Generic placeholder image

Current Neuropharmacology

Editor-in-Chief

ISSN (Print): 1570-159X
ISSN (Online): 1875-6190

Systematic Review Article

The Role of High Mobility Group Box 1 (HMGB1) in Neurodegeneration: A Systematic Review

Author(s): Fathimath Zaha Ikram, Alina Arulsamy, Thaarvena Retinasamy and Mohd. Farooq Shaikh*

Volume 20, Issue 11, 2022

Published on: 21 April, 2022

Page: [2221 - 2245] Pages: 25

DOI: 10.2174/1570159X20666220114153308

Price: $65

Abstract

Background: High mobility group box 1 (HMGB1) protein is a damage-associated molecular pattern (DAMP) that plays an important role in the repair and regeneration of tissue injury. It also acts as a pro-inflammatory cytokine through the activation of toll-like receptor 4 (TLR4) and receptor for advanced glycation end products (RAGE), to elicit the neuroinflammatory response. HMGB1 may aggravate several cellular responses, which may lead to pathological inflammation and cellular death. Thus, there have been a considerable amount of research into the pathological role of HMGB1 in diseases. However, whether the mechanism of action of HMGB1 is similar in all neurodegenerative disease pathology remains to be determined.

Objective: Therefore, this systematic review aimed to critically evaluate and elucidate the role of HMGB1 in the pathology of neurodegeneration based on the available literature.

Methods: A comprehensive literature search was performed on four databases; EMBASE, PubMed, Scopus, and CINAHL Plus.

Results: A total of 85 articles were selected for critical appraisal, after subjecting to the inclusion and exclusion criteria in this study. The selected articles revealed that HMGB1 levels were found elevated in most neurodegeneration except in Huntington’s disease and Spinocerebellar ataxia, where the levels were found decreased. This review also showcased that HMGB1 may act on distinctive pathways to elicit its pathological response leading to the various neurodegeneration processes/ diseases.

Conclusion: While there have been promising findings in HMGB1 intervention research, further studies may still be required before any HMGB1 intervention may be recommended as a therapeutic target for neurodegenerative diseases.

Keywords: Neurodegenerative disease, externally induced neurodegeneration, RAGE/TLR4, nuclear factor-κB (NFκB) pathway, TNF-α, therapeutic strategies, high mobility group box 1 (HMGB1).

