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Journal articles on the topic 'Apolipoprotein F'

Author: Grafiati

Published: 7 September 2022

Last updated: 18 September 2022

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1

Puchois, P., C. Luley, and P. Alaupovic. "Comparison of four procedures for separating apolipoprotein A- and apolipoprotein B-containing lipoproteins in plasma." Clinical Chemistry 33, no. 9 (September 1, 1987): 1597–602. http://dx.doi.org/10.1093/clinchem/33.9.1597.

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Abstract Because lipoproteins containing apolipoprotein A (ApoA-I + ApoA-II) or apolipoprotein B (ApoB) seem to exert opposite effects as risk factors for coronary heart disease, we decided to determine the separability of these two major plasma lipoproteins by procedures originally designed to separate high-density from low- and very-low-density lipoproteins. The presumably ApoB-free lipoproteins isolated from normal plasma by (a) ultracentrifugation at d = 1.063; precipitation with (b) heparin-Mn2+ or (c) phosphotungstate-Mg2+; or (d) immunoprecipitation with antibodies to ApoB were characterized by quantifying cholesterol and apolipoproteins A-I, A-II, B, C-II, C-III, D, E, F, and Lp(a). ApoA- and ApoB-containing lipoproteins were completely separated only by immunoprecipitation with antibodies to ApoB. The ApoB-containing lipoproteins isolated by other procedures always contained 4% to 20% of total plasma ApoA-I and differed substantially from one another with respect to the content of some of the minor apolipoproteins. Measuring apolipoproteins was more reliable than measuring cholesterol for monitoring this separation and for expressing the concentrations of ApoA- and ApoB-containing lipoproteins.

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2

Barbaras, R., P. Puchois, J. C. Fruchart, A. Pradines-Figueres, and G. Ailhaud. "Purification of an apolipoprotein A binding protein from mouse adipose cells." Biochemical Journal 269, no. 3 (August 1, 1990): 767–73. http://dx.doi.org/10.1042/bj2690767.

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A protein recognizing apolipoproteins AI, AII and AIV was purified from cultured mouse adipose cells of the Ob17MT18 clonal line. Apolipoprotein A binding sites were solubilized in the presence of proteinase inhibitors using the non-denaturating detergent CHAPS. Chromatography of the soluble extract on DEAE-Trisacryl was followed by immunoaffinity chromatography of the complex apolipoprotein AI-binding proteins on anti-(apolipoprotein AI) coupled to Sepharose 4B and then by h.p.l.c. on an RP-Select B column. A 1400-fold purification over the starting crude homogenate was achieved. The purified material contained two proteins that were both able to bind apolipoproteins AI, AII and AIV, but not low-density lipoprotein. Glycopeptidase F treatment showed the existence of a single protein bearing either N-linked high-mannose or complex oligosaccharide chains. The purified material showed an apparent molecular mass of 80 +/- 9 kDa by h.p.l.c. on a TSKG 3000 SW column. Rabbit polyclonal antibodies directed against the purified material revealed two protein bands of 80 and 92 kDa after SDS/PAGE under reducing conditions and immunoblotting. These bands were undetectable in growing Ob17PY cells previously shown not to bind the various apolipoproteins A and not to undergo cholesterol efflux, whereas they were conspicuous in growth-arrested Ob17PY cells which have recovered these properties.

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3

Day, J. R., J. J. Albers, T. L. Gilbert, T. E. Whitmore, W. J. Mcconathy, and G. Wolfbauer. "Purification and Molecular-Cloning of Human Apolipoprotein F." Biochemical and Biophysical Research Communications 203, no. 2 (September 1994): 1146–51. http://dx.doi.org/10.1006/bbrc.1994.2302.

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4

Blanchard, Valentin, Damien Garçon, Catherine Jaunet, Kevin Chemello, Stéphanie Billon-Crossouard, Audrey Aguesse, Aya Garfa, et al. "A high-throughput mass spectrometry-based assay for large-scale profiling of circulating human apolipoproteins." Journal of Lipid Research 61, no. 7 (May 13, 2020): 1128–39. http://dx.doi.org/10.1194/jlr.d120000835.

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Apolipoproteins govern lipoprotein metabolism and are promising biomarkers of metabolic and cardiovascular diseases. Unlike immunoassays, MS enables the quantification and phenotyping of multiple apolipoproteins. Hence, here, we aimed to develop a LC-MS/MS assay that can simultaneously quantitate 18 human apolipoproteins [A-I, A-II, A-IV, A-V, B48, B100, C-I, C-II, C-III, C-IV, D, E, F, H, J, L1, M, and (a)] and determined apoE, apoL1, and apo(a) phenotypes in human plasma and serum samples. The plasma and serum apolipoproteins were trypsin digested through an optimized procedure and peptides were extracted and analyzed by LC-MS/MS. The method was validated according to standard guidelines in samples spiked with known peptide amounts. The LC-MS/MS results were compared with those obtained with other techniques, and reproducibility, dilution effects, and stabilities were also assessed. Peptide markers were successfully selected for targeted apolipoprotein quantification and phenotyping. After optimization, the assay was validated for linearity, lower limits of quantification, accuracy (biases: –14.8% to 12.1%), intra-assay variability [coefficients of variation (CVs): 1.5–14.2%], and inter-assay repeatability (CVs: 4.1–14.3%). Bland-Altman plots indicated no major statistically significant differences between LC-MS/MS and other techniques. The LC-MS/MS results were reproducible over five repeated experiments (CVs: 1.8–13.7%), and we identified marked differences among the plasma and serum samples. The LC-MS/MS assay developed here is rapid, requires only small sampling volumes, and incurs reasonable costs, thus making it amenable for a wide range of studies of apolipoprotein metabolism. We also highlight how this assay can be implemented in laboratories.

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5

Lagor, William R., Robert J. Brown, Sue-Anne Toh, John S. Millar, Ilia V. Fuki, Margarita de la Llera-Moya, Tiffany Yuen, George Rothblat, Jeffrey T. Billheimer, and Daniel J. Rader. "Overexpression of Apolipoprotein F Reduces HDL Cholesterol Levels In Vivo." Arteriosclerosis, Thrombosis, and Vascular Biology 29, no. 1 (January 2009): 40–46. http://dx.doi.org/10.1161/atvbaha.108.177105.

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6

Wu, Tiyun, Chun G. Lee, Alicia Buckler-White, and Christine A. Kozak. "Genetic Control of a Mouse Serum Lipoprotein Factor That Inactivates Murine Leukemia Viruses: Evaluation of Apolipoprotein F as a Candidate." Journal of Virology 76, no. 5 (March 1, 2002): 2279–86. http://dx.doi.org/10.1128/jvi.76.5.2279-2286.2002.

