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ApoA1, ApoJ and ApoE Plasma Levels and Genotype Frequencies in Cerebral Amyloid Angiopathy
- 作者:Alex Montañola ; Sofía Fernández de Retana ; Antonio López-Rueda…
- 关键词:apoA1 ; apoJ ; Clusterin ; apoE ; APOA1 ; APOJ ; CLU ; APOE ; Cerebral Amyloid Angiopathy ; Alzheimer’s disease
- 刊名:NeuroMolecular Medicine
- 出版年:2016
- 出版时间:March 2016
- 年:2016
- 卷:18
- 期:1
- 页码:99-108
- 全文大小:527 KB
- 参考文献:Bell, R. D., Sagare, A. P., Friedman, A. E., Bedi, G. S., Holtzman, D. M., Deane, R., et al. (2007). Transport pathways for clearance of human Alzheimer’s amyloid beta-peptide and apolipoproteins E and J in the mouse central nervous system. Journal of Cerebral Blood Flow and Metabolism, 27(5), 909–918.PubMedCentral PubMed
Biffi, A., Sonni, A., Anderson, C. D., Kissela, B., Jagiella, J. M., Schmidt, H., et al. (2010). Variants at APOE influence risk of deep and lobar intracerebral hemorrhage. Annals of Neurology, 68(6), 934–943.PubMedCentral PubMed CrossRef Calero, M., Rostagno, A., Matsubara, E., Zlokovic, B., Frangione, B., & Ghiso, J. (2000). Apolipoprotein J (clusterin) and Alzheimer’s disease. Microscopy Research and Technique, 50(4), 305–315.PubMed CrossRef Charidimou, A., Jäger, R. H., Fox, Z., Peeters, A., Vandermeeren, Y., Laloux, P., et al. (2013). Prevalence and mechanisms of cortical superficial siderosis in cerebral amyloid angiopathy. Neurology, 81(7), 626–632.PubMed CrossRef Charnay, Y., Imhof, A., Vallet, P. G., Kovari, E., Bouras, C., & Giannakopoulos, P. (2012). Clusterin in neurological disorders: Molecular perspectives and clinical relevance. Brain Research Bulletin, 88(5), 434–443.PubMed CrossRef Corder, E. H., Saunders, A. M., Risch, N. J., Strittmatter, W. J., Schmechel, D. E., Gaskell, P. C, Jr, et al. (1994). Protective effect of apolipoprotein E type 2 allele for late onset Alzheimer disease. Nature Genetics, 7(2), 180–184.PubMed CrossRef Cordonnier, C., Potter, G. M., Jackson, C. A., Doubal, F., Keir, S., Sudlow, C. L., et al. (2009). Improving interrater agreement about brain microbleeds: Development of the Brain Observer MicroBleed Scale (BOMBS). Stroke, 40(1), 94–99.PubMed CrossRef Craggs, L. J., Taylor, J. L., Slade, J. Y., Chen, A., Hagel, C., Kuhlenbaeumer, G., et al. (2015). Clusterin/Apolipoprotein J immunoreactivity is associated with white matter damage in cerebral small vessel diseases. Neuropathology and Applied Neurobiology. doi:10.1111/nan.12248 . da Costa, G., Ribeiro-Silva, C., Ribeiro, R., Gilberto, S., Gomes, R. A., Ferreira, A., et al. (2015). Transthyretin amyloidosis: Chaperone concentration changes and increased proteolysis in the pathway to disease. PLoS One, 10(7), e0125392.PubMedCentral PubMed CrossRef Deane, R., Sagare, A., Hamm, K., Parisi, M., Lane, S., Finn, M. B., et al. (2008). apoE isoform–specific disruption of amyloid β peptide clearance from mouse brain. Journal of Clinical Investigation, 118(12), 4002–4013.PubMedCentral PubMed CrossRef Devan, W. J., Falcone, G. J., Anderson, C. D., Jagiella, J. M., Schmidt, H., Hansen, B. M., et al. (2013). Heritability estimates identify a substantial genetic contribution to risk and outcome of intracerebral hemorrhage. Stroke, 44(6), 1578–1583.PubMedCentral PubMed CrossRef Fagan, A. M., Christopher, E., Taylor, J. W., Parsadanian, M., Spinner, M., Watson, M., et al. (2004). ApoAI deficiency results in marked reductions in plasma cholesterol but no alterations in amyloid-beta pathology in a mouse model of Alzheimer’s disease-like cerebral amyloidosis. The American