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Effect of High Cholesterol Regulation of LRP1 and RAGE on Aβ Transport Across the Blood-Brain Barrier in Alzheimer’s Disease

Zhou, Rui, Chen, Li-li, Yang, Hai, Li, Ling, Liu, Juan, Chen, Le, Hong, Wen-Juan, Wang, Cong-guo, Ma, Jing-Jing, Huang, Jie, Zhou, Xin-Fu, Liu, Dong, Zhou, Hua-Dong·2021·Current Alzheimer Research
DOI 10.2174/1567205018666210906092940
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Abstract

Background: High cholesterol aggravates the risk development of Alzheimer's disease (AD). AD is closely related to the transport impairment of Amyloid-β (Aβ) in the blood-brain barrier. It is unclear whether high cholesterol affects the risk of cognitive impairment in AD by affecting Aβ transport. The purpose of the study is to investigate whether high cholesterol regulates Aβ transport through low-density Lipoprotein Receptor-Related Protein 1 (LRP1) and Receptor for Advanced Glycation End products (RAGE) in the risk development of AD. Methods: We established high cholesterol AD mice model. The learning and memory functions were evaluated by Morris Water Maze (MWM). Cerebral microvascular endothelial cells were isolated, cultured, and observed. The expression levels of LRP1 and RAGE of endothelial cells and their effect on Aβ transport in vivo were observed. The expression level of LRP1 and RAGE was detected in cultured microvessels after using Wnt inhibitor DKK-1 and β-catenin inhibitor XAV-939. Results: Hypercholesterolemia exacerbated spatial learning and memory impairment. Hypercholesterolemia increased serum Aβ40 level, while serum Aβ42 level did not change significantly. Hypercholesterolemia decreased LRP1 expression and increased RAGE expression in cerebral microvascular endothelial cells. Hypercholesterolemia increased brain apoptosis in AD mice. In in vitro experiment, high cholesterol decreased LRP1 expression and increased RAGE expression, increased Aβ40 expression in cerebral microvascular endothelial cells. High cholesterol regulated the expressions of LRP1 and RAGE and transcriptional activity of LRP1 and RAGE promoters by the Wnt/β-catenin signaling pathway. Conclusion : High cholesterol decreased LRP1 expression and increased RAGE expression in cerebral microvascular endothelial cells, which led to Aβ transport disorder in the blood-brain barrier. Increased Aβ deposition in the brain aggravated apoptosis in the brain, resulting to cognitive impairment of AD mice.

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Research works printed but not linked: 66

  1. Jia L.; Quan M.; Fu Y.; Dementia in China: Epidemiology, clinical management, and research advances. Lancet Neurol 2020,19(1),81-92 · DOI · Paper page
  2. Zhou M.; Wang H.; Zeng X.; Mortality, morbidity, and risk factors in China and its provinces, 1990-2017: A systematic analysis for the Global Burden of Disease Study 2017. Lancet 2019,394(10204),1145-1158 · DOI
  3. Wang J.; Jin W.S.; Bu X.L.; Physiological clearance of tau in the periphery and its therapeutic potential for tauopathies. Acta Neuropathol 2018,136(4),525-536 · DOI
  4. Liu Y.H.; Giunta B.; Zhou H.D.; Tan J.; Wang Y.J.; Immunotherapy for Alzheimer disease: The challenge of adverse effects. Nat Rev Neurol 2012,8(8),465-469 · DOI
