder, et al. "Phospholipid dysregulation contributes to ApoE4-associated cognitive deficits in Alzheimer’s disease pathogenesis." Proceedings of the National Academy of Sciences 112, no. 38 (2015): 11965–70. http://dx.doi.org/10.1073/pnas.1510011112.

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The apolipoprotein E4 (ApoE4) allele is the strongest genetic risk factor for developing sporadic Alzheimer’s disease (AD). However, the mechanisms underlying the pathogenic nature of ApoE4 are not well understood. In this study, we have found that ApoE proteins are critical determinants of brain phospholipid homeostasis and that the ApoE4 isoform is dysfunctional in this process. We have found that the levels of phosphoinositol biphosphate (PIP2) are reduced in postmortem human brain tissues of ApoE4 carriers, in the brains of ApoE4 knock-in (KI) mice, and in primary neurons expressing ApoE4

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Mori, Takashi, Terrence Town, Mariko Kobayashi, Jun Tan, Shinobu C. Fujita, and Takao Asano. "Augmented Delayed Infarct Expansion and Reactive Astrocytosis after Permanent Focal Ischemia in Apolipoprotein E4 Knock-In Mice." Journal of Cerebral Blood Flow & Metabolism 24, no. 6 (2004): 646–56. http://dx.doi.org/10.1097/01.wcb.0000120787.53851.a4.

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Using homozygous human apolipoprotein E2 (apoE2) (2/2)-, apoE3 (3/3)-, or apoE4 (4/4)-knock-in (KI) mice, we aimed to examine whether an apoE isoform-specific exacerbation of delayed infarct expansion occurs after permanent middle cerebral artery occlusion (pMCAO). Compared with 2/2- or 3/3-KI mice, 4/4-KI mice exhibited significantly larger infarct volumes and worse neurologic deficits after pMCAO, with no significant differences between the latter two groups. Infarct volume in 4/4-KI mice was significantly increased from 1 to 5 days after pMCAO, whereas that in 2/2- or 3/3-KI mice was not si

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McLean, John W., Avnish Bhattrai, Francesca Vitali, Adam C. Raikes, Jean-Paul L. Wiegand, and Roberta Diaz Brinton. "Contributions of sex and genotype to exploratory behavior differences in an aged humanized APOE mouse model of late-onset Alzheimer's disease." Learning & Memory 29, no. 9 (2022): 321–31. http://dx.doi.org/10.1101/lm.053588.122.

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Age, genetics, and chromosomal sex have been identified as critical risk factors for late-onset Alzheimer's disease (LOAD). The predominant genetic risk factor for LOAD is the apolipoprotein E ε4 allele (APOE4), and the prevalence of LOAD is higher in females. However, the translational validity of APOE4 mouse models for AD-related cognitive impairment remains to be fully determined. The present study investigated the role of both sex and genotype on learning and memory in aged, humanized APOE knock-in mice. Aged (23.27 mo ± 1.21 mo; 39 male/37 female) APOE3/3, APOE3/4, and APOE4/4 mice perfor

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Chang, Ya-Hsuan, Jared Hoffman, Lucille Yanckello, et al. "Apolipoprotein E Genotype-Dependent Nutrigenetic Effects to Prebiotic Inulin for Reducing Risk for Alzheimer's Disease in a Mouse Model." Current Developments in Nutrition 4, Supplement_2 (2020): 1197. http://dx.doi.org/10.1093/cdn/nzaa057_013.

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Abstract Objectives Apolipoprotein E ε4 (APOE4) allele is the strongest genetic risk factor for Alzheimer's disease (AD). Cognitively normal APOE4 carriers show an early decline in brain metabolic functions and gut microbiome dysbiosis before the onset of AD compared to APOE3 carriers. Our laboratory previously found that inulin, a prebiotic, is effective to restore metabolic functions and gut microbiome balance, and thus reduce risk for AD in an ApoE4 mouse model. However, whether the responses to the inulin are APOE allele-dependent remains unknown. Therefore, our objective was to identify w

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Yang, Hong, Ningya Zhang, Emmanuel Okoro, and Zhongmao Guo. "Transport of Apolipoprotein B-Containing Lipoproteins through Endothelial Cells Is Associated with Apolipoprotein E-Carrying HDL-Like Particle Formation." International Journal of Molecular Sciences 19, no. 11 (2018): 3593. http://dx.doi.org/10.3390/ijms19113593.