Journal of Pathology, 165(4), 1413–1422.PubMedCentral PubMed CrossRef Folstein, M. F., Folstein, S. E., & McHugh, P. R. (1975). “Mini-mental state”. A practical method for grading the cognitive state of patients for the clinician. Journal of Psychiatric Research, 12(3), 189–198.PubMed CrossRef Ghiso, J., Matsubara, E., Koudinov, A., Choi-Miura, N. H., Tomita, M., Wisniewski, T., et al. (1993). The cerebrospinal-fluid soluble form of Alzheimer’s amyloid beta is complexed to SP-40,40 (apolipoprotein J), an inhibitor of the complement membrane-attack complex. Biochemical Journal, 293(Pt1), 27–30.PubMedCentral PubMed CrossRef Golabek, A., Marques, M. A., Lalowski, M., & Wianiewski, T. (1995). Amyloid beta binding proteins in vitro and in normal human cerebrospinal fluid. Neuroscience Letters, 191(1–2), 79–82.PubMed CrossRef Greenberg, S. M., Gurol, M. E., Rosand, J., & Smith, E. E. (2004). Amyloid angiopathy-related vascular cognitive impairment. Stroke, 35(11 Suppl 1), 2616–2619.PubMed CrossRef Greenberg, S. M., Rebeck, G. W., Vonsattel, J. P., Gomez-Isla, T., & Hyman, B. T. (1995). Apolipoprotein E epsilon 4 and cerebral hemorrhage associated with amyloid angiopathy. Annals of Neurology, 38(2), 254–259.PubMed CrossRef Greenberg, S. M., Vonsattel, J. P., Segal, A. Z., Chiu, R. I., Clatworthy, A. E., Liao, A., et al. (1998). Association of apolipoprotein E epsilon2 and vasculopathy in cerebral amyloid angiopathy. Neurology, 50(4), 961–965.PubMed CrossRef Grinberg, L. T., & Thal, D. R. (2010). Vascular pathology in the aged human brain. Acta Neuropathologica, 119(3), 277–290.PubMedCentral PubMed CrossRef Gupta, V. B., Laws, S. M., Villemagne, V. L., Ames, D., Bush, A. I., Ellis, K. A., et al. (2011). Plasma apolipoprotein E and Alzheimer disease risk: The AIBL study of aging. Neurology, 76(12), 1091–1098.PubMed CrossRef Harold, D., Abraham, R., Hollingworth, P., Sims, R., Gerrish, A., Hamshere, M. L., et al. (2009). Genome-wide association study identifies variants at CLU and PICALM associated with Alzheimer’s disease. Nature Genetics, 41(10), 1088–1093.PubMedCentral PubMed CrossRef Hernandez-Guillamon, M., Delgado, P., Penalba, A., Rodriguez-Luna, D., Molina, C. A., Rovira, A., et al. (2012). Plasma β-amyloid levels in cerebral amyloid angiopathy-associated hemorrhagic stroke. Neurodegenerative Diseases, 10(1–4), 320–323.PubMed CrossRef Kawano, M., Kawakami, M., Otsuka, M., Yashima, H., Yaginuma, T., & Ueki, A. (1995). Marked decrease of plasma apolipoprotein AI and AII in Japanese patients with late-onset non-familial Alzheimer’s disease. Clinica Chimica Acta, 239(2), 209–211.CrossRef Killick, R., Ribe, E. M., Al-Shawi, R., Malik, B., Hooper, C., Fernandes, C., et al. (2014). Clusterin regulates β-amyloid toxicity via Dickkopf-1-driven induction of the wnt-PCP-JNK pathway. Molecular Psychiatry, 19(1), 88–98.PubMedCentral PubMed CrossRef Koldamova, R. P., Lefterov, I. M., Lefterov, M. I., & Lazo, J. S. (2001). Apolipoprotein A-I directly interacts with amyloid precursor protein and inhibits A beta aggregation and toxicity. Biochemistry, 40(12), 3553–3560.PubMed CrossRef Koudinov, A. R., Berezov, T. T., Kumar, A., & Koudinova, N. V. (1998). Alzheimer’s amyloid beta interaction with normal human plasma high density lipoprotein: Association with apolipoprotein and lipids. Clinica Chimica Acta, 270(2), 75–84.CrossRef Koudinov, A., Matsubara, E., Frangione, B., & Ghiso, J. (1994). The soluble form of Alzheimer’s amyloid beta protein is complexed to high density lipoprotein 3 and very high density