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ABSTRACT Mice contain a serum factor capable of inactivating some subgroups of murine leukemia viruses. This leukemia virus-inactivating factor (LVIF) is distinct from immunoglobulin and complement; it has been associated with lipoprotein serum fractions and may be an apolipoprotein. The present study demonstrates that some Swiss-derived inbred strains are LVIF negative. Genetic crosses show this factor to be under control of a single gene that maps to distal chromosome 10 at or near the gene encoding a minor serum apolipoprotein, apolipoprotein F (ApoF). To evaluate this gene as a potential candidate for LVIF, the mouse ApoF gene was cloned and sequenced and its expression was assessed in LVIF-positive and -negative mice; no obvious differences were detected, suggesting that LVIF is under the control of a distinct linked gene.

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7

Backus, J. W., M. J. Eagleton, S. G. Harris, C. E. Sparks, J. D. Sparks, and H. C. Smith. "Quantitation of endogenous liver apolipoprotein B mRNA editing." Biochemical and Biophysical Research Communications 170, no. 2 (July 1990): 513–18. http://dx.doi.org/10.1016/0006-291x(90)92121-f.

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8

Hoe, Hyang-Sook, David Wessner, Uwe Beffert, Amanda G. Becker, Yasuji Matsuoka, and G. William Rebeck. "F-Spondin Interaction with the Apolipoprotein E Receptor ApoEr2 Affects Processing of Amyloid Precursor Protein." Molecular and Cellular Biology 25, no. 21 (November 1, 2005): 9259–68. http://dx.doi.org/10.1128/mcb.25.21.9259-9268.2005.

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ABSTRACT A recent study showed that F-spondin, a protein associated with the extracellular matrix, interacted with amyloid precursor protein (APP) and inhibited β-secretase cleavage. F-spondin contains a thrombospondin domain that we hypothesized could interact with the family of receptors for apolipoprotein E (apoE). Through coimmunoprecipitation experiments, we demonstrated that F-spondin interacts with an apoE receptor (apoE receptor 2 [ApoEr2]) through the thrombospondin domain of F-spondin and the ligand binding domain of ApoEr2. Full-length F-spondin increased coimmunoprecipitation of ApoEr2 and APP in transfected cells and primary neurons and increased surface expression of APP and ApoEr2. Full-length F-spondin, but none of the individual F-spondin domains, increased cleavage of APP and ApoEr2, resulting in more secreted forms of APP and ApoEr2 and more C-terminal fragments (CTF) of these proteins. In addition, full-length F-spondin, but not the individual domains, decreased production of the β-CTF of APP and Aβ in transfected cells and primary neurons. The reduction in APP β-CTF was blocked by receptor-associated protein (RAP), an inhibitor of lipoprotein receptors, implicating ApoEr2 in the altered proteolysis of APP. ApoEr2 coprecipitated with APP α- and β-CTF, and F-spondin reduced the levels of APP intracellular domain signaling, suggesting that there are also intracellular interactions between APP and ApoEr2, perhaps involving adaptor proteins. These studies suggest that the extracellular matrix molecule F-spondin can cluster APP and ApoEr2 together on the cell surface and affect the processing of each, resulting in decreased production of Aβ.

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9

DEKNIJFF, P., A. KAPTEIN, D. BOOMSMA, H. PRINCEN, R. FRANTS, and L. HAVEKES. "Apolipoprotein E polymorphism affects plasma levels of lipoprotein(a)." Atherosclerosis 90, no. 2-3 (October 1991): 169–74. http://dx.doi.org/10.1016/0021-9150(91)90111-f.

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10

Kamboh, M. Ilyas, Rhobert W. Evans, and Christopher E. Aston. "Genetic effect of apolipoprotein(a) and apolipoprotein E polymorphisms on plasma quantitative risk factors for coronary heart disease in American Black women." Atherosclerosis 117, no. 1 (September 1995): 73–81. http://dx.doi.org/10.1016/0021-9150(95)05559-f.

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11

Apfelbaum, Terri F., Nicholas O. Davidson, and Robert M. Glickman. "Apolipoprotein A-IV synthesis in rat intestine: regulation by dietary triglyceride." American Journal of Physiology-Gastrointestinal and Liver Physiology 253, no. 1 (December 1, 1987): 1. http://dx.doi.org/10.1152/ajpgi.1987.253.1.1-a.

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Page G662: Terri F. Apfelbaum, Nicholas O. Davidson, and Robert M. Glickman. “Apolipoprotein A-IV synthesis in rat intestine: regulation by dietary triglyceride.” Page G663: sentence beginning on line 10, second column, should read “Data are expressed as mean ± 1 SD, and comparisons for both paired and unpaired means were made by Students t test.”

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12

Kujiraoka, Takeshi, Takaaki Nakamoto, Hiroyuki Sugimura, Tadao Iwasaki, Mitsuaki Ishihara, Toshiyasu Hoshi, Yasuto Horie, et al. "Clinical Significance of Plasma Apolipoprotein F in Japanese Healthy and Hypertriglyceridemic Subjects." Journal of Atherosclerosis and Thrombosis 20, no. 4 (2013): 380–90. http://dx.doi.org/10.5551/jat.13706.

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13

Morton, Richard E., Hannah M. Gnizak, Diane J. Greene, Kyung-Hyun Cho, and Victor M. Paromov. "Lipid transfer inhibitor protein (apolipoprotein F) concentration in normolipidemic and hyperlipidemic subjects." Journal of Lipid Research 49, no. 1 (September 27, 2007): 127–35. http://dx.doi.org/10.1194/jlr.m700258-jlr200.

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14

Yuan, Zuyi, Chiharu Kishimoto, Hideto Sano, Keisuke Shioji, Yang Xu, and Masayuki Yokode. "Immunoglobulin treatment suppresses atherosclerosis in apolipoprotein E-deficient mice via the Fc portion." American Journal of Physiology-Heart and Circulatory Physiology 285, no. 2 (August 2003): H899—H906. http://dx.doi.org/10.1152/ajpheart.00926.2002.