« Previous
Graphical Abstract
[1]
Dumitriu, I.E.; Baruah, P.; Manfredi, A.A.; Bianchi, M.E.; Rovere-Querini, P. HMGB1: guiding immunity from within. Trends Immunol., 2005, 26(7), 381-387.
[http://dx.doi.org/10.1016/j.it.2005.04.009] [PMID: 15978523]
[2]
Paudel, Y.N.; Angelopoulou, E.; Piperi, C.; Othman, I.; Aamir, K.; Shaikh, M.F. Impact of HMGB1, RAGE, and TLR4 in Alzheimer’s disease (AD): from risk factors to therapeutic targeting. Cells, 2020, 9(2), E383.
[http://dx.doi.org/10.3390/cells9020383] [PMID: 32046119]
[3]
Bianchi, M.E.; Agresti, A. HMG proteins: dynamic players in gene regulation and differentiation. Curr. Opin. Genet. Dev., 2005, 15(5), 496-506.
[http://dx.doi.org/10.1016/j.gde.2005.08.007] [PMID: 16102963]
[4]
Vénéreau, E.; Ceriotti, C.; Bianchi, M.E. DAMPs from cell death to new life. Front. Immunol., 2015, 6, 422.
[http://dx.doi.org/10.3389/fimmu.2015.00422] [PMID: 26347745]
[5]
Paudel, Y.N.; Angelopoulou, E.; Piperi, C.; Othman, I.; Shaikh, M.F. Implication of HMGB1 signaling pathways in Amyotrophic lateral sclerosis (ALS): From molecular mechanisms to pre-clinical results. Pharmacol. Res., 2020, 156, 104792.
[http://dx.doi.org/10.1016/j.phrs.2020.104792] [PMID: 32278047]
[6]
Paudel, Y.N.; Angelopoulou, E.; Piperi, C.; Balasubramaniam, V.R.M.T.; Othman, I.; Shaikh, M.F. Enlightening the role of high mobility group box 1 (HMGB1) in inflammation: Updates on receptor signalling. Eur. J. Pharmacol., 2019, 858, 172487.
[http://dx.doi.org/10.1016/j.ejphar.2019.172487] [PMID: 31229535]
[7]
VanPatten, S.; Al-Abed, Y. High Mobility Group Box-1 (HMGb1): current wisdom and advancement as a potential drug target. J. Med. Chem., 2018, 61(12), 5093-5107.
[http://dx.doi.org/10.1021/acs.jmedchem.7b01136] [PMID: 29268019]
[8]
Skaper, S.D.; Facci, L.; Zusso, M.; Giusti, P. An inflammation-centric view of neurological disease: beyond the neuron. Front. Cell. Neurosci., 2018, 12, 72.
[http://dx.doi.org/10.3389/fncel.2018.00072] [PMID: 29618972]
[9]
Furman, D.; Campisi, J.; Verdin, E.; Carrera-Bastos, P.; Targ, S.; Franceschi, C.; Ferrucci, L.; Gilroy, D.W.; Fasano, A.; Miller, G.W.; Mil-ler, A.H.; Mantovani, A.; Weyand, C.M.; Barzilai, N.; Goronzy, J.J.; Rando, T.A.; Effros, R.B.; Lucia, A.; Kleinstreuer, N.; Slavich, G.M. Chronic inflammation in the etiology of disease across the life span. Nat. Med., 2019, 25(12), 1822-1832.
[http://dx.doi.org/10.1038/s41591-019-0675-0] [PMID: 31806905]
[10]
Gao, H-M.; Hong, J-S. Why neurodegenerative diseases are progressive: uncontrolled inflammation drives disease progression. Trends Immunol., 2008, 29(8), 357-365.
[http://dx.doi.org/10.1016/j.it.2008.05.002] [PMID: 18599350]
[11]
Dugger, B.N.; Dickson, D.W. Pathology of neurodegenerative diseases. Cold Spring Harb. Perspect. Biol., 2017, 9(7), a028035.
[http://dx.doi.org/10.1101/cshperspect.a028035] [PMID: 28062563]
[12]
Przedborski, S.; Vila, M.; Jackson-Lewis, V. Neurodegeneration: what is it and where are we? J. Clin. Invest., 2003, 111(1), 3-10.
[http://dx.doi.org/10.1172/JCI200317522] [PMID: 12511579]
[13]
Hou, Y.; Dan, X.; Babbar, M.; Wei, Y.; Hasselbalch, S.G.; Croteau, D.L.; Bohr, V.A. Ageing as a risk factor for neurodegenerative disease. Nat. Rev. Neurol., 2019, 15(10), 565-581.
[http://dx.doi.org/10.1038/s41582-019-0244-7] [PMID: 31501588]
[14]
Wyss-Coray, T.; Mucke, L. Inflammation in neurodegenerative disease--a double-edged sword. Neuron, 2002, 35(3), 419-432.
[http://dx.doi.org/10.1016/S0896-6273(02)00794-8] [PMID: 12165466]
[15]
Garwood, C.J.; Pooler, A.M.; Atherton, J.; Hanger, D.P.; Noble, W. Astrocytes are important mediators of Aβ-induced neurotoxicity and tau phosphorylation in primary culture. Cell Death Dis., 2011, 2(6), e167.