lipoprotein in normal human plasma. Biochemical and Biophysical Research Communications, 205(2), 1164–1171.PubMed CrossRef Lambert, J. C., Heath, S., Even, G., Campion, D., Sleegers, K., Hiltunen, M., et al. (2009). Genome-wide association study identifies variants at CLU and CR1 associated with Alzheimer’s disease. Nature Genetics, 41(10), 1094–1099.PubMed CrossRef Lambert, J. C., Ibrahim-Verbaas, C. A., Harold, D., Naj, A. C., Sims, R., Bellenguez, C., et al. (2013). Meta-analysis of 74,046 individuals identifies 11 new susceptibility loci for Alzheimer’s disease. Nature Genetics, 45(12), 1452–1458.PubMedCentral PubMed CrossRef Lefterov, I., Fitz, N. F., Cronican, A. A., Fogg, A., Lefterov, P., Kodali, R., et al. (2010). Apolipoprotein A-I deficiency increases cerebral amyloid angiopathy and cognitive deficits in APP/PS1DeltaE9 mice. The Journal of Biological Chemistry, 285(47), 36945–36957.PubMedCentral PubMed CrossRef Lewis, T. L., Cao, D., Lu, H., Mans, R. A., Su, Y. R., Jungbauer, L., et al. (2010). Overexpression of human apolipoprotein A-I preserves cognitive function and attenuates neuroinflammation and cerebral amyloid angiopathy in a mouse model of Alzheimer disease. The Journal of Biological Chemistry, 285(47), 36958–36968.PubMedCentral PubMed CrossRef Linn, J., Halpin, A., Demaerel, P., Ruhland, J., Giese, A. D., Dichgans, M., et al. (2010). Prevalence of superficial siderosis in patients with cerebral amyloid angiopathy. Neurology, 74(17), 1346–1350.PubMedCentral PubMed CrossRef Liu, H. C., Hu, C. J., Chang, J. G., Sung, S. M., Lee, L. S., Yuan, R. Y., et al. (2006). Proteomic identification of lower apolipoprotein A-I in Alzheimer’s disease. Dementia and Geriatric Cognitive Disorders, 21(3), 155–161.PubMed CrossRef Matsubara, E., Frangione, B., & Ghiso, J. (1995). Characterization of apolipoprotein J-Alzheimer’s A beta interaction. The Journal of Biological Chemistry, 270(13), 7563–7567.PubMed CrossRef Matsubara, E., Soto, C., Governale, S., Frangione, B., & Chiso, J. (1996). Apolipoprotein J and Alzheimer’s amyloid beta solubility. Biochemical Journal, 316(Pt 2), 671–679.PubMedCentral PubMed CrossRef Maxwell, S. S., Jackson, C. A., Paternoster, L., Cordonnier, C., Thijs, V., Al-Shahi Salman, R., et al. (2011). Genetic associations with brain microbleeds: Systematic review and meta-analyses. Neurology, 77(2), 158–167.PubMedCentral PubMed CrossRef McKhann, G., Drachman, D., Folstein, M., Katzman, R., Price, D., & Stadlan, E. M. (1984). Clinical diagnosis of Alzheimer’s disease: Report of the NINCDS-ADRDA Work Group under the auspices of Department of Health and Human Services Task Force on Alzheimer’s Disease. Neurology, 34(7), 939–944.PubMed CrossRef Merched, A., Xia, Y., Visvikis, S., Serot, J. M., & Siest, G. (2000). Decreased high-density lipoprotein cholesterol and serum apolipoprotein AI concentrations are highly correlated with the severity of Alzheimer’s disease. Neurobiology of Aging, 21(1), 27–30.PubMed CrossRef Michaelson, D. M. (2014). APOE ε4: The most prevalent yet understudied risk factor for Alzheimer’s disease. Alzheimer’s & Dementia, 10(6), 861–868.CrossRef Miyata, M., & Smith, J. D. (1996). Apolipoprotein E allele-specific antioxidante activity and effects on cytotoxicity by oxidative insults and beta-amyloid peptides. Nature Genetics, 14(1), 55–61.PubMed CrossRef Naj, A. C., Jun, G., Beecham, G. W., Wang, L. S., Vardarajan, B. N., Buros, J., et al. (2011). Common variants at MS4A4/MS4A6E, CD2AP, CD33 and EPHA1 are associated with late-onset Alzheimer’s disease. Nature