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Atherosclerosis is associated with immune activation. Immunoglobulin is used for the treatment of immune-mediated diseases. The mechanisms and importance of the Fc portion of immunoglobulin upon experimental atherosclerosis in apolipoprotein E-deficient mice were examined. Experimental atherosclerosis was induced in mice fed a high-fat diet containing 0.3% cholesterol. Over 8, 12, and 16 wk, on alternate days, mice were treated with an intraperitoneal injection of either 1 g·kg–1·day–1of human intact immunoglobulin or F(ab′)2fragments of human immunoglobulin. Fatty streak formation and fibrofatty plaques were markedly suppressed in mice that received intact immunoglobulin for 8, 12, and 16 wk. In contrast, atherosclerotic lesions were not ameliorated in mice that received F(ab′)2fragments. Immunohistochemical analysis revealed that macrophage accumulation in the fatty streak lesions was suppressed in mice received intact immunoglobulin but not in those that received F(ab′)2fragments. In addition, the cytotoxic activities of splenocytes from immunoglobulin-treated mice, but not from F(ab′)2fragment-treated mice, were significantly suppressed compared with those from human serum albumin-treated mice. Differences in lesion area did not correlate with any significant alterations in serum lipid levels. Immunoglobulin therapy markedly suppressed atherosclerosis due to Fc receptor-mediated anti-inflammatory and immunomodulating actions. The antiatherosclerotic effects of immunoglobulin may be related to the suppression of cytotoxic activity of atherogenic T cells and the reduction of macrophage accumulation in the lesions.

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15

Sawashita, Jinko, Beiru Zhang, Kazuhiro Hasegawa, Masayuki Mori, Hironobu Naiki, Fuyuki Kametani, and Keiichi Higuchi. "C-terminal sequence of amyloid-resistant type F apolipoprotein A-II inhibits amyloid fibril formation of apolipoprotein A-II in mice." Proceedings of the National Academy of Sciences 112, no. 8 (February 9, 2015): E836—E845. http://dx.doi.org/10.1073/pnas.1416363112.

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In murine senile amyloidosis, misfolded serum apolipoprotein (apo) A-II deposits as amyloid fibrils (AApoAII) in a process associated with aging. Mouse strains carrying type C apoA-II (APOA2C) protein exhibit a high incidence of severe systemic amyloidosis. Previously, we showed that N- and C-terminal sequences of apoA-II protein are critical for polymerization into amyloid fibrils in vitro. Here, we demonstrate that congenic mouse strains carrying type F apoA-II (APOA2F) protein, which contains four amino acid substitutions in the amyloidogenic regions of APOA2C, were absolutely resistant to amyloidosis, even after induction of amyloidosis by injection of AApoAII. In vitro fibril formation tests showed that N- and C-terminal APOA2F peptides did not polymerize into amyloid fibrils. Moreover, a C-terminal APOA2F peptide was a strong inhibitor of nucleation and extension of amyloid fibrils during polymerization. Importantly, after the induction of amyloidosis, we succeeded in suppressing amyloid deposition in senile amyloidosis-susceptible mice by treatment with the C-terminal APOA2F peptide. We suggest that the C-terminal APOA2F peptide might inhibit further extension of amyloid fibrils by blocking the active ends of nuclei (seeds). We present a previously unidentified model system for investigating inhibitory mechanisms against amyloidosis in vivo and in vitro and believe that this system will be useful for the development of novel therapies.

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16

Garai, Kanchan, Sourajit M. Mustafi, Berevan Baban, and Carl Frieden. "Structural differences between apolipoprotein E3 and E4 as measured by 19 F NMR." Protein Science 19, no. 1 (November 10, 2009): 66–74. http://dx.doi.org/10.1002/pro.283.

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17

Gambert, Philippe, Michel Farnier, Gilbert Girardot, Jean-Marvel Brun, and Christian Lallemant. "Effects of gemfibrozil on serum apolipoprotein E distribution in hypercholesterolemic patients." Atherosclerosis 89, no. 2-3 (August 1991): 267–69. http://dx.doi.org/10.1016/0021-9150(91)90069-f.

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18

Skoryukova, S. A., M. V. Kim, A. A. Bystrova, A. Yu Babenko, E. I. Baranova, and S. N. Pchelina. "Polymorphism of S19W of apolipoprotein A5gene in patients with type 2 diabetes mellitus - connection with metabolic parameters and triglyceride levels." Scientific Notes of the I. P. Pavlov St. Petersburg State Medical University 22, no. 2 (June 30, 2015): 60–63. http://dx.doi.org/10.24884/1607-4181-2015-22-2-60-63.

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The article deals with genetic aspects of the influence of S19W polymorphic variants of apolipoprotein A5 gene, on the blood lipids in patients with type 2 diabetes mellitus, as well as influence of various clinical and anamnestic parameters on the blood lipids determining the development f atherogenic dyslipidemia.. The study revealed interrelation between 19W allele and hypertriglyceridemia development in patients with type 2 diabetes mellitus.

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19

Plubell, Deanna L., Alex M. Fenton, Sara Rosario, Paige Bergstrom, Phillip A. Wilmarth, Wayne M. Clark, Neil A. Zakai, et al. "High-Density Lipoprotein Carries Markers That Track With Recovery From Stroke." Circulation Research 127, no. 10 (October 23, 2020): 1274–87. http://dx.doi.org/10.1161/circresaha.120.316526.

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Rationale: Prospective cohort studies question the value of HDL-C (high-density lipoprotein cholesterol) for stroke risk prediction. Objective: Investigate the relationship between long-term functional recovery and HDL proteome and function. Methods and Results: Changes in HDL protein composition and function (cholesterol efflux capacity) in patients after acute ischemic stroke at 2 time points (24 hours, 35 patients; 96 hours, 20 patients) and in 35 control subjects were measured. The recovery from stroke was assessed by 3 months, the National Institutes of Health Stroke Scale and modified Rankin scale scores. When compared with control subject after adjustments for sex and HDL-C levels, 12 proteins some of which participate in acute phase response and platelet activation (APMAP [adipocyte plasma membrane-associated protein], GPLD1 [phosphate inositol-glycan specific phospholipase D], APOE [apolipoprotein E], IHH [Indian hedgehog protein], ITIH4 [inter-alpha-trypsin inhibitor chain H4], SAA2 [serum amyloid A2], APOA4 [apolipoprotein A-IV], CLU [clusterin], ANTRX2 [anthrax toxin receptor 2], PON1 [serum paraoxonase/arylesterase], SERPINA1 [alpha-1-antitrypsin], and APOF [apolipoprotein F]) were significantly (adjusted P <0.05) altered in stroke HDL at 96 hours. The first 8 of these proteins were also significantly altered at 24 hours. Consistent with inflammatory remodeling, cholesterol efflux capacity was reduced by 32% ( P <0.001) at both time points. Baseline stroke severity adjusted regression model showed that changes within 96-hour poststroke in APOF, APOL1, APMAP, APOC4 (apolipoprotein C4), APOM (apolipoprotein M), PCYOX1 (prenylcysteine oxidase 1), PON1, and APOE correlate with stroke recovery scores ( R 2 =0.38–0.73, adjusted P <0.05). APOF ( R 2 =0.73) and APOL1 ( R 2 =0.60) continued to significantly correlate with recovery scores after accounting for tPA (tissue-type plasminogen activator) treatment. Conclusions: Changes in HDL proteins during early acute phase of stroke associate with recovery. Monitoring HDL proteins may provide clinical biomarkers that inform on stroke recuperation.