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Passage of apolipoprotein B-containing lipoproteins (apoB-LPs), i.e., triglyceride-rich lipoproteins (TRLs), intermediate-density lipoproteins (IDLs), and low-density lipoproteins (LDLs), through the endothelial monolayer occurs in normal and atherosclerotic arteries. Among these lipoproteins, TRLs and IDLs are apoE-rich apoB-LPs (E/B-LPs). Recycling of TRL-associated apoE has been shown to form apoE-carrying high-density lipoprotein (HDL)-like (HDLE) particles in many types of cells. The current report studied the formation of HDLE particles by transcytosis of apoB-LPs through mouse aortic en

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Braunersreuther, Vincent, Fabienne Burger, Sébastien Lenglet, et al. "Anti-apoA-1 auto-antibodies increase mouse atherosclerotic plaque vulnerability, myocardial necrosis and mortality triggering TLR2 and TLR4." Thrombosis and Haemostasis 114, no. 08 (2015): 410–22. http://dx.doi.org/10.1160/th14-12-1039.

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SummaryAuto-antibodies to apolipoprotein A-1 (anti-apoA-1 IgG) were shown to promote inflammation and atherogenesis, possibly through innate immune receptors signalling. Here, we aimed at investigating the role of Toll-like receptors (TLR) 2 and 4 on anti-apoA-1 IgG-induced athero-sclerotic plaque vulnerability, myocardial necrosis and mortality in mice. Adult male apolipoprotein E knockout (ApoE)-/- (n=72), TLR2-/-ApoE-/- (n=36) and TLR4-/-Apo-/- (n=28) mice were intravenously injected with 50 µg/mouse of endotoxin-free polyclonal anti-apoA-1 IgG or control isotype IgG (CTL IgG) every two wee

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Rijpma, A., D. Jansen, I. A. C. Arnoldussen, et al. "Sex Differences in Presynaptic Density and Neurogenesis in Middle-Aged ApoE4 and ApoE Knockout Mice." Journal of Neurodegenerative Diseases 2013 (January 27, 2013): 1–9. http://dx.doi.org/10.1155/2013/531326.

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Atherosclerosis and apolipoprotein E ε4 (APOE4) genotype are risk factors for Alzheimer’s disease (AD) and cardiovascular disease (CVD). Sex differences exist in prevalence and manifestation of both diseases. We investigated sex differences respective to aging, focusing on cognitive parameters in apoE4 and apoE knockout (ko) mouse models of AD and CVD. Presynaptic density and neurogenesis were investigated immunohistochemically in male and female apoE4, apoE ko, and wild-type mice. Middle-aged female apoE4 mice showed decreased presynaptic density in the inner molecular layer of the dentate gy

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Guardia-Escote, Laia, Jordi Blanco, Pia Basaure, et al. "Sex and Exposure to Postnatal Chlorpyrifos Influence the Epigenetics of Feeding-Related Genes in a Transgenic APOE Mouse Model: Long-Term Implications on Body Weight after a High-Fat Diet." International Journal of Environmental Research and Public Health 18, no. 1 (2020): 184. http://dx.doi.org/10.3390/ijerph18010184.

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Developmental exposure to toxicants and diet can interact with an individual’s genetics and produce long-lasting metabolic adaptations. The different isoforms of the apolipoprotein E (APOE) are an important source of variability in metabolic disorders and influence the response to the pesticide chlorpyrifos (CPF). We aimed to study the epigenetic regulation on feeding control genes and the influence of postnatal CPF exposure, APOE genotype, and sex, and how these modifications impact on the metabolic response to a high-fat diet (HFD). Both male and female apoE3- and apoE4-TR mice were exposed

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Hewes, Amanda, Kate Foley, Jennifer Thompson, et al. "6 Exercise Induced Growth Factor Increases Directly and Indirectly Reduce Systemic Vascular Risk Parameters: Translational Project Amongst Midlife Human and Animal Models of Preclinical Alzheimer’s disease and Vascular Dementia." Journal of the International Neuropsychological Society 29, s1 (2023): 218–19. http://dx.doi.org/10.1017/s1355617723003259.