[http://dx.doi.org/10.1038/cddis.2011.50] [PMID: 21633390]
[16]
Kitazawa, M.; Yamasaki, T.R.; LaFerla, F.M. Microglia as a potential bridge between the amyloid beta-peptide and tau. Ann. N. Y. Acad. Sci., 2004, 1035, 85-103.
[http://dx.doi.org/10.1196/annals.1332.006] [PMID: 15681802]
[17]
Lema Tomé, C.M.; Tyson, T.; Rey, N.L.; Grathwohl, S.; Britschgi, M.; Brundin, P. Inflammation and α-synuclein’s prion-like behavior in Parkinson’s disease--is there a link? Mol. Neurobiol., 2013, 47(2), 561-574.
[http://dx.doi.org/10.1007/s12035-012-8267-8] [PMID: 22544647]
[18]
Kempuraj, D.; Thangavel, R.; Natteru, P.A.; Selvakumar, G.P.; Saeed, D.; Zahoor, H.; Zaheer, S.; Iyer, S.S.; Zaheer, A. Neuroinflammation induces neurodegeneration. J. Neurol. Neurosurg. Spine., 2016, 1(1), 1003.
[PMID: 28127589]
[19]
Moher, D.; Shamseer, L.; Clarke, M.; Ghersi, D.; Liberati, A.; Petticrew, M.; Shekelle, P.; Stewart, L.A. Preferred reporting items for sys-tematic review and meta-analysis protocols (PRISMA-P) 2015 statement. Syst. Rev., 2015, 4(1), 1.
[http://dx.doi.org/10.1186/2046-4053-4-1] [PMID: 25554246]
[20]
Project, EPHP Quality assessment tool for quantitative studies., 1998.
[21]
Hooijmans, C.R.; Rovers, M.M.; de Vries, R.B.M.; Leenaars, M.; Ritskes-Hoitinga, M.; Langendam, M.W. SYRCLE’s risk of bias tool for animal studies. BMC Med. Res. Methodol., 2014, 14(1), 43.
[http://dx.doi.org/10.1186/1471-2288-14-43] [PMID: 24667063]
[22]
Festoff, B.W.; Sajja, R.K.; van Dreden, P.; Cucullo, L. HMGB1 and thrombin mediate the blood-brain barrier dysfunction acting as bi-omarkers of neuroinflammation and progression to neurodegeneration in Alzheimer’s disease. J. Neuroinflammation, 2016, 13(1), 194.
[http://dx.doi.org/10.1186/s12974-016-0670-z] [PMID: 27553758]
[23]
Minjarez, B.; Calderón-González, K.G.; Rustarazo, M.L.V.; Herrera-Aguirre, M.E.; Labra-Barrios, M.L.; Rincon-Limas, D.E.; Del Pino, M.M.; Mena, R.; Luna-Arias, J.P. Identification of proteins that are differentially expressed in brains with Alzheimer’s disease using iTRAQ labeling and tandem mass spectrometry. J. Proteomics, 2016, 139, 103-121.
[http://dx.doi.org/10.1016/j.jprot.2016.03.022] [PMID: 27012543]
[24]
Takata, K.; Takada, T.; Ito, A.; Asai, M.; Tawa, M.; Saito, Y.; Ashihara, E.; Tomimoto, H.; Kitamura, Y.; Shimohama, S. Microglial Amy-loid-β1-40 Phagocytosis Dysfunction Is Caused by High-Mobility Group Box Protein-1: Implications for the Pathological Progression of Alzheimer’s Disease. Int. J. Alzheimers Dis., 2012, 2012, 685739.
[http://dx.doi.org/10.1155/2012/685739] [PMID: 22645697]
[25]
Takata, K.; Kitamura, Y.; Kakimura, J.; Shibagaki, K.; Tsuchiya, D.; Taniguchi, T.; Smith, M.A.; Perry, G.; Shimohama, S. Role of high mobility group protein-1 (HMG1) in amyloid-beta homeostasis. Biochem. Biophys. Res. Commun., 2003, 301(3), 699-703.
[http://dx.doi.org/10.1016/S0006-291X(03)00024-X] [PMID: 12565837]
[26]
Nilson, A.N.; English, K.C.; Gerson, J.E.; Barton Whittle, T.; Nicolas Crain, C.; Xue, J.; Sengupta, U.; Castillo-Carranza, D.L.; Zhang, W.; Gupta, P.; Kayed, R. Tau oligomers associate with inflammation in the brain and retina of tauopathy mice and in neurodegenerative dis-eases. J. Alzheimers Dis., 2017, 55(3), 1083-1099.
[http://dx.doi.org/10.3233/JAD-160912] [PMID: 27716675]
[27]
Fujita, K.; Motoki, K.; Tagawa, K.; Chen, X.; Hama, H.; Nakajima, K.; Homma, H.; Tamura, T.; Watanabe, H.; Katsuno, M.; Matsumi, C.; Kajikawa, M.; Saito, T.; Saido, T.; Sobue, G.; Miyawaki, A.; Okazawa, H. HMGB1, a pathogenic molecule that induces neurite degenera-tion via TLR4-MARCKS, is a potential therapeutic target for Alzheimer’s disease. Sci. Rep., 2016, 6(1), 31895.
[http://dx.doi.org/10.1038/srep31895] [PMID: 27557632]
[28]