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20

Lagor, William R., David W. Fields, Sumeet A. Khetarpal, Arthi Kumaravel, Wen Lin, Nathaniel Weintraub, Kaijin Wu, et al. "The Effects of Apolipoprotein F Deficiency on High Density Lipoprotein Cholesterol Metabolism in Mice." PLoS ONE 7, no. 2 (February 20, 2012): e31616. http://dx.doi.org/10.1371/journal.pone.0031616.

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21

Crouse, Stephen F., Barbara C. O’Brien, Peter W. Grandjean, Robert C. Lowe, J. James Rohack, and John S. Green. "Effects of training and a single session of exercise on lipids and apolipoproteins in hypercholesterolemic men." Journal of Applied Physiology 83, no. 6 (December 1, 1997): 2019–28. http://dx.doi.org/10.1152/jappl.1997.83.6.2019.

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Crouse, Stephen F., Barbara C. O’Brien, Peter W. Grandjean, Robert C. Lowe, J. James Rohack, and John S. Green. Effects of training and a single session of exercise on lipids and apolipoproteins in hypercholesterolemic men. J. Appl. Physiol. 83(6): 2019–2028, 1997.—To differentiate between transient (acute) and training (chronic) effects of exercise at two different intensities on blood lipids and apolipoproteins (apo), 26 hypercholesterolemic men (cholesterol = 258 mg/dl, age = 47 yr, weight = 81.9 kg) trained three times per week for 24 wk, 350 kcal/session at high (80% maximal O2uptake, n = 12) or moderate (50% maximal O2uptake, n = 14) intensity. Serum lipid and apolipoprotein (apo) concentrations (plasma volume adjusted) were measured before and immediately, 24, and 48 h after exercise on four different occasions corresponding to 0, 8, 16, and 24 wk of training. Data were analyzed using three-way repeated-measures multivariate analysis of variance followed by analysis of variance and Duncan’s procedures (α = 0.05). A transient 6% rise in low-density-lipoprotein cholesterol measured before training at the 24-h time point was no longer evident after training. Triglycerides fell and total cholesterol, high-density-lipoprotein cholesterol (HDL-C), HDL3-C, apo A-I, and apo B rose 24–48 h after exercise regardless of training or intensity. Total cholesterol, HDL3-C, apo A-I, and apo B were lower and HDL2-C was higher after training than before training. Thus exercise training and a single session of exercise exert distinct and interactive effects on lipids and apolipoproteins. These results support the practice of training at least every other day to obtain optimal exercise benefits.

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22

Wang, Xinxing, Donna M. Driscoll, and Richard E. Morton. "Molecular Cloning and Expression of Lipid Transfer Inhibitor Protein Reveals Its Identity with Apolipoprotein F." Journal of Biological Chemistry 274, no. 3 (January 15, 1999): 1814–20. http://dx.doi.org/10.1074/jbc.274.3.1814.

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23

Morton, Richard E., and Daniel Mihna. "Apolipoprotein F concentration, activity, and the properties of LDL controlling ApoF activation in hyperlipidemic plasma." Journal of Lipid Research 63, no. 2 (February 2022): 100166. http://dx.doi.org/10.1016/j.jlr.2021.100166.

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24

Murray, R. W., and K. R. Marotti. "Nucleotide sequence of the cynomolgus monkey apolipoprotein A-I gene and corresponding flanking regions." Biochimica et Biophysica Acta (BBA) - Gene Structure and Expression 1131, no. 2 (June 1992): 207–10. http://dx.doi.org/10.1016/0167-4781(92)90079-f.

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25

Wilson, Peter W. F., Richard H. Myers, Martin G. Larson, Jose M. Ordovas, Philip A. Wolf, and Ernst J. Schaefer. "750-5 Apolipoprotein E Alleles, Dyslipidemia, and Coronary Heart Disease: The Framingham Offspring Study." Journal of the American College of Cardiology 25, no. 2 (February 1995): 196A. http://dx.doi.org/10.1016/0735-1097(95)92270-f.

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Kota, Lakshmi Narayanan, Bhagyalakshmi Mallapura Shankarappa, Prafulla Shivakumar, Shilpa Sadanand, Bhavani Shankara Bagepally, Srinivas Brahmadevarahalli Krishnappa, Meera Purushottam, et al. "Dementia and Diabetes Mellitus: Association with Apolipoprotein E4 Polymorphism from a Hospital in Southern India." International Journal of Alzheimer's Disease 2012 (2012): 1–4. http://dx.doi.org/10.1155/2012/702972.

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Objective. To evaluate the association of Apolipoprotein E4 (ApoE4) in Alzheimer's dementia (AD) with comorbid diabetes mellitus (DM).Methods. The study included subjects with Alzheimer's dementia (AD) (n=209), individuals with non-Alzheimer's dementia (nAD) (n=122), individuals with parental history of AD (f/hAD) (n=70), and control individuals who had normal cognitive functions and no parental history of dementia (NC) (n=193). Dementia was diagnosed using International Classification of Diseases-10 revision (ICD-10) criteria. DM was assessed on the basis of self-report and/or use of antidiabetic medications. ApoE genotyping was done using sequence-specific primer polymerase chain reaction.Results. ApoE4 allele frequencies were highest among AD with comorbid DM (0.35) followed by AD without DM (0.25), nAD with DM (0.13), nAD without comorbid DM (0.12), and NC (0.08). Frequency of ApoE4 in persons with f/hAD was 0.13. The association of AD with co-morbid DM in ApoE4 carriers was more in comparison to NC with DM (OR=5.68,P=0.04).Conclusion. There is a significant association between AD with co-morbid DM and ApoE4 genotype.

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27

Zhu, H., L. Xie, Z.-Q. Liu, B. Wang, M.-Q. Gao, and Y. Lu. "Population pharmacokinetics of bedaquiline in patients with drug-resistant TB." International Journal of Tuberculosis and Lung Disease 25, no. 12 (December 1, 2021): 1006–12. http://dx.doi.org/10.5588/ijtld.21.0158.