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Objective:Using a humanized APOE3/4 (Alzheimer’s disease genetic risk allele) mouse model we investigated the potential modulating effects of exercise on systemic risk factors and the ability of this mouse model to translate to active or sedentary, midlife, human participants. We present preliminary results of an ongoing, translational pilot study.Participants and Methods:26 Midlife individuals, ages 40-65, were recruited from the community and dichotomized into active or sedentary groups following health screening and cognitive assessment. Blood samples were drawn from human participants for

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wang, chao, Aimin Li, Rebecca Spellman, et al. "Effects of human LDLR overexpression on apoE-related tau pathology and brain dysfunction." Journal of Immunology 204, no. 1_Supplement (2020): 64.6. http://dx.doi.org/10.4049/jimmunol.204.supp.64.6.

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Abstract ApoE4 is the strongest genetic risk factor for late-onset Alzheimer Disease. It has been reported that apoE isoforms directly affect tauopathy and tau-mediated neurodegeneration in P301S tau transgenic mice expressing different human apoE isoforms, with apoE4 resulting in markedly increased tau-mediated neurodegeneration and the absence of apoE being marked protective against neurodegeneration. In the brain, low-density lipoprotein receptor (LDLR) is one of the main apoE receptors that regulates apoE levels, but LDLR has very few identified ligands compared to other apoE receptors. LD

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Liu, Min, David G. Kuhel, Ling Shen, David Y. Hui, and Stephen C. Woods. "Apolipoprotein E does not cross the blood-cerebrospinal fluid barrier, as revealed by an improved technique for sampling CSF from mice." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 303, no. 9 (2012): R903—R908. http://dx.doi.org/10.1152/ajpregu.00219.2012.

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Apolipoprotein E (apoE) is a 34-kDa glycoprotein that is important in lipoprotein metabolism both peripherally and centrally. Because it is primarily produced in the liver, apoE observed in the brain or cerebrospinal fluid (CSF) could have originated in the periphery; i.e., circulating apoE may cross the blood-brain barrier (BBB) and/or enter CSF and be taken up by brain cells. To determine whether this occurs, a second-generation adenovirus encoding human apoE3 was administered intravenously (iv) to C57BL/6J mice, and the detection of human apoE3 in the CSF was used as a surrogate measure of

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Provost, Pierre R., Eric Boucher, and Yves Tremblay. "Apolipoprotein A-I, A-II, C-II, and H expression in the developing lung and sex difference in surfactant lipids." Journal of Endocrinology 200, no. 3 (2008): 321–30. http://dx.doi.org/10.1677/joe-08-0238.

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A sex difference in surfactant lipids is associated with a higher incidence of respiratory distress syndrome for males in cases of preterm birth. In animal models, the sex difference in surfactant lipids was shown to be androgen receptor-dependent. This report examines expression of apolipoprotein (apo)A-I, apoA-II, apoC-II, apoE, apoH, and lipoprotein lipase (LPL) by quantitative real-time PCR in pools of male and female fetal lung tissues from various mouse litters from gestation day (GD) 15.5 to 18.5, and in various adult tissues. Although the expression profiles of ApoA-I, ApoA-II, ApoC-II

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Liu, Ke, Bangzhu Chen, Fanwen Zeng, et al. "ApoE/NOS3 Knockout Mice as a Novel Cardiovascular Disease Model of Hypertension and Atherosclerosis." Genes 13, no. 11 (2022): 1998. http://dx.doi.org/10.3390/genes13111998.

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Hypertension is an independent risk factor for atherosclerosis. However, few models of hypertensive atherosclerosis have been established in medical research. In this study, we crossed the ApoE knockout (ApoE-KO; ApoE−/−) atherosclerotic mouse model with the NOS3 knockout (NOS3-KO; NOS3−/−) hypertensive mouse model to establish an ApoE/NOS3 double knockout (ApoE/NOS3-KO; ApoE/NOS3−/−) hypertensive atherosclerosis mouse model. We found that ApoE/NOS3−/− mice reproduced normally, had a blood pressure of 133.00 ± 3.85 mmHg, and developed hypertensive fundus retinopathy and hypertensive nephropath

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Marottoli, Felecia M., Yuriko Katsumata, Kevin P. Koster, Riya Thomas, David W. Fardo та Leon M. Tai. "Peripheral Inflammation, Apolipoprotein E4, and Amyloid-β Interact to Induce Cognitive and Cerebrovascular Dysfunction". ASN Neuro 9, № 4 (2017): 175909141771920. http://dx.doi.org/10.1177/1759091417719201.