Kong, Z.H.; Chen, X.; Hua, H.P.; Liang, L.; Liu, L.J. The oral pretreatment of glycyrrhizin prevents surgery-induced cognitive impairment in aged mice by reducing neuroinflammation and Alzheimer’s-related pathology via HMGB1 inhibition. J. Mol. Neurosci., 2017, 63(3-4), 385-395.
[http://dx.doi.org/10.1007/s12031-017-0989-7] [PMID: 29034441]
[29]
Lee, Y-S.; Choi, J-Y.; Mankhong, S.; Moon, S.; Kim, S.; Koh, Y.H.; Kim, J.H.; Kang, J.H. Sirtuin 1-dependent regulation of high mobility box 1 in hypoxia-reoxygenated brain microvascular endothelial cells: roles in neuronal amyloidogenesis. Cell Death Dis., 2020, 11(12), 1072.
[http://dx.doi.org/10.1038/s41419-020-03293-0] [PMID: 33318474]
[30]
Meneghini, V.; Bortolotto, V.; Francese, M.T.; Dellarole, A.; Carraro, L.; Terzieva, S.; Grilli, M. High-mobility group box-1 protein and β-amyloid oligomers promote neuronal differentiation of adult hippocampal neural progenitors via receptor for advanced glycation end products/nuclear factor-κB axis: relevance for Alzheimer’s disease. J. Neurosci., 2013, 33(14), 6047-6059.
[http://dx.doi.org/10.1523/JNEUROSCI.2052-12.2013] [PMID: 23554486]
[31]
Nan, K.; Han, Y.; Fang, Q.; Huang, C.; Yu, L.; Ge, W.; Xiang, F.; Tao, Y.X.; Cao, H.; Li, J. HMGB1 gene silencing inhibits neuroinflamma-tion via down-regulation of NF-κB signaling in primary hippocampal neurons induced by Aβ25-35. Int. Immunopharmacol., 2019, 67, 294-301.
[http://dx.doi.org/10.1016/j.intimp.2018.12.027] [PMID: 30572254]
[32]
Oh, S.; Son, M.; Choi, J.; Lee, S.; Byun, K. sRAGE prolonged stem cell survival and suppressed RAGE-related inflammatory cell and T lymphocyte accumulations in an Alzheimer’s disease model. Biochem. Biophys. Res. Commun., 2018, 495(1), 807-813.
[http://dx.doi.org/10.1016/j.bbrc.2017.11.035] [PMID: 29127006]
[33]
Takata, K.; Kitamura, Y.; Tsuchiya, D.; Kawasaki, T.; Taniguchi, T.; Shimohama, S. High mobility group box protein-1 inhibits microglial Abeta clearance and enhances Abeta neurotoxicity. J. Neurosci. Res., 2004, 78(6), 880-891.
[http://dx.doi.org/10.1002/jnr.20340] [PMID: 15499593]
[34]
Zhang, J.; Hua, X.F.; Gu, J.; Chen, F.; Gu, J.; Gong, C.X.; Liu, F.; Dai, C.L. High mobility group box 1 ameliorates cognitive impairment in the 3×Tg-AD mouse model. J. Alzheimers Dis., 2020, 74(3), 851-864.
[http://dx.doi.org/10.3233/JAD-191110] [PMID: 32116254]
[35]
Zhang, Y.Y.; Bao, H.L.; Dong, L.X.; Liu, Y.; Zhang, G.W.; An, F.M. Silenced lncRNA H19 and up-regulated microRNA-129 accelerates viability and restrains apoptosis of PC12 cells induced by Aβ25-35 in a cellular model of Alzheimer’s disease. Cell Cycle, 2021, 20(1), 112-125.
[http://dx.doi.org/10.1080/15384101.2020.1863681] [PMID: 33410377]
[36]
Zhang, Z.; Liu, H.; Zhao, Z.; Zang, C.; Ju, C.; Li, F.; Wang, L.; Yang, H.; Bao, X.; Yu, Y.; Yao, X.; Zhang, D. GJ-4 alleviates Aβ25-35-induced memory dysfunction in mice through protecting the neurovascular unit. Biomed. Pharmacother., 2020, 127, 110131.
[http://dx.doi.org/10.1016/j.biopha.2020.110131] [PMID: 32325348]
[37]
Zhou, Z.; Hou, J.; Mo, Y.; Ren, M.; Yang, G.; Qu, Z.; Hu, Y. Geniposidic acid ameliorates spatial learning and memory deficits and allevi-ates neuroinflammation via inhibiting HMGB-1 and downregulating TLR4/2 signaling pathway in APP/PS1 mice. Eur. J. Pharmacol., 2020, 869, 172857.
[http://dx.doi.org/10.1016/j.ejphar.2019.172857] [PMID: 31837991]
[38]
Jang, A.; Liew, H.; Kim, Y.M.; Choi, H.; Kim, S.; Lee, S.H.; Ohshima, T.; Mikoshiba, K.; Suh, Y.H. p35 deficiency accelerates HMGB-1-mediated neuronal death in the early stages of an Alzheimer’s disease mouse model. Curr. Alzheimer Res., 2013, 10(8), 829-843.
[http://dx.doi.org/10.2174/15672050113109990135] [PMID: 23905994]
[39]