  5. Ingelsson M.; Fukumoto H.; Newell K.L.; Early Abeta accumulation and progressive synaptic loss, gliosis, and tangle formation in AD brain. Neurology 2004,62(6),925-931 · DOI · Paper page
  6. Jeong S.; Molecular and cellular basis of neurodegeneration in alzheimer’s disease. Mol Cells 2017,40(9),613-620 · DOI
  7. Donohue M.C.; Sperling R.A.; Petersen R.; Sun C.K.; Weiner M.W.; Aisen P.S.; Association between elevated brain amyloid and subsequent cognitive decline among cognitively normal persons. JAMA 2017,317(22),2305-2316 · DOI · Paper page
  8. O’Brien J.T.; Markus H.S.; Vascular risk factors and Alzheimer’s disease. BMC Med 2014,12,218 · DOI
  9. Zambón D.; Quintana M.; Mata P.; Higher incidence of mild cognitive impairment in familial hypercholesterolemia. Am J Med 2010,123(3),267-274 · DOI · Paper page
  10. Llorente-Cortes V.; Casani L.; Cal R.; Cholesterol-lowering strategies reduce vascular LRP1 overexpression induced by hypercholesterolaemia. Eur J Clin Invest 2011,41(10),1087-1097 · DOI
  11. Yang H.; Wang Y.; Kar S.; Effects of cholesterol transport inhibitor U18666A on APP metabolism in rat primary astrocytes. Glia 2017,65(11),1728-1743 · DOI
  12. Chang T.Y.; Yamauchi Y.; Hasan M.T.; Chang C.; Cellular cholesterol homeostasis and Alzheimer’s disease. J Lipid Res 2017,58(12),2239-2254 · DOI · Paper page
  13. Pedrini S.; Thomas C.; Brautigam H.; Dietary composition modulates brain mass and solubilizable Abeta levels in a mouse model of aggressive Alzheimer’s amyloid pathology. Mol Neurodegener 2009,4,40 · DOI
  14. Wang R.; Li J.J.; Diao S.; Metabolic stress modulates Alzheimer’s β-secretase gene transcription via SIRT1-PPARγ-PGC-1 in neurons. Cell Metab 2013,17(5),685-694 · DOI
  15. Park H.J.; Shabashvili D.; Nekorchuk M.D.; Retention in endoplasmic reticulum 1 (RER1) modulates amyloid-β (Aβ) production by altering trafficking of γ-secretase and amyloid precursor protein (APP). J Biol Chem 2012,287(48),40629-40640 · DOI
  16. Löffler T.; Flunkert S.; Temmel M.; Hutter-Paier B.; Decreased plasma Aβ in hyperlipidemic APPSL transgenic mice is associated with BBB dysfunction. Front Neurosci 2016,10,232 · DOI
  17. Do T.M.; Dodacki A.; Alata W.; Age-dependent regulation of the blood-brain barrier influx/efflux equilibrium of amyloid-β peptide in a mouse model of Alzheimer’s disease (3xTg-AD). J Alzheimers Dis 2016,49(2),287-300 · DOI
  18. Kut C.; Grossman S.A.; Blakeley J.; How critical is the blood-brain barrier to the development of neurotherapeutics? JAMA Neurol 2015,72(4),381-382 · DOI
  19. Erickson M.A.; Hansen K.; Banks W.A.; Inflammation-induced dysfunction of the low-density lipoprotein receptor-related protein-1 at the blood-brain barrier: Protection by the antioxidant N-acetylcysteine. Brain Behav Immun 2012,26(7),1085-1094 · DOI
  20. Chen C.; Li X.H.; Tu Y.; Aβ-AGE aggravates cognitive deficit in rats via RAGE pathway. Neuroscience 2014,257,1-10 · DOI
  21. Kim D.E.; Priefer R.; Therapeutic potential of direct clearance of the amyloid-β in Alzheimer’s disease. Brain Sci 2020,10(2) · DOI
  22. Jaya Prasanthi R.P.; Schommer E.; Thomasson S.; Thompson A.; Feist G.; Ghribi O.; Regulation of beta-amyloid levels in the brain of cholesterol-fed rabbit, a model system for sporadic Alzheimer’s disease. Mech Ageing Dev 2008,129(11),649-655 · DOI