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Cerebrovascular dysfunction is rapidly reemerging as a major process of Alzheimer’s disease (AD). It is, therefore, crucial to delineate the roles of AD risk factors in cerebrovascular dysfunction. While apolipoprotein E4 ( APOE4), Amyloid-β (Aβ), and peripheral inflammation independently induce cerebrovascular damage, their collective effects remain to be elucidated. The goal of this study was to determine the interactive effect of APOE4, Aβ, and chronic repeated peripheral inflammation on cerebrovascular and cognitive dysfunction in vivo. EFAD mice are a well-characterized mouse model that e

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Martinsen, Anneloes, Rasha N. M. Saleh, Raphael Chouinard-Watkins, et al. "The Influence of APOE Genotype, DHA, and Flavanol Intervention on Brain DHA and Lipidomics Profile in Aged Transgenic Mice." Nutrients 15, no. 9 (2023): 2032. http://dx.doi.org/10.3390/nu15092032.

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The apolipoprotein E4 (APOE4) genotype is predictive of Alzheimer’s disease (AD). The brain is highly enriched with the omega-3 polyunsaturated fatty acid (n3-PUFA), docosahexaenoic acid (DHA). DHA’s metabolism is defective in APOE4 carriers. Flavanol intake can play a role in modulating DHA levels. However, the impact of flavanol co-supplementation with fish oil on brain DHA uptake, status and partitioning, and according to APOE genotype is currently unknown. Here, using a humanised APOE3 and APOE4 targeted replacement transgenic mouse model, the interactive influence of cocoa flavanols (FLAV

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Williams, Tristan, Tim Bathe, Quan Vo, et al. "Humanized APOE genotypes influence lifespan independently of tau aggregation in the P301S mouse model of tauopathy." Acta Neuropathologica Communications 11, no. 1 (2023). http://dx.doi.org/10.1186/s40478-023-01581-2.

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AbstractApolipoprotein (APOE) E4 isoform is a major risk factor of Alzheimer’s disease and contributes to metabolic and neuropathological abnormalities during brain aging. To provide insights into whether APOE4 genotype is related to tau-associated neurodegeneration, we have generated human P301S mutant tau transgenic mice (PS19) that carry humanized APOE alleles (APOE2, APOE3 or APOE4). In aging mice that succumbed to paralysis, PS19 mice homozygous for APOE3 had the longest lifespan when compared to APOE4 and APOE2 homozygous mice (APOE3 > APOE4 ~ APOE2). Heterozygous mice with one human

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Medegan Fagla, Bani, Jason York, Amy Christensen, et al. "Apolipoprotein E polymorphisms and female fertility in a transgenic mouse model of Alzheimer’s disease." Scientific Reports 14, no. 1 (2024). http://dx.doi.org/10.1038/s41598-024-66489-w.

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AbstractApolipoprotein E (APOE) is a major cholesterol carrier responsible for lipid transport and injury repair in the brain. The human APOE gene (h-APOE) has 3 naturally occurring alleles: ε3, the common allele; ε4, which increases Alzheimer’s disease (AD) risk up to 15-fold; and ε2, the rare allele which protects against AD. Although APOE4 has negative effects on neurocognition in old age, its persistence in the population suggests a survival advantage. We investigated the relationship between APOE genotypes and fertility in EFAD mice, a transgenic mouse model expressing h-APOE. We show tha

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Adaku, Nneoma, Benjamin N. Ostendorf, Wenbin Mei, and Sohail F. Tavazoie. "Apolipoprotein E2 Stimulates Protein Synthesis and Promotes Melanoma Progression." Cancer Research, June 19, 2023. http://dx.doi.org/10.1158/0008-5472.can-23-1252.