Yang, Y.; Han, C.; Guo, L.; Guan, Q. High expression of the HMGB1-TLR4 axis and its downstream signaling factors in patients with Parkinson’s disease and the relationship of pathological staging. Brain Behav., 2018, 8(4), e00948.
[http://dx.doi.org/10.1002/brb3.948] [PMID: 29670828]
[40]
Santoro, M.; Maetzler, W.; Stathakos, P.; Martin, H.L.; Hobert, M.A.; Rattay, T.W.; Gasser, T.; Forrester, J.V.; Berg, D.; Tracey, K.J.; Riedel, G.; Teismann, P. In-vivo evidence that high mobility group box 1 exerts deleterious effects in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine model and Parkinson’s disease which can be attenuated by glycyrrhizin. Neurobiol. Dis., 2016, 91, 59-68.
[http://dx.doi.org/10.1016/j.nbd.2016.02.018] [PMID: 26921471]
[41]
Gan, P.; Ding, L.; Hang, G.; Xia, Q.; Huang, Z.; Ye, X.; Qian, X. Oxymatrine attenuates dopaminergic neuronal damage and microglia-mediated neuroinflammation through cathepsin D-dependent HMGB1/TLR4/NF-κB pathway in Parkinson’s disease. Front. Pharmacol., 2020, 11, 776.
[http://dx.doi.org/10.3389/fphar.2020.00776] [PMID: 32528295]
[42]
Gao, H-M.; Zhou, H.; Zhang, F.; Wilson, B.C.; Kam, W.; Hong, J-S. HMGB1 acts on microglia Mac1 to mediate chronic neuroinflamma-tion that drives progressive neurodegeneration. J. Neurosci., 2011, 31(3), 1081-1092.
[http://dx.doi.org/10.1523/JNEUROSCI.3732-10.2011] [PMID: 21248133]
[43]
Huang, J.; Yang, J.; Shen, Y.; Jiang, H.; Han, C.; Zhang, G.; Liu, L.; Xu, X.; Li, J.; Lin, Z.; Xiong, N.; Zhang, Z.; Xiong, J.; Wang, T. HMGB1 mediates autophagy dysfunction via perturbing Beclin1-Vps34 complex in dopaminergic cell model. Front. Mol. Neurosci., 2017, 10(13), 13.
[http://dx.doi.org/10.3389/fnmol.2017.00013] [PMID: 28197072]
[44]
Huang, M.; Guo, M.; Wang, K.; Wu, K.; Li, Y.; Tian, T.; Wang, Y.; Yan, W.; Zhou, Z.; Yang, H. HMGB1 mediates paraquat-induced neu-roinflammatory responses via activating RAGE signaling pathway. Neurotox. Res., 2020, 37(4), 913-925.
[http://dx.doi.org/10.1007/s12640-019-00148-1] [PMID: 31858421]
[45]
Kim, S.J.; Ryu, M.J.; Han, J.; Jang, Y.; Lee, M.J.; Ju, X.; Ryu, I.; Lee, Y.L.; Oh, E.; Chung, W.; Heo, J.Y.; Kweon, G.R. Non-cell autonomous modulation of tyrosine hydroxylase by HMGB1 released from astrocytes in an acute MPTP-induced Parkinsonian mouse model. Lab. Invest., 2019, 99(9), 1389-1399.
[http://dx.doi.org/10.1038/s41374-019-0254-5] [PMID: 31043679]
[46]
Lv, R.; Du, L.; Liu, X.; Zhou, F.; Zhang, Z.; Zhang, L. Rosmarinic acid attenuates inflammatory responses through inhibiting HMGB1/TLR4/NF-κB signaling pathway in a mouse model of Parkinson’s disease. Life Sci., 2019, 223, 158-165.
[http://dx.doi.org/10.1016/j.lfs.2019.03.030] [PMID: 30880023]
[47]
Sasaki, T.; Liu, K.; Agari, T.; Yasuhara, T.; Morimoto, J.; Okazaki, M.; Takeuchi, H.; Toyoshima, A.; Sasada, S.; Shinko, A.; Kondo, A.; Kameda, M.; Miyazaki, I.; Asanuma, M.; Borlongan, C.V.; Nishibori, M.; Date, I. Anti-high mobility group box 1 antibody exerts neuro-protection in a rat model of Parkinson’s disease. Exp. Neurol., 2016, 275(Pt 1), 220-231.
[http://dx.doi.org/10.1016/j.expneurol.2015.11.003] [PMID: 26555088]
[48]
Guan, Y.; Li, Y.; Zhao, G.; Li, Y. HMGB1 promotes the starvation-induced autophagic degradation of α-synuclein in SH-SY5Y cells Atg 5-dependently. Life Sci., 2018, 202, 1-10.
[http://dx.doi.org/10.1016/j.lfs.2018.03.031] [PMID: 29551576]
[49]
Tian, Y.; Cao, Y.; Chen, R.; Jing, Y.; Xia, L.; Zhang, S. HMGB1 A box protects neurons by potently inhibiting both microglia and T cell-mediated inflammation in a mouse Parkinson’s disease model. Clin. Sci. (Lond.), 2020, 134(15), 2075-2090.
[http://dx.doi.org/10.1042/CS20200553] [PMID: 32706028]
[50]