  23. Wang Y.J.; Zhou H.D.; Zhou X.F.; Clearance of amyloid-beta in Alzheimer’s disease: Progress, problems and perspectives. Drug Discov Today 2006,11(19-20),931-938 · DOI
  24. Shin E.J.; Park J.H.; Sung M.J.; Chung M.Y.; Hwang J.T.; Citrus junos Tanaka peel ameliorates hepatic lipid accumulation in HepG2 cells and in mice fed a high-cholesterol diet. BMC Complement Altern Med 2016,16(1),499 · DOI
  25. Cui H.; Zhu Y.; Jiang D.; The RIP1-RIP3 complex mediates osteocyte necroptosis after ovariectomy in rats. PLoS One 2016,11(3) · DOI
  26. Morales-Corraliza J.; Schmidt S.D.; Mazzella M.J.; Immunization targeting a minor plaque constituent clears β-amyloid and rescues behavioral deficits in an Alzheimer’s disease mouse model. Neurobiol Aging 2013,34(1),137-145 · DOI
  27. Taylor S.C.; Posch A.; The design of a quantitative western blot experiment. BioMed Res Int 2014,2014 · DOI
  28. Xue-Shan Z.; Juan P.; Qi W.; Imbalanced cholesterol metabolism in Alzheimer’s disease. Clin Chim Acta 2016,456,107-114 · DOI
  29. Solomon A.; Kåreholt I.; Ngandu T.; Serum cholesterol changes after midlife and late-life cognition: Twenty-one-year follow-up study. Neurology 2007,68(10),751-756 · DOI
  30. Helzner E.P.; Luchsinger J.A.; Scarmeas N.; Contribution of vascular risk factors to the progression in Alzheimer disease. Arch Neurol 2009,66(3),343-348 · DOI
  31. Shepardson N.E.; Shankar G.M.; Selkoe D.J.; Cholesterol level and statin use in Alzheimer disease: I. Review of epidemiological and preclinical studies. Arch Neurol 2011,68(10),1239-1244 · DOI
  32. Longenberger J.; Shah Z.A.; Simvastatin and other HMG-CoA reductase inhibitors on brain cholesterol levels in Alzheimer’s disease. Curr Alzheimer Res 2011,8(4),434-442 · DOI
  33. Lin F.C.; Chuang Y.S.; Hsieh H.M.; Early statin use and the progression of alzheimer disease: A total population-based case-control study. Medicine (Baltimore) 2015,94(47) · DOI
  34. Ismail N.; Ismail M.; Azmi N.H.; Thymoquinone-rich fraction nanoemulsion (TQRFNE) decreases Aβ40 and Aβ42 levels by modulating APP processing, up-regulating IDE and LRP1, and down-regulating BACE1 and RAGE in response to high fat/cholesterol diet-induced rats. Biomed Pharmacother 2017,95,780-788 · DOI
  35. Yin K.; Jin J.; Zhu X.; CART modulates beta-amyloid metabolism-associated enzymes and attenuates memory deficits in APP/PS1 mice. Neurol Res 2017,39(10),885-894 · DOI
  36. Ashok A.; Rai N.K.; Raza W.; Pandey R.; Bandyopadhyay S.; Chronic cerebral hypoperfusion-induced impairment of Aβ clearance requires HB-EGF-dependent sequential activation of HIF1α and MMP9. Neurobiol Dis 2016,95,179-193 · DOI
  37. Donahue J.E.; Flaherty S.L.; Johanson C.E.; RAGE, LRP-1, and amyloid-beta protein in Alzheimer’s disease. Acta Neuropathol 2006,112(4),405-415 · DOI · Paper page
  38. Ma L.Y.; Fei Y.L.; Wang X.Y.; The Research on the Relationship of RAGE, LRP-1, and Aβ Accumulation in the Hippocampus, Prefrontal Lobe, and Amygdala of STZ-Induced Diabetic Rats. J Mol Neurosci 2017,62(1),1-10 · DOI
  39. Moir R.D.; Tanzi R.E.; LRP-mediated clearance of Abeta is inhibited by KPI-containing isoforms of APP. Curr Alzheimer Res 2005,2(2),269-273 · DOI