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Abstract The secreted lipid transporter apolipoprotein E (APOE) plays important roles in atherosclerosis and Alzheimer’s disease and has been implicated as a suppressor of melanoma progression. The APOE germline genotype predicts human melanoma outcomes, with APOE4 and APOE2 allele carriers exhibiting prolonged and reduced survival, respectively, relative to APOE3 homozygotes. While the APOE4 variant was recently shown to suppress melanoma progression by enhancing anti-tumor immunity, further work is needed to fully characterize the melanoma cell-intrinsic effects of APOE variants on cancer pr

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Williams, Tristan, Alejandra Jolie Ruiz, Angelica Maria Ruiz, et al. "Impact of APOE genotype on prion-type propagation of tauopathy." Acta Neuropathologica Communications 10, no. 1 (2022). http://dx.doi.org/10.1186/s40478-022-01359-y.

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AbstractApolipoprotein (APOE) is a major risk factor of Alzheimer’s disease (AD), with the E2, E3 and E4 isoforms differentially regulating the burden of AD-associated neuropathologies, such as amyloid β and tau. In AD, pathological tau is thought to spread along neuroanatomic connections following a prion-like mechanism. To provide insights into whether APOE isoforms differentially regulate the prion properties of tau and determine trans-synaptic transmission of tauopathy, we have generated human P301S mutant tau transgenic mice (PS19) that carry human APOE (APOE2, APOE3 or APOE4) or mouse Ap

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Litvinchuk, Alexandra. "The relationship between ApoE4 and lipid dysregulation in glia of the PS19 mouse model of tauopathy." Alzheimer's & Dementia 19, S13 (2023). http://dx.doi.org/10.1002/alz.071023.

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AbstractBackgroundApolipoprotein E4 (apoE), the major lipoprotein in the brain, plays an essential role in brain`s lipid homeostasis; furthermore, the presence of the apoE4 allele is the strongest genetic risk factor for developing late‐onset AD compared to most common apoE3 and protective apoE2 alleles. Recent studies in iPSC microglia and astrocytes demonstrate that apoE modulates cholesterol dysfunction and inflammatory responses in an isoform‐specific fashion. However, it is not known if lipid accumulation in glia mediates toxic effects in vivo in the context of tauopathy and neurodegenera

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Siano, Dahlia, Lesley R. Golden, Steven M. MacLean, Gabriela Hernandez, and Lance A. Johnson. "Validation of Various Pan‐ApoE and Isoform‐Specific ApoE Antibodies." Alzheimer's & Dementia 20, S1 (2024). https://doi.org/10.1002/alz.091634.

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AbstractBackgroundApolipoprotein E (ApoE) exists in three protein isoforms: E2, E3, and E4, which differ by only one or two amino acids. These slight differences profoundly effect protein structure and function, allowing each isoform to differentially impact Alzheimer’s Disease (AD) risk. Relative to the most common E3 isoform, E4 dramatically increases risk, while E2 confers a substantial decrease in risk. The close similarity between protein isoforms makes it difficult to develop isoform‐specific antibodies that are reliable and selective. Here, we aim to validate and optimize a number of co

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Rueter, Johanna, Gerald Rimbach, Christian Treitz, et al. "The mitochondrial BCKD complex interacts with hepatic apolipoprotein E in cultured cells in vitro and mouse livers in vivo." Cellular and Molecular Life Sciences 80, no. 3 (2023). http://dx.doi.org/10.1007/s00018-023-04706-x.

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Abstract Background and aims Apolipoprotein E (APOE) is known for its role in lipid metabolism and its association with age-related disease pathology. The aim of the present work was to identify previously unknown functions of APOE based on the detection of novel APOE protein–protein interaction candidates. Approach and results APOE targeted replacement mice and transfected cultured hepatocytes expressing the human isoforms APOE3 and APOE4 were used. For 7 months, APOE3 and APOE4 mice were fed a high-fat and high-sugar diet to induce obesity, while a subgroup was subjected to 30% dietary restr

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WANG, NA, Sydney V. Doss, Yuzhou Chang та ін. "Specific expression of APOE in astrocytes reduces Aβ accumulation and plaque‐related pathology in a mouse model of amyloidosis". Alzheimer's & Dementia 20, S1 (2024). https://doi.org/10.1002/alz.090129.