Lindersson, E.K. Højrup, P.; Gai, W.P.; Locker, D.; Martin, D.; Jensen, P.H. α-Synuclein filaments bind the transcriptional regulator HMGB-1. Neuroreport, 2004, 15(18), 2735-2739.
[PMID: 15597044]
[51]
Goula, A.V.; Berquist, B.R.; Wilson, D.M., III; Wheeler, V.C.; Trottier, Y.; Merienne, K. Stoichiometry of base excision repair proteins correlates with increased somatic CAG instability in striatum over cerebellum in Huntington’s disease transgenic mice. PLoS Genet., 2009, 5(12), e1000749.
[http://dx.doi.org/10.1371/journal.pgen.1000749] [PMID: 19997493]
[52]
Kalathur, R.K.; Giner-Lamia, J.; Machado, S.; Barata, T.; Ayasolla, K.R.; Futschik, M.E. The unfolded protein response and its potential role in Huntington’s disease elucidated by a systems biology approach. F1000 Res., 2015, 4, 103.
[http://dx.doi.org/10.12688/f1000research.6358.1] [PMID: 26949515]
[53]
Son, S.; Bowie, L.E.; Maiuri, T.; Hung, C.L.K.; Desmond, C.R.; Xia, J.; Truant, R. High-mobility group box 1 links sensing of reactive oxygen species by huntingtin to its nuclear entry. J. Biol. Chem., 2019, 294(6), 1915-1923.
[http://dx.doi.org/10.1074/jbc.RA117.001440] [PMID: 30538129]
[54]
Min, H.J.; Ko, E.A.; Wu, J.; Kim, E.S.; Kwon, M.K.; Kwak, M.S.; Choi, J.E.; Lee, J.E.; Shin, J.S. Chaperone-like activity of high-mobility group box 1 protein and its role in reducing the formation of polyglutamine aggregates. J. Immunol., 2013, 190(4), 1797-1806.
[http://dx.doi.org/10.4049/jimmunol.1202472] [PMID: 23303669]
[55]
Qi, M.L.; Tagawa, K.; Enokido, Y.; Yoshimura, N.; Wada, Y.; Watase, K.; Ishiura, S.; Kanazawa, I.; Botas, J.; Saitoe, M.; Wanker, E.E.; Okazawa, H. Proteome analysis of soluble nuclear proteins reveals that HMGB1/2 suppress genotoxic stress in polyglutamine diseases. Nat. Cell Biol., 2007, 9(4), 402-414.
[http://dx.doi.org/10.1038/ncb1553] [PMID: 17384639]
[56]
Hwang, C.S.; Liu, G.T.; Chang, M.D.; Liao, I.L.; Chang, H.T. Elevated serum autoantibody against high mobility group box 1 as a potent surrogate biomarker for amyotrophic lateral sclerosis. Neurobiol. Dis., 2013, 58, 13-18.
[http://dx.doi.org/10.1016/j.nbd.2013.04.013] [PMID: 23639787]
[57]
Juranek, J.K.; Daffu, G.K.; Wojtkiewicz, J.; Lacomis, D.; Kofler, J.; Schmidt, A.M. Receptor for advanced glycation end products and its inflammatory ligands are upregulated in amyotrophic lateral sclerosis. Front. Cell. Neurosci., 2015, 9, 485.
[http://dx.doi.org/10.3389/fncel.2015.00485] [PMID: 26733811]
[58]
Casula, M.; Iyer, A.M.; Spliet, W.G.; Anink, J.J.; Steentjes, K.; Sta, M.; Troost, D.; Aronica, E. Toll-like receptor signaling in amyotrophic lateral sclerosis spinal cord tissue. Neuroscience, 2011, 179, 233-243.
[http://dx.doi.org/10.1016/j.neuroscience.2011.02.001] [PMID: 21303685]
[59]
Lee, J.D.; Liu, N.; Levin, S.C.; Ottosson, L.; Andersson, U.; Harris, H.E.; Woodruff, T.M. Therapeutic blockade of HMGB1 reduces early motor deficits, but not survival in the SOD1G93A mouse model of amyotrophic lateral sclerosis. J. Neuroinflammation, 2019, 16(1), 45.
[http://dx.doi.org/10.1186/s12974-019-1435-2] [PMID: 30782181]
[60]
Lo Coco, D.; Veglianese, P.; Allievi, E.; Bendotti, C. Distribution and cellular localization of high mobility group box protein 1 (HMGB1) in the spinal cord of a transgenic mouse model of ALS. Neurosci. Lett., 2007, 412(1), 73-77.
[http://dx.doi.org/10.1016/j.neulet.2006.10.063] [PMID: 17196331]
[61]
Meyer, M.; Lara, A.; Hunt, H.; Belanoff, J.; de Kloet, E.R.; Gonzalez Deniselle, M.C.; De Nicola, A.F. The selective glucocorticoid receptor modulator cort 113176 reduces neurodegeneration and neuroinflammation in wobbler mice spinal cord. Neuroscience, 2018, 384, 384-396.
[http://dx.doi.org/10.1016/j.neuroscience.2018.05.042] [PMID: 29890290]
[62]