  40. Sharma H.S.; Castellani R.J.; Smith M.A.; Sharma A.; The blood-brain barrier in Alzheimer’s disease: Novel therapeutic targets and nanodrug delivery. Int Rev Neurobiol 2012,102,47-90 · DOI
  41. Van Gool B.; Storck S.E.; Reekmans S.M.; LRP1 has a predominant role in production over clearance of aβ in a mouse model of alzheimer’s disease. Mol Neurobiol 2019,56(10),7234-7245 · DOI · Paper page
  42. Candela P.; Gosselet F.; Saint-Pol J.; Apical-to-basolateral transport of amyloid-β peptides through blood-brain barrier cells is mediated by the receptor for advanced glycation end-products and is restricted by P-glycoprotein. J Alzheimers Dis 2010,22(3),849-859 · DOI · Paper page
  43. Cui L.; Cai Y.; Cheng W.; A novel, multi-target natural drug candidate, matrine, improves cognitive deficits in alzheimer’s disease transgenic mice by inhibiting aβ aggregation and blocking the rage/aβ axis. Mol Neurobiol 2017,54(3),1939-1952 · DOI
  44. Derk J.; MacLean M.; Juranek J.; Schmidt A.M.; The receptor for advanced glycation endproducts (rage) and mediation of inflammatory neurodegeneration. J Alzheimers Dis Parkinsonism 2018,8(1),421 · DOI · Paper page
  45. Ding B.; Lin C.; Liu Q.; Tanshinone IIA attenuates neuroinflammation via inhibiting RAGE/NF-κB signaling pathway in vivo and in vitro. J Neuroinflammation 2020,17(1),302 · DOI
  46. Fani Maleki A.; Cisbani G.; Plante M.M.; Muramyl dipeptide-mediated immunomodulation on monocyte subsets exerts therapeutic effects in a mouse model of Alzheimer’s disease. J Neuroinflammation 2020,17(1),218 · DOI
  47. Wang H.; Chen F.; Du Y.F.; Targeted inhibition of RAGE reduces amyloid-β influx across the blood-brain barrier and improves cognitive deficits in db/db mice. Neuropharmacology 2018,131,143-153 · DOI
  48. Yan S.D.; Chen X.; Fu J.; RAGE and amyloid-beta peptide neurotoxicity in Alzheimer’s disease. Nature 1996,382(6593),685-691 · DOI · Paper page
  49. Lukose B, Rani P. G82S RAGE polymorphism influences amyloid-RAGE interactions relevant in Alzheimer’s disease pathology. PLoS One C RC2020,15(10) · DOI
  50. Zhang H.; Wang Y.; Yan S.; Genetic deficiency of neuronal RAGE protects against AGE-induced synaptic injury. Cell Death Dis 2014,5(6) · DOI
  51. Wang P.; Huang R.; Lu S.; RAGE and AGEs in mild cognitive impairment of diabetic patients: A cross-sectional study. PLoS One 2016,11(1) · DOI
  52. Wahrle S.E.; Jiang H.; Parsadanian M.; Deletion of Abca1 increases Abeta deposition in the PDAPP transgenic mouse model of Alzheimer disease. J Biol Chem 2005,280(52),43236-43242 · DOI · Paper page
  53. Zhang J.; Liu Q.; Cholesterol metabolism and homeostasis in the brain. Protein Cell 2015,6(4),254-264 · DOI · Paper page
  54. Jiang X.; Guo M.; Su J.; Simvastatin blocks blood-brain barrier disruptions induced by elevated cholesterol both in vivo and in vitro. Int J Alzheimers Dis 2012,2012 · DOI
  55. Loera-Valencia R.; Goikolea J.; Parrado-Fernandez C.; Merino-Serrais P.; Maioli S.; Alterations in cholesterol metabolism as a risk factor for developing Alzheimer’s disease: Potential novel targets for treatment. J Steroid Biochem Mol Biol 2019,190,104-114 · DOI · Paper page