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AbstractBackgroundAccumulation of the amyloid‐β (Aβ) peptide into amyloid plaque is one of the key pathological markers of Alzheimer’s disease (AD). Apolipoprotein E (APOE) is known to modify AD risk and has been reported to influence Aβ accumulation in the brain in an isoform‐dependent manner. ApoE can be produced by various cell types in the brain, with astrocytes being the main producer. Increasing studies show that altering apoE levels can influence Aβ plaque pathology. However, it is not fully understood how apoE produced by specific cell types, such as astrocytes, contributes to amyloid

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Wang, Shaowei, Boyang Li, Victoria Solomon, et al. "Calcium-dependent cytosolic phospholipase A2 activation is implicated in neuroinflammation and oxidative stress associated with ApoE4." Molecular Neurodegeneration 17, no. 1 (2022). http://dx.doi.org/10.1186/s13024-022-00549-5.

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Abstract Background Apolipoprotein E4 (APOE4) is associated with a greater response to neuroinflammation and the risk of developing late-onset Alzheimer’s disease (AD), but the mechanisms for this association are not clear. The activation of calcium-dependent cytosolic phospholipase A2 (cPLA2) is involved in inflammatory signaling and is elevated within the plaques of AD brains. The relation between APOE4 genotype and cPLA2 activity is not known. Methods Mouse primary astrocytes, mouse and human brain samples differing by APOE genotypes were collected for measuring cPLA2 expression, phosphoryl

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Avila‐Munoz, Maria Evangelina, Deebika Balu, Jason York, Shivesh Ghura, Nicole Collins, and Mary Jo Ladu. "The effect of sex on APOE‐modulated AD pathology in EFAD mice." FASEB Journal 31, S1 (2017). http://dx.doi.org/10.1096/fasebj.31.1_supplement.814.3.

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APOE4 allele of apolipoprotein E (apoE) is the greatest genetic risk factor for Alzheimer's disease (AD) and is associated with accelerated accumulation of both amyloid plaques and and soluble oligomeric forms of the amyloid‐β peptide (oAβ), likely a proximal neurotoxin. Importantly, female APOE4 carriers have a greater lifetime risk for developing AD, an increased rate of cognitive decline and accelerated accumulation of Aβ compared to male APOE4 carriers. In vivo progress has been limited by the lack of a tractable familial AD‐transgenic (FAD‐Tg) mouse model expressing human (h)‐ rather than

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Peng, Katherine Y., Braison Liemisa, Jonathan Pasato, et al. "Apolipoprotein E2 Expression Alters Endosomal Pathways in a Mouse Model With Increased Brain Exosome Levels During Aging." Traffic 25, no. 5 (2024). http://dx.doi.org/10.1111/tra.12937.

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ABSTRACTThe polymorphic APOE gene is the greatest genetic determinant of sporadic Alzheimer's disease risk: the APOE4 allele increases risk, while the APOE2 allele is neuroprotective compared with the risk‐neutral APOE3 allele. The neuronal endosomal system is inherently vulnerable during aging, and APOE4 exacerbates this vulnerability by driving an enlargement of early endosomes and reducing exosome release in the brain of humans and mice. We hypothesized that the protective effects of APOE2 are, in part, mediated through the endosomal pathway. Messenger RNA analyses showed that APOE2 leads t

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Davies, Caitlin, Jane Tulloch, Ellie Yip, et al. "Apolipoprotein E isoform does not influence trans-synaptic spread of tau pathology in a mouse model." Brain and Neuroscience Advances 7 (January 2023). http://dx.doi.org/10.1177/23982128231191046.

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A key hallmark of Alzheimer’s disease (AD) is the accumulation of hyperphosphorylated tau in neurofibrillary tangles. This occurs alongside neuroinflammation and neurodegeneration. Pathological tau propagates through the AD brain in a defined manner, which correlates with neuron and synapse loss and cognitive decline. One proposed mechanism of tau spread is through synaptically connected brain structures. Apolipoprotein E4 ( APOE4) genotype is the strongest genetic risk factor for late-onset AD and is associated with increased tau burden. Whether the apolipoprotein E ( APOE) genotype influence

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Fotakis, Panagiotis, Dimitris Kardassis, and Vassilis Zannis. "Abstract 584: ApoE3[K146N/R147W] Acts as a Dominant Negative ApoE Form that Prevents Remnant Clearance and Inhibits the Biogenesis of HDL." Arteriosclerosis, Thrombosis, and Vascular Biology 34, suppl_1 (2014). http://dx.doi.org/10.1161/atvb.34.suppl_1.584.