Genetics, 43(5), 436–441.PubMedCentral PubMed CrossRef Nicoll, J. A., Burnett, C., Love, S., Graham, D. I., Ironside, J. W., & Vinters, H. V. (1996). High frequency of apolipoprotein E epsilon 2 in patients with cerebral hemorrhage due to cerebral amyloid angiopathy. Annals of Neurology, 39(5), 682–683.PubMed CrossRef Paula-Lima, A. C., Tricerri, M. A., Brito-Moreira, J., Bomfim, T. R., Oliveira, F. F., Magdesian, M. H., et al. (2009). Human apolipoprotein A-I binds amyloid-beta and prevents Abeta-induced neurotoxicity. The International Journal of Biochemistry & Cell Biology, 41(6), 1361–1370.CrossRef Rannikmäe, K., Kalaria, R. N., Greenberg, S. M., Chui, H. C., Schmitt, F. A., Samarasekera, N., et al. (2014). APOE associations with severe CAA-associated vasculopathic changes: Collaborative meta-analysis. Journal of Neurology, Neurosurgery and Psychiatry, 85(3), 300–305.PubMedCentral PubMed CrossRef Rasmussen, K. L., Tybjaerg-Hansen, A., Nordestgaard, B. G., & Frikke-Schmidt, R. (2015). Plasma levels of apolipoprotein E and risk of dementia in the general population. Annals of Neurology, 77(2), 301–311.PubMed CrossRef Saczynski, J. S., White, L., Peila, R. L., Rodriguez, B. L., & Launer, L. J. (2007). The relation between apolipoprotein A-I and dementia: The Honolulu-Asia aging study. American Journal of Epidemiology, 165(9), 985–992.PubMed CrossRef Schilling, S., DeStefano, A. L., Sachdev, P. S., Choi, S. H., Mather, K. A., DeCarli, C. D., et al. (2013). APOE genotype and MRI markers of cerebrovascular disease: Systematic review and meta-analysis. Neurology, 81(3), 292–300.PubMedCentral PubMed CrossRef Schmechel, D. E., Saunders, A. M., Strittmatter, W. J., Crain, B. J., Hulette, C. M., Joo, S. H., et al. (1993). Increased amyloid beta-peptide deposition in cerebral cortex as a consequence of apolipoprotein E genotype in late-onset Alzheimer disease. Proceedings of the National Academy of Sciences, 90(20), 9649–9653.CrossRef Schrijvers, E. M., Koudstaal, P. J., Hofman, A., & Breteler, M. M. (2011). Plasma clusterin and the risk of Alzheimer disease. JAMA Network, 305(13), 1322–1326. Shoamanesh, A., Martinez-Ramirez, S., Oliveira-Filho, J., Reijmer, Y., Falcone, G. J., Ayres, A., et al. (2014). Interrelationship of superficial siderosis and microbleeds in cerebral amyloid angiopathy. Neurology, 83(20), 1838–1843.PubMedCentral PubMed CrossRef Silajdžić, E., Minthon, L., Björkqvist, M., & Hansson, O. (2012). No diagnostic value of plasma clusterin in Alzheimer’s disease. PLoS One, 7(11), e50237.PubMedCentral PubMed CrossRef Smach, M. A., Edziri, H., Charfeddine, B., Ben Othman, L., Lammouchi, T., Ltaief, A., et al. (2011). Polymorphism in apoA1 Influences High-Density Lipoprotein Cholesterol Levels but Is Not a Major Risk Factor of Alzheimer’s Disease. Dementia and Geriatric Cognitive Disorders Extra, 1(1), 249–257.PubMedCentral PubMed CrossRef Thambisetty, M., Simmons, A., Velayudhan, L., Hye, A., Campell, J., Zhang, Y., et al. (2010). Association of plasma clusterin concentration with severity, pathology, and progression in Alzheimer disease. Archives of General Psychiatry, 67(7), 739–748.PubMedCentral PubMed CrossRef Verbeek, M. M., Otte-Höller, I., Veerhuis, R., Ruiter, D. J., & De Waal, R. M. (1998). Distribution of A beta-associated proteins in cerebrovascular amyloid of Alzheimer’s disease. Acta Neuropathologica, 96(6), 628–636.PubMed CrossRef Wahlund, L. O., Barkhof, F., Fazekas, F., Bronge, L., Augustin, M., Sjögren, M., et al. (2001). A new rating scale for age-related white matter