Brambilla, L.; Martorana, F.; Guidotti, G.; Rossi, D. Dysregulation of astrocytic HMGB1 signaling in amyotrophic lateral sclerosis. Front. Neurosci., 2018, 12, 622.
[http://dx.doi.org/10.3389/fnins.2018.00622] [PMID: 30210286]
[63]
Gomes, C.; Cunha, C.; Nascimento, F.; Ribeiro, J.A.; Vaz, A.R.; Brites, D. Cortical neurotoxic astrocytes with early ALS pathology and miR-146a deficit replicate gliosis markers of symptomatic SOD1G93A mouse model. Mol. Neurobiol., 2019, 56(3), 2137-2158.
[http://dx.doi.org/10.1007/s12035-018-1220-8] [PMID: 29995256]
[64]
Lee, J.D.; McDonald, T.S.; Fung, J.N.T.; Woodruff, T.M. Absence of receptor for advanced glycation end product (RAGE) reduces in-flammation and extends survival in the hSOD1G93A mouse model of amyotrophic lateral sclerosis. Mol. Neurobiol., 2020, 57(10), 4143-4155.
[http://dx.doi.org/10.1007/s12035-020-02019-9] [PMID: 32676989]
[65]
Lee, J.Y.; Lee, J.D.; Phipps, S.; Noakes, P.G.; Woodruff, T.M. Absence of toll-like receptor 4 (TLR4) extends survival in the hSOD1 G93A mouse model of amyotrophic lateral sclerosis. J. Neuroinflammation, 2015, 12, 90.
[http://dx.doi.org/10.1186/s12974-015-0310-z] [PMID: 25962427]
[66]
Cunha, C.; Santos, C.; Gomes, C.; Fernandes, A.; Correia, A.M.; Sebastião, A.M.; Vaz, A.R.; Brites, D. Downregulated glia interplay and increased miRNA-155 as promising markers to track ALS at an early stage. Mol. Neurobiol., 2018, 55(5), 4207-4224.
[PMID: 28612258]
[67]
Andersson, A.; Covacu, R.; Sunnemark, D.; Danilov, A.I.; Dal Bianco, A.; Khademi, M.; Wallström, E.; Lobell, A.; Brundin, L.; Lass-mann, H.; Harris, R.A. Pivotal advance: HMGB1 expression in active lesions of human and experimental multiple sclerosis. J. Leukoc. Biol., 2008, 84(5), 1248-1255.
[http://dx.doi.org/10.1189/jlb.1207844] [PMID: 18644848]
[68]
Asouri, M.; Alinejad Rokni, H.; Sahraian, M.A.; Fattahi, S.; Motamed, N.; Doosti, R.; Rahimi, H.; Lotfi, M.; Moslemi, A.; Karimpoor, M.; Mahboudi, F.; Akhavan-Niaki, H. Analysis of single nucleotide polymorphisms in HLA-DRA, IL2RA, and HMGB1 genes in multiple scle-rosis. Rep. Biochem. Mol. Biol., 2020, 9(2), 198-208.
[http://dx.doi.org/10.29252/rbmb.9.2.199] [PMID: 33178870]
[69]
Bucova, M.; Majernikova, B.; Durmanova, V.; Cudrakova, D.; Gmitterova, K.; Lisa, I.; Klimova, E.; Kluckova, K.; Buc, M. HMGB1 as a potential new marker of disease activity in patients with multiple sclerosis. Neurol. Sci., 2020, 41(3), 599-604.
[http://dx.doi.org/10.1007/s10072-019-04136-3] [PMID: 31728855]
[70]
D’Angelo, C.; Reale, M.; Costantini, E.; Di Nicola, M.; Porfilio, I.; de Andrés, C.; Fernández-Paredes, L.; Sánchez-Ramón, S.; Pasquali, L. 9(JUN), 1240.
[http://dx.doi.org/10.3389/fimmu.2018.01240] [PMID: 29915590]
[71]
Glasnović A.; Cvija, H.; Stojić M.; Tudorić-Đeno, I.; Ivčević S.; Romić D.; Tičinović N.; Vuletić V.; Lazibat, I.; Grčević D. Decreased level of sRAGE in the cerebrospinal fluid of multiple sclerosis patients at clinical onset. Neuroimmunomodulation, 2014, 21(5), 226-233.
[http://dx.doi.org/10.1159/000357002] [PMID: 24603633]
[72]
Hamid, K.M.; Nejati, A.; Shoja, Z.; Mollaei-Kandelousd, Y.; Doosti, R.; Mirshafiey, A.; Tafakhori, A.; Sahraian, M.A.; Marashi, S.M. Quantitative Evaluation of BAFF, HMGB1, TLR 4 AND TLR 7 Expression in Patients with Relapsing Remitting Multiple Sclerosis. Iran. J. Allergy Asthma Immunol., 2016, 15(1), 75-81.
[PMID: 26996115]
[73]
Malhotra, S.; Fissolo, N.; Tintoré, M.; Wing, A.C.; Castilló, J.; Vidal-Jordana, A.; Montalban, X.; Comabella, M. Role of high mobility group box protein 1 (HMGB1) in peripheral blood from patients with multiple sclerosis. J. Neuroinflammation, 2015, 12, 48.
[http://dx.doi.org/10.1186/s12974-015-0269-9] [PMID: 25879961]
[74]