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OBJECTIVE: To develop a population pharmacokinetic (PK) model for bedaquiline (BDQ) to describe the concentration-time data from patients with multidrug-resistant TB (MDR-TB) in China.METHOD: A total of 306 PK observations from 69 patients were used in a non-linear, mixed-effects modelling (NONMEM) approach. BDQ PK can be adequately described by a three-compartment model with a transit absorption model. The impact of baseline covariates, including age, sex, height, weight, alanine aminotransferase (ALT), aspartate aminotransferase (AST), apolipoprotein (ALP), total bilirubin (TBIL), direct bilirubin (DBIL), creatinine (CR), potassium (K+), calcium (Ca++) and magnesium (Mg++) on the oral clearance (CL/F) of BDQ were investigated.RESULTS: In final population PK model, no significant covariates were found in the population PK model for BDQ. The population PK parameter estimate values for oral clearance (CL/F); CL/F between central compartment and peripheral compartment (Q1/F, Q2/F); peripheral volume of distribution (Vp1/F, VP2/F) were respectively 1.50 L/h (95% CI 1.07–1.93), 2.54 L/h (95% CI 1.67–3.41), 1,250 L (95% CI 616.9–1883.1), 2.00 L/h (95% CI 1.10–2.90) and 4,960 L (95% CI 1647.6–8272.4). Inter-individual variability on CL/F was 65.0%.CONCLUSION: This is the first study to establish a population PK model for BDQ in Chinese patients with MDR-TB. The final model adequately described the data and had good simulation characteristics. Despite some limitations, the final population PK model was stable with good accuracy of parameter estimation.

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28

Morton, Richard E., and Diane J. Greene. "Conversion of lipid transfer inhibitor protein (apolipoprotein F) to its active form depends on LDL composition." Journal of Lipid Research 52, no. 12 (September 21, 2011): 2262–71. http://dx.doi.org/10.1194/jlr.m018283.

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29

Shen, Xue-Bin, Ling Huang, Shao-Hong Zhang, De-Ping Wang, Yun-Li Wu, Wan-Nan Chen, Shang-Hua Xu, and Xu Lin. "Transcriptional regulation of the apolipoprotein F (ApoF) gene by ETS and C/EBPα in hepatoma cells." Biochimie 112 (May 2015): 1–9. http://dx.doi.org/10.1016/j.biochi.2015.02.013.

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30

Kumar, Abhinav, Bevin Gangadharan, and Nicole Zitzmann. "Multiple reaction monitoring and multiple reaction monitoring cubed based assays for the quantitation of apolipoprotein F." Journal of Chromatography B 1033-1034 (October 2016): 278–86. http://dx.doi.org/10.1016/j.jchromb.2016.08.038.

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31

Rainwater, David L. "Genetic basis for multimodal relationship between apolipoprotein (a) size and lipoprotein (a) concentration in Mexican-Americans." Atherosclerosis 115, no. 2 (June 1995): 165–71. http://dx.doi.org/10.1016/0021-9150(94)05507-f.

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Zisman, Sophie, Karen Marom, Oshri Avraham, Lilah Rinsky-Halivni, Uri Gai, Gilit Kligun, Vered Tzarfaty-Majar, Tatsuo Suzuki, and Avihu Klar. "Proteolysis and membrane capture of F-spondin generates combinatorial guidance cues from a single molecule." Journal of Cell Biology 178, no. 7 (September 17, 2007): 1237–49. http://dx.doi.org/10.1083/jcb.200702184.

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The formation of neuronal networks is governed by a limited number of guidance molecules, yet it is immensely complex. The complexity of guidance cues is augmented by posttranslational modification of guidance molecules and their receptors. We report here that cleavage of the floor plate guidance molecule F-spondin generates two functionally opposing fragments: a short-range repellent protein deposited in the membrane of floor plate cells and an adhesive protein that accumulates at the basement membrane. Their coordinated activity, acting respectively as a short-range repellant and a permissive short-range attractant, constricts commissural axons to the basement membrane beneath the floor plate cells. We further demonstrate that the repulsive activity of the inhibitory fragment of F-spondin requires its presentation by the lipoprotein receptor–related protein (LRP) receptors apolipoprotein E receptor 2, LRP2/megalin, and LRP4, which are expressed in the floor plate. Thus, proteolysis and membrane interaction coordinate combinatorial guidance signaling originating from a single guidance cue.

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Farrer, M., F. L. Game, P. C. Adams, M. F. Laker, and K. G. M. M. Alberti. "A simple, sensitive technique for classification of apolipoprotein(a) isoforms by sodium dodecyl sulphate-polyacrylamide gel electrophoresis." Clinica Chimica Acta 207, no. 3 (May 1992): 215–25. http://dx.doi.org/10.1016/0009-8981(92)90120-f.

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Izem, Lahoucine, and Richard E. Morton. "Molecular cloning of hamster lipid transfer inhibitor protein (apolipoprotein F) and regulation of its expression by hyperlipidemia." Journal of Lipid Research 50, no. 4 (November 13, 2008): 676–84. http://dx.doi.org/10.1194/jlr.m800429-jlr200.

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Liu, Yan, and Richard E. Morton. "Apolipoprotein F: a natural inhibitor of cholesteryl ester transfer protein and a key regulator of lipoprotein metabolism." Current Opinion in Lipidology 31, no. 4 (June 9, 2020): 194–99. http://dx.doi.org/10.1097/mol.0000000000000688.

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Tenkanen, H., P. Koskinene, J. Metso, M. Baumann, M. Lukka, R. Kauppinen-Mäkelin, K. Kontula, et al. "A novel polymorphism of apolipoprotein A-IV is the result of an asparagine to serine substitution at residue 127." Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease 1138, no. 1 (January 1992): 27–33. http://dx.doi.org/10.1016/0925-4439(92)90147-f.

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Borghini, Isabelle, Richard W. James, Marie-Claude Blatter, and Daniel Pometta. "Distribution of apolipoprotein E between free and A-II complexed forms in very-low- and high-density lipoproteins: functional implications." Biochimica et Biophysica Acta (BBA) - Lipids and Lipid Metabolism 1083, no. 2 (May 1991): 139–46. http://dx.doi.org/10.1016/0005-2760(91)90034-f.

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Inbal, Aida, Dov Freimark, Baruch Modan, Angela Chetrit, Shlomi Matetzky, Nurit Rosenberg, Rima Dardik, Zvia Baron, and Uri Seligsohn. "Synergistic Effects of Prothrombotic Polymorphisms and Atherogenic Factors on the Risk of Myocardial Infarction in Young Males." Blood 93, no. 7 (April 1, 1999): 2186–90. http://dx.doi.org/10.1182/blood.v93.7.2186.407k28_2186_2190.