changes applicable to MRI and CT. Stroke, 32(6), 1318–1322.PubMed CrossRef Wang, C., Yu, J. T., Wang, H. F., Jiang, T., Tan, C. C., Meng, X. F., et al. (2014). Meta-analysis of peripheral blood apolipoprotein E levels in Alzheimer’s disease. PLoS One, 9(2), e89041.PubMedCentral PubMed CrossRef Wisniewski, T., Castaño, E. M., Golabek, A., Vogel, T., & Frangione, B. (1994). Acceleration of Alzheimer’s fibril formation by apolipoprotein E in vitro. The American Journal of Pathology, 145(5), 1030–1035.PubMedCentral PubMed Yamada, M. (2000). Cerebral amyloid angiopathy: An overview. Neuropathology, 20(1), 8–22.PubMed CrossRef Zhang, R., Wang, X., Tang, Z., Liu, J., Yang, S., Zhang, Y., et al. (2014). Apolipoprotein E gene polymorphism and the risk of intracerebral hemorrhage: a meta-analysis of epidemiologic studies. Lipids in Health and Disease, 13, 47.PubMedCentral PubMed CrossRef
- 作者单位:Alex Montañola (1)
Sofía Fernández de Retana (1) Antonio López-Rueda (1) Cristina Merino-Zamorano (1) Anna Penalba (1) Paula Fernández-Álvarez (4) David Rodríguez-Luna (2) Ana Malagelada (3) Francesc Pujadas (3) Joan Montaner (1) (2) Mar Hernández-Guillamon (1)
1. Neurovascular Research Laboratory, Vall d’Hebron Research Institute, Universitat Autònoma de Barcelona, Pg. Vall d’Hebron 119-129, 08035, Barcelona, Spain 4. Department of Clinical and Molecular Genetics, Vall d’Hebron Hospital, Barcelona, Spain 2. Neurovascular Unit, Neurology Department, Vall d’Hebron Hospital, Barcelona, Spain 3. Dementia Unit, Neurology Department, Vall d’Hebron Hospital, Barcelona, Spain
- 刊物主题:Neurosciences; Neurology; Internal Medicine;
- 出版者:Springer US
- ISSN:1559-1174
文摘
The involvement of apolipoproteins, such as the ApoE4 isoform, in Alzheimer’s disease (AD) and cerebral amyloid angiopathy (CAA) highlights the fact that certain lipid carriers may participate in soluble β-amyloid (Aβ) transport. Our general aim was to characterize the soluble levels of the apolipoproteins apoE, apoA1 and apoJ/clusterin and their genotype status in patients with CAA. We analyzed the genotypes frequency of APOA1 (rs5069, rs670), CLU (rs11136000, rs1532278, rs7012010, rs9331888) and APOE (rs429358, rs7412) in a cohort of patients with CAA-associated intracerebral hemorrhage (ICH) (n = 59) and compared the results with those from hypertension-associated ICH (n = 42), AD patients (n = 73) and controls (n = 88). In a subgroup of patients, we also determined the plasma concentrations of apoE, apoA1 and apoJ/clusterin. We found increased plasma apoJ/clusterin levels in CAA patients compared to AD patients or controls after adjusting for sex and age (CAA vs. controls, p = 0.033; CAA vs. AD, p = 0.013). ApoA1 levels were not altered between groups, although a strong correlation was observed between plasma Aβ(1-40) and apoA1 among CAA patients (r = 0.583, p = 0.007). Regarding plasma apoE concentration, a robust association between circulating levels and genotype status was confirmed (p < 0.001). Whereas the APOE4 frequency was higher in AD (p < 0.001) and CAA (p = 0.013), the APOA1 and CLU genotypes were not different among groups. In the CAA cohort, the risk-linked CLU variant (C) rs11136000 was associated with white matter hyperintensities (p = 0.045) and the presence of lobar microbleeds (p = 0.023) on MRI. In summary, our findings suggest that apoA1 may act as a physiological transporter of Aβ(1-40) and that apoJ/clusterin appears to be a chaperone related to distinctive lesions in CAA brains.
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