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Introduction: The K146N/R147W substitutions in human apolipoproteinE3 (apoE3) have been associated with a dominant form of type III hyperlipoproteinemia which is expressed at an early age. Methods: The effects of the K146N,R147W substitutions on the lipid and lipoprotein profiles and the HDL phenotypes were studied by adenovirus mediated gene transfer of the full length and a truncated apoE3[K146N/R147W]-202 mutant using different mouse models. Results: A low dose of adenovirus expressing the apoE3[K146N/R147W] mutant in apoE deficient or in apoA-I x apoE double deficient mice exacerbated the

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Golden, Lesley R., Steven M. MacLean, Cathryn T. Smith, et al. "Mid‐life APOE4 to APOE2 ‘Switching’ Alters the Cerebral Transcriptome and Lipidome in a Transgenic Mouse Model." Alzheimer's & Dementia 19, S12 (2023). http://dx.doi.org/10.1002/alz.074217.

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AbstractBackgroundCompared to the ‘neutral’ E3, the E4 allele of Apolipoprotein E (APOE) confers up to a 15‐fold increase in Alzheimer’s Disease (AD) risk. Conversely, the neuroprotective E2 allele decreases AD risk by a similar degree. APOE’s strong risk profile and multitude of effects make it a promising therapeutic target. Here, we aimed to assess the therapeutic potential of allelic ‘switching’ by investigating the physiological changes associated with an inducible, in vivo APOE4 to APOE2 transition in a novel transgenic mouse model.MethodThe APOE “switch mouse” (APOE4s2) uses the Cre‐lox

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Balu, Deebika, Ana Valencia‐Olvera, Nicole Collins, Ryan Salzman, Jason York, and Mary Jo Ladu. "The effect of aging on APOE‐modulated AD pathology in EFAD mice." FASEB Journal 31, S1 (2017). http://dx.doi.org/10.1096/fasebj.31.1_supplement.814.5.

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The APOE ɛ4 allele of apolipoprotein E (apoE) is the greatest genetic risk factor for Alzheimer's disease (AD) compared to APOE3, with APOE2 providing a protective effect. APOE4 is associated with accelerated amyloid‐β (Aβ) accumulation, both as amyloid plaque and soluble oligomeric forms of Aβ (oAβ), the latter considered a proximal neurotoxin. Using EFAD mice, a novel, tractable human‐APOE/familial AD‐transgenic (FAD‐Tg) preclinical mouse model, we have developed the mechanistic hypothesis that APOE4 causes a reduction in apoE lipidation, resulting in inefficient clearance of soluble Aβ, syn

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Konings, Sabine C., Laura Torres-Garcia, Isak Martinsson, and Gunnar K. Gouras. "Astrocytic and Neuronal Apolipoprotein E Isoforms Differentially Affect Neuronal Excitability." Frontiers in Neuroscience 15 (September 21, 2021). http://dx.doi.org/10.3389/fnins.2021.734001.

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Synaptic changes and neuronal network dysfunction are among the earliest changes in Alzheimer’s disease (AD). Apolipoprotein E4 (ApoE4), the major genetic risk factor in AD, has been shown to be present at synapses and to induce hyperexcitability in mouse knock-in brain regions vulnerable to AD. ApoE in the brain is mainly generated by astrocytes, however, neurons can also produce ApoE under stress conditions such as aging. The potential synaptic function(s) of ApoE and whether the cellular source of ApoE might affect neuronal excitability remain poorly understood. Therefore, the aim of this s

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Chen, Junru, Haibing Chen, Qinjun Wei, et al. "APOE4 impairs macrophage lipophagy and promotes demyelination of spiral ganglion neurons in mouse cochleae." Cell Death Discovery 11, no. 1 (2025). https://doi.org/10.1038/s41420-025-02454-4.

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Abstract The ApoE-ε4 gene is a well-established genetic risk factor for neurodegenerative diseases, such as Alzheimer’s disease and multiple sclerosis, which are characterized by axonal demyelination in the central nervous system. Recent studies have implicated ApoE-ε4 in age-related hearing loss (ARHL), suggesting a potential role of APOE4 isoform in peripheral nervous system degeneration. However, the role of APOE4 in ARHL are still unclear. In this study, we explored the potential role of APOE4 in axonal demyelination of spiral ganglion neurons (SGNs). ApoE-ε4/ε4 (APOE4) and ApoE-ε3/ε3 (APO

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