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Several recent studies evaluated a possible effect of the prothrombotic polymorphisms such as 5,10 methylenetetrahydrofolate reductase (MTHFR) nt 677C → T, factor V (F V) nt 1691G → A (F V Leiden), and factor II (F II) nt 20210 G → A on the risk of myocardial infarction. In the present study, we analyzed the effect of these prothrombotic polymorphisms, as well as apolipoprotein (Apo) E4, smoking, hypertension, diabetes mellitus, and hypercholesterolemia, on the risk of myocardial infarction in young males. We conducted a case-control study of 112 young males with first acute myocardial infarction (AMI) before the age of 52 and 187 healthy controls of similar age. The prevalences of heterozygotes for F V G1691A and F II G20210A were not significantly different between cases and controls (6.3% v 6.4% and 5.9% v 3.4% among cases and controls, respectively). In contrast, the prevalence of MTHFR 677T homozygosity and the allele frequency of Apo E4 were significantly higher among patients (24.1% v 10.7% and 9.4% v5.3% among cases and controls, respectively). Concomitant presence of hypertension, hypercholesterolemia, or diabetes and one or more of the four examined polymorphisms increased the risk by almost ninefold (odds ratio [OR] = 8.66; 95% confidence interval [CI], 3.49 to 21.5) and concomitant smoking by almost 18-fold (OR = 17.6; 95% CI, 6.30 to 48.9). When all atherogenic risk factors were analyzed simultaneously by a logistic model, the combination of prothrombotic and Apo E4 polymorphisms with current smoking increased the risk 25-fold (OR = 24.7; 95% CI, 7.17 to 84.9).The presented data suggest a synergistic effect between atherogenic and thrombogenic risk factors in the pathogenesis of AMI, as was recently found in a similar cohort of women.

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Takeda, Eri, Sachiyo Tsuji-Kawahara, Mayumi Sakamoto, Marc-André Langlois, Michael S. Neuberger, Cristina Rada, and Masaaki Miyazawa. "Mouse APOBEC3 Restricts Friend Leukemia Virus Infection and Pathogenesis In Vivo." Journal of Virology 82, no. 22 (September 10, 2008): 10998–1008. http://dx.doi.org/10.1128/jvi.01311-08.

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ABSTRACT Several members of the apolipoprotein B mRNA-editing enzyme catalytic polypeptide-like complex 3 (APOBEC3) family in primates act as potent inhibitors of retroviral replication. However, lentiviruses have evolved mechanisms to specifically evade host APOBEC3. Likewise, murine leukemia viruses (MuLV) exclude mouse APOBEC3 from the virions and cleave virion-incorporated APOBEC3. Although the betaretrovirus mouse mammary tumor virus has been shown to be susceptible to mouse APOBEC3, it is not known if APOBEC3 has a physiological role in restricting more widely distributed and long-coevolved mouse gammaretroviruses. The pathogenicity of Friend MuLV (F-MuLV) is influenced by several host genes: some directly restrict the cell entry or integration of the virus, while others influence the host immune responses. Among the latter, the Rfv3 gene has been mapped to chromosome 15 in the vicinity of the APOBEC3 locus. Here we have shown that polymorphisms at the mouse APOBEC3 locus indeed influence F-MuLV replication and pathogenesis: the APOBEC3 alleles of F-MuLV-resistant C57BL/6 and -susceptible BALB/c mice differ in their sequences and expression levels in the hematopoietic tissues and in their abilities to restrict F-MuLV replication both in vitro and in vivo. Furthermore, upon infection with the pathogenic Friend virus complex, (BALB/c × C57BL/6)F1 mice displayed an exacerbated erythroid cell proliferation when the mice carried a targeted disruption of the C57BL/6-derived APOBEC3 allele. These results indicate, for the first time, that mouse APOBEC3 is a physiologically functioning restriction factor to mouse gammaretroviruses.

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Namba, Yoshio, Masanori Tomonaga, Hiroshi Kawasaki, Eiichi Otomo, and Kazuhiko Ikeda. "Apolipoprotein E immunoreactivity in cerebral amyloid deposits and neurofibrillary tangles in Alzheimer's disease and kuru plaque amyloid in Creutzfeldt-Jakob disease." Brain Research 541, no. 1 (February 1991): 163–66. http://dx.doi.org/10.1016/0006-8993(91)91092-f.

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41

Inbal, Aida, Dov Freimark, Baruch Modan, Angela Chetrit, Shlomi Matetzky, Nurit Rosenberg, Rima Dardik, Zvia Baron, and Uri Seligsohn. "Synergistic Effects of Prothrombotic Polymorphisms and Atherogenic Factors on the Risk of Myocardial Infarction in Young Males." Blood 93, no. 7 (April 1, 1999): 2186–90. http://dx.doi.org/10.1182/blood.v93.7.2186.

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Abstract Several recent studies evaluated a possible effect of the prothrombotic polymorphisms such as 5,10 methylenetetrahydrofolate reductase (MTHFR) nt 677C → T, factor V (F V) nt 1691G → A (F V Leiden), and factor II (F II) nt 20210 G → A on the risk of myocardial infarction. In the present study, we analyzed the effect of these prothrombotic polymorphisms, as well as apolipoprotein (Apo) E4, smoking, hypertension, diabetes mellitus, and hypercholesterolemia, on the risk of myocardial infarction in young males. We conducted a case-control study of 112 young males with first acute myocardial infarction (AMI) before the age of 52 and 187 healthy controls of similar age. The prevalences of heterozygotes for F V G1691A and F II G20210A were not significantly different between cases and controls (6.3% v 6.4% and 5.9% v 3.4% among cases and controls, respectively). In contrast, the prevalence of MTHFR 677T homozygosity and the allele frequency of Apo E4 were significantly higher among patients (24.1% v 10.7% and 9.4% v5.3% among cases and controls, respectively). Concomitant presence of hypertension, hypercholesterolemia, or diabetes and one or more of the four examined polymorphisms increased the risk by almost ninefold (odds ratio [OR] = 8.66; 95% confidence interval [CI], 3.49 to 21.5) and concomitant smoking by almost 18-fold (OR = 17.6; 95% CI, 6.30 to 48.9). When all atherogenic risk factors were analyzed simultaneously by a logistic model, the combination of prothrombotic and Apo E4 polymorphisms with current smoking increased the risk 25-fold (OR = 24.7; 95% CI, 7.17 to 84.9).The presented data suggest a synergistic effect between atherogenic and thrombogenic risk factors in the pathogenesis of AMI, as was recently found in a similar cohort of women.

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42

Fattori, Bruno, Andrea Nacci, Augusto Casani, Renza Cristofani, and Andrea Sagripanti. "Hemostatic Alterations in Patients with Acute, Unilateral Vestibular Paresis." Otolaryngology–Head and Neck Surgery 124, no. 4 (April 2001): 401–7. http://dx.doi.org/10.1067/mhn.2001.114795.