  56. Chang K.W.; Zong H.F.; Ma K.G.; Activation of α7 nicotinic acetylcholine receptor alleviates Aβ-induced neurotoxicity via downregulation of p38 and JNK MAPK signaling pathways. Neurochem Int 2018,120,238-250 · DOI
  57. Yang T.T.; Hsu C.T.; Kuo Y.M.; Cell-derived soluble oligomers of human amyloid-beta peptides disturb cellular homeostasis and induce apoptosis in primary hippocampal neurons. J Neural Transm (Vienna) 2009,116(12),1561-1569 · DOI
  58. Long Z.; Zheng M.; Zhao L.; Valproic acid attenuates neuronal loss in the brain of APP/PS1 double transgenic Alzheimer’s disease mice model. Curr Alzheimer Res 2013,10(3),261-269 · DOI
  59. LaFerla F.M.; Hall C.K.; Ngo L.; Jay G.; Extracellular deposition of beta-amyloid upon p53-dependent neuronal cell death in transgenic mice. J Clin Invest 1996,98(7),1626-1632 · DOI
  60. Zhou L.; Chen D.; Huang X.M.; Wnt5a promotes cortical neuron survival by inhibiting cell-cycle activation. Front Cell Neurosci 2017,11,281 · DOI
  61. Borrell-Pagès M.; Romero J.C.; Badimon L.; LRP5 deficiency down-regulates Wnt signalling and promotes aortic lipid infiltration in hypercholesterolaemic mice. J Cell Mol Med 2015,19(4),770-777 · DOI · Paper page
  62. Liu L.; Wan W.; Xia S.; Kalionis B.; Li Y.; Dysfunctional Wnt/β-catenin signaling contributes to blood-brain barrier breakdown in Alzheimer’s disease. Neurochem Int 2014,75,19-25 · DOI
  63. Vallon M.; Yuki K.; Nguyen T.D.; A RECK-WNT7 receptor-ligand interaction enables isoform-specific regulation of wnt bioavailability. Cell Rep 2018,25(2),339-349.e9 · DOI
  64. Patel M.M.; Behar A.R.; Silasi R.; Role of ADTRP (androgen-dependent tissue factor pathway inhibitor regulating protein) in vascular development and function. J Am Heart Assoc 2018,7(22) · DOI
  65. Li H.F.; Liu J.Y.; Effects of MiR-26a on respiratory distress syndrome in neonatal rats via the wnt/β-catenin signaling pathway. Eur Rev Med Pharmacol Sci 2019,23(6),2525-2531
  66. Azizian-Farsani F.; Abedpoor N.; Hasan Sheikhha M.; Gure A.O.; Nasr-Esfahani M.H.; Ghaedi K.; Receptor for advanced glycation end products acts as a fuel to colorectal cancer development. Front Oncol 2020,10 · DOI

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Metadata

Authors
Zhou, R., Chen, L.-L., Yang, H., Li, L., Liu, J., Chen, L., Hong, W.-J., Wang, C.-G., Ma, J.-J., Huang, J., Zhou, X.-F., Liu, D., & Zhou, H.-D.
Affiliations
  • Department of Orthopedics, The Orthopedic Surgery Center of Chinese PLA, Southwest Hospital, Army Medical University, Chongqing 400042,China
  • Department of Neurology, Daping Hospital, Army Medical University, Chongqing 400042,China
  • Postgraduate School, Bengbu Medical College, Anhui 233004,China
  • School of Pharmacy and Medical Sciences and Sansom Institute, University of South Australia, Adelaide, SA,Australia
  • Laboratory of Field Surgery Institute, Army Medical University, Chongqing 400042,China
Venue
Current Alzheimer Research
Publisher
Bentham Science Publishers Ltd.
Published
2021-05
Volume
18
Issue
5
Pages
428-442
ISSN
1567-2050
DOI
10.2174/1567205018666210906092940
Cited by
43
References
13
Language
en
Funders
  • Excellent Youth Fund of Third Military Medical University (2017YQRC-04)
  • Natural Science Foundation of China (81571258, 81771177)

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