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OBJECTIVES: The etiopathogenesis of acute unilateral peripheral vestibulopathy (APV) still remains a matter of debate; ischemic changes in the circulation of the labyrinth may play a role. We consequently looked for possible hemostasis alterations in a group of patients with APV of an unknown nature. METHODS: We evaluated blood parameters known to be involved in circulation disorders, including total and HDL cholesterol, tryglycerides, apolipoprotein A and B, lipoprotein(a), homocysteine, folate, prothrombin time, activated partial thromboplastin time, fibrinogen, D-dimer, antithrombin III, protein C, protein S, activated protein C resistance, and anticardiolipin IgG and IgM antibodies. A series of 23 patients affected with APV were consecutively referred to our department, in the acute phase, before treatment, and in the follow-up phase after 4 to 6 weeks of pharmacologic washout. The aforementioned blood parameters were also measured in a series of 15 patients with Menière's disease. RESULTS: The patients with APV in the acute phase compared with the patients with Menière's disease in the acute phase exhibited increased plasma levels of fibrinogen (mean, 338.3 ± 135.9 SD vs 271.3 ± 69.8 SD mg/dL, P = 0.05), increased plasma levels of D-dimer (mean, 320 ± 207.8 SD vs 226.7 ± 138.7 SD NG/mL), enhanced plasma levels of lipoprotein(a) (41.4 ± 38.6 SD vs 16 ± 18.2 SD mg/dL, F = 5.67, P = 0.02), high leukocyte count (9.1 ± 2.7 SD vs 6.5 ± 1.3 SD x 10 3 /μL; F = 8.42, P < 0.006), and low serum folate concentration (5.3 ± 1.8 SD vs 7.1 ± 2.7 NG/mg; F = 4.34, P = 0.04). During follow-up the prothrombin time was prolonged (F = 4.34, P = 0.04) and leukocyte count decreased (F = 7.39, P < 0.019) in the APV patients, whereas fibrinogen, D-dimer, lipoprotein(a), and folate were unchanged. CONCLUSION: Our results provide evidence suggesting an involvement of the hemostatic system in APV.

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Bard, J. M., H. J. Parra, P. Douste-Blazy, and J. C. Fruchart. "Effect of pravastatin, an HMG CoA reductase inhibitor, and cholestyramine, a bile acid sequestrant, on lipoprotein particles defined by their apolipoprotein composition." Metabolism 39, no. 3 (March 1990): 269–73. http://dx.doi.org/10.1016/0026-0495(90)90046-f.

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Crouse, Stephen F., Barbara C. O’Brien, Peter W. Grandjean, Robert C. Lowe, J. James Rohack, John S. Green, and Homer Tolson. "Training intensity, blood lipids, and apolipoproteins in men with high cholesterol." Journal of Applied Physiology 82, no. 1 (January 1, 1997): 270–77. http://dx.doi.org/10.1152/jappl.1997.82.1.270.

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Crouse, Stephen F., Barbara C. O’Brien, Peter W. Grandjean, Robert C. Lowe, J. James Rohack, John S. Green, and Homer Tolson.Training intensity, blood lipids, and apolipoproteins in men with high cholesterol. J. Appl. Physiol.82(1): 270–277, 1997.—Twenty-six hypercholesterolemic men (mean cholesterol, 258 mg/dl; age, 47 yr; weight, 81.9 kg) completed 24 wk of cycle ergometer training (3 days/wk, 350 kcal/session) at either high ( n = 12) or moderate ( n = 14) intensity (80 and 50% maximal O2uptake, respectively, randomly assigned) to test the influence of training intensity on blood lipid and apolipoprotein (apo) concentrations. All physiological, lipid, and apo measurements were completed at 0, 8, 16, and 24 wk. Lipid data were analyzed via two × four repeated-measures analysis of variance (∝ = 0.0031). Training produced a significant decrease in body weight and increase in maximal O2uptake. No interactions between intensity and weeks of training were noted for any lipid or apo variable, and no between-group differences were significant before or throughout training. Therefore, intensity did not affect the training response. Regardless of intensity, apo AI and apo B fell 9 and 13%, respectively, by week 16 and remained lower through week 24( P < 0.0003). Total cholesterol fell transiently (−5.5%) by week 16( P < 0.0021) but returned to initial levels by week 24. Triglyceride, low-density-lipoprotein cholesterol, and high-density-lipoprotein (HDL) cholesterol did not change with training. In contrast, HDL2cholesterol rose 79% above initial levels by week 8 and 82% above initial levels by week 24( P < 0.0018); HDL3cholesterol fell 8 and 13% over the same training intervals ( P< 0.0026). These data show that changes in blood lipid and apo concentrations that accompany training in hypercholesterolemic men are not influenced by exercise intensity when caloric expenditure is held constant.

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Walcher, Thomas, Peter Bernhardt, Dusica Vasic, Helga Bach, Renate Durst, Wolfgang Rottbauer, and Daniel Walcher. "Ivabradine Reduces Chemokine-Induced CD4-Positive Lymphocyte Migration." Mediators of Inflammation 2010 (2010): 1–8. http://dx.doi.org/10.1155/2010/751313.

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Aims.Migration of CD4-positive lymphocytes into the vessel wall is a critical step in atherogenesis. Recent data suggest that ivabradine, a selective I(f)-channel blocker, reduces atherosclerotic plaque formation in apolipoprotein E-deficient mice, hitherto nothing is known about the mechanism by which ivabradine modulates plaque formation. Therefore, the present study investigated whether ivabradine regulates chemokine-induced migration of lymphocytes.Methods and results.Stimulation of CD4-positive lymphocytes with SDF-1 leads to a2.0±0.1fold increase in cell migration (P<.01;n=7). Pretreatment of cells with ivabradine reduces this effect to a maximal1.2±0.1fold induction at 0.1 µmol/L ivabradine (P<.01compared to SDF-1-treated cells,n=7). The effect of ivabradine on CD4-positive lymphocyte migration was mediated through an early inhibition of chemokine-induced PI-3 kinase activity as determined by PI-3 kinase activity assays. Downstream, ivabradine inhibits activation of the small GTPase Rac and phosphorylation of the Myosin Light Chain (MLC). Moreover, ivabradine treatment reduces f-actin formation as well as ICAM3 translocation to the uropod of the cell, thus interfering with two important steps in T cell migration.Conclusion.Ivabradine inhibits chemokine-induced migration of CD4-positive lymphocytes. Given the crucial importance of chemokine-induced T-cell migration in early atherogenesis, ivabradine may be a promising tool to modulate this effect.

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Seferovic-Mitrovic, Jelena, Nebojsa Lalic, Bosiljka Vujisic-Tesic, Katarina Lalic, Aleksandra Jotic, Arsen Ristic, Vojislav Giga, et al. "Asymptomatic cardiovascular manifestations in diabetes mellitus: Left ventricular diastolic dysfunction and silent myocardial ischemia." Srpski arhiv za celokupno lekarstvo 139, no. 9-10 (2011): 599–604. http://dx.doi.org/10.2298/sarh1110599s.

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Introduction. Several cardiovascular manifestations in patients with diabetes may be asymptomatic. Left ventricular diastolic dysfunction (LVDD) is considered to be the earliest metabolic myocardial lesion in these patients, and can be diagnosed with tissue Doppler echocardiography. Silent myocardial ischemia (SMI) is a characteristic and frequently described form of ischemic heart disease in patients with diabetes. Objective. The aim of the study was to assess the prevalence of LVDD and SMI in patients with type 2 diabetes, as well as to compare demographic, clinical, and metabolic data among defined groups (patients with LVDD, patients with SMI and patients with type 2 diabetes, without LVDD and SMI). Methods. We investigated 104 type 2 diabetic patients (mean age 55.4?9.1 years, 64.4% males) with normal blood pressure, prehypertension and arterial hypertension stage I. Study design included basic laboratory assessment and cardiological workup (transthoracic echocardiography and tissue Doppler, as well as the exercise stress echocardiography). Results. LVDD was diagnosed in twelve patients (11.5%), while SMI was revealed in six patients (5.8%). Less patients with LVDD were using metformin, in comparison to other two groups (?2 =12.152; p=0.002). Values of HDL cholesterol (F=4.515; p=0.013) and apolipoprotein A1 (F=5.128; p= 0.008) were significantly higher in patients with LVDD. Conclusion. The study confirmed asymptomatic cardiovascular complications in 17.3% patients with type 2 diabetes.

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Марусин, А. В., О. А. Макеева, К. В. Вагайцева, А. В. Бочарова, and В. А. Степанов. "Cognitive domains association with genetic variability of apolipoprotein E in a sample of elderly Russians." Nauchno-prakticheskii zhurnal «Medicinskaia genetika», no. 4(213) (April 30, 2020): 27–29. http://dx.doi.org/10.25557/2073-7998.2020.04.27-29.

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Актуальным является поиск генетических вариантов связывающих снижение различных сфер мыслительных процессов с возрастом и болезнью Альцгеймера. Цель исследования - поиск взаимосвязи белковых гаплотипов двух полиморфных вариантов гена APOE с вариабельностью восьми доменов когнитивных функций пожилых людей, определяемых по баллам батареи тестов Монреальской шкалы оценки когнитивных функций (МоСА). Две наиболее высоко статистически значимые ассоциации выявлены для генотипа ε3/ε3 в сравнении с носителями аллеля ε4. Это домены памяти (р=0,002) и зрительно конструктивных навыков (р=0,007). Не обнаружено статистически значимых ассоциаций для когнитивных сфер: внимание и концентрация, исполнительные функции, язык, абстрактное мышление, счет и ориентация. Возможно, обнаруженные ассоциации обуславливают общую генетическую природу наследования болезни Альцгеймера, психических расстройств, деменции и интеллекта у пожилых людей. The search for genetic variants linking the decline in various areas of cognitive processes with age and Alzheimer’s disease is relevant. The aim was to search for the relationship of protein haplotypes of two polymorphic variants in the APOE gene with the eight cognitive function domains variability in f the elderly. Domains were determined by the battery score of the Montreal Cognitive Assessmnet (MoCA). The two most highly statistically significant associations were identified for the ε3/ε3 genotype in comparison with carriers of the ε4 allele. These are memory (p = 0.002) and visuospatial abilities (p = 0.007) domains. No statistically significant associations were revealed for cognitive domains: attention and concentration, executive functions, language, abstraction, calculations and orientation. Possibly, the identified associations determine the general genetic baseline of inheritance of Alzheimer’s disease, mental disorders, dementia and intelligence in the elderly.

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Julian, LJ, L. Vella, D. Frankel, SL Minden, JR Oksenberg, and DC Mohr. "ApoE alleles, depression and positive affect in multiple sclerosis." Multiple Sclerosis Journal 15, no. 3 (January 19, 2009): 311–15. http://dx.doi.org/10.1177/1352458508099478.

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Background The role of apolipoprotein E (ApoE) alleles has received recent attention in depressive disorders, the ApoE ε4 conferring greater risk for poorer outcomes, and the ApoE ε2 allele providing some protective effects. Depression is common in multiple sclerosis (MS) and the role of ApoE alleles is unknown. Aims To evaluate ApoE alleles in relation to symptoms of depression in a cohort of patients with MS participating in the Sonya Slifka Longitudinal Multiple Sclerosis Study (Slifka Study). To examine risk and protection, depressed mood and positive affect were each investigated with respect to the ApoE ε4 and ApoE ε2 alleles, respectively. Results Of the total 101 participants, 22.8% were ApoE ε2 carriers and 21.8% were ApoE ε4 carriers. Hierarchical linear regression analyses suggested that after controlling for demographics, disease duration, and disability, ApoE ε2 significantly predicted increased positive affect (R2Δ = 0.05, F(1,94) = 5.44, P = 0.02) and was associated with decreased severity of depressive symptoms, although this did not reach statistical significance (R2Δ = 0.03, F(1,94) = 3.44, P = 0.06). ApoE ε4 did not significantly predict depression status. Conclusion The presence of the ApoE ε2 allele in this study is suggested to be protective against depressive symptoms in our subsample of patients recruited from the Slifka Study. These findings are consistent with reports in psychiatric populations linking ApoE ε2 with decreased incidence of depressive disorders. Further investigation would be warranted to understand the role of ApoE genotypes and risk for depressive symptoms.

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Chiwata, Tsuyoshi, Katsumi Aragane, Koji Fujinami, Kazuhiro Kojima, Shun Ishibashi, Nobuhiro Yamada, and Jun Kusunoki. "Direct effect of an acyl-CoA:cholesterol acyltransferase inhibitor, F-1394, on atherosclerosis in apolipoprotein E and low density lipoprotein receptor double knockout mice." British Journal of Pharmacology 133, no. 7 (August 2001): 1005–12. http://dx.doi.org/10.1038/sj.bjp.0704160.

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Kardassis, Dimitris, Iphigenia Tzameli, Margarita Hadzopoulou-Cladaras, Iannis Talianidis, and Vassilis Zannis. "Distal Apolipoprotein C-III Regulatory Elements F to J Act as a General Modular Enhancer for Proximal Promoters That Contain Hormone Response Elements." Arteriosclerosis, Thrombosis, and Vascular Biology 17, no. 1 (January 1997): 222–32. http://dx.doi.org/10.1161/01.atv.17.1.222.

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