Nasi, M.; Bianchini, E.; De Biasi, S.; Gibellini, L.; Neroni, A.; Mattioli, M.; Pinti, M.; Iannone, A.; Mattioli, A.V.; Simone, A.M.; Ferraro, D.; Vitetta, F.; Sola, P.; Cossarizza, A. Increased plasma levels of mitochondrial DNA and pro-inflammatory cytokines in patients with progressive multiple sclerosis. J. Neuroimmunol., 2020, 338, 577107.
[http://dx.doi.org/10.1016/j.jneuroim.2019.577107] [PMID: 31726376]
[75]
Sternberg, Z.; Sternberg, D.; Chichelli, T.; Drake, A.; Patel, N.; Kolb, C.; Chadha, K.; Yu, J.; Hojnacki, D. High-mobility group box 1 in multiple sclerosis. Immunol. Res., 2016, 64(2), 385-391.
[http://dx.doi.org/10.1007/s12026-015-8673-x] [PMID: 26100980]
[76]
Sternberg, Z.; Kolb, C.; Chadha, K.; Nir, A.; Nir, R.; George, R.; Johnson, J.; Yu, J.; Hojnacki, D. Fingolimod anti-inflammatory and neu-roprotective effects modulation of RAGE axis in multiple sclerosis patients. Neuropharmacology, 2018, 130, 71-76.
[http://dx.doi.org/10.1016/j.neuropharm.2017.11.047] [PMID: 29197515]
[77]
Wang, H.; Wang, K.; Wang, C.; Xu, F.; Zhong, X.; Qiu, W.; Hu, X. Cerebrospinal fluid high-mobility group box protein 1 in neuromyelitis optica and multiple sclerosis. Neuroimmunomodulation, 2013, 20(2), 113-118.
[http://dx.doi.org/10.1159/000345994] [PMID: 23328212]
[78]
Wang, K.C.; Tsai, C.P.; Lee, C.L.; Chen, S.Y.; Chin, L.T.; Chen, S.J. Elevated plasma high-mobility group box 1 protein is a potential marker for neuromyelitis optica. Neuroscience, 2012, 226, 510-516.
[http://dx.doi.org/10.1016/j.neuroscience.2012.08.041] [PMID: 23122444]
[79]
Bucova, M.; Durmanova, V.; Cudrakova, D.; Blazickova, S.; Gmitterova, K.; Klimova, E.; Lisa, I.; Kluckova, K.; Majernikova, B. De-creased plasma levels of 25(OH)D in multiple sclerosis patients. Correlation with disease severity expressed by EDSS, MSSS, progression index and Herbert’s scale severity grade. Bratisl. Lek Listy, 2019, 120(10), 723-729.
[http://dx.doi.org/10.4149/BLL_2019_120] [PMID: 31663345]
[80]
Uzawa, A.; Mori, M.; Masuda, S.; Muto, M.; Kuwabara, S. CSF high-mobility group box 1 is associated with intrathecal inflammation and astrocytic damage in neuromyelitis optica. J. Neurol. Neurosurg. Psychiatry, 2013, 84(5), 517-522.
[http://dx.doi.org/10.1136/jnnp-2012-304039] [PMID: 23255728]
[81]
Nicaise, A.M.; Wagstaff, L.J.; Willis, C.M.; Paisie, C.; Chandok, H.; Robson, P.; Fossati, V.; Williams, A.; Crocker, S.J. Cellular senescence in progenitor cells contributes to diminished remyelination potential in progressive multiple sclerosis. Proc. Natl. Acad. Sci. USA, 2019, 116(18), 9030-9039.
[http://dx.doi.org/10.1073/pnas.1818348116] [PMID: 30910981]
[82]
Chu, Y.; Jing, Y.; Zhao, X.; Wang, M.; Zhang, M.; Ma, R.; Ma, W.; Lv, Y.; Zhu, L. Modulation of the HMGB1/TLR4/NF-κB signaling pathway in the CNS by matrine in experimental autoimmune encephalomyelitis. J. Neuroimmunol., 2021, 352, 577480.
[http://dx.doi.org/10.1016/j.jneuroim.2021.577480] [PMID: 33493985]
[83]
Djedović N.; Stanisavljevic, S.; Jevtić B.; Momčilović M.; Lavrnja, I.; Miljković D. Anti-encephalitogenic effects of ethyl pyruvate are reflected in the central nervous system and the gut. Biomed. Pharmacother., 2017, 96, 78-85.
[http://dx.doi.org/10.1016/j.biopha.2017.09.110] [PMID: 28965011]
[84]
Latha, T.S.; Lomada, D.; Dharani, P.K.; Muthukonda, S.V.; Reddy, M.C. Ti-O based nanomaterials ameliorate experimental autoimmune encephalomyelitis and collagen-induced arthritis. RSC Advances, 2016, 6(11), 8870-8880.
[http://dx.doi.org/10.1039/C5RA18974H]
[85]
Robinson, A.P.; Caldis, M.W.; Harp, C.T.; Goings, G.E.; Miller, S.D. High-mobility group box 1 protein (HMGB1) neutralization amelio-rates experimental autoimmune encephalomyelitis. J. Autoimmun., 2013, 43, 32-43.
[http://dx.doi.org/10.1016/j.jaut.2013.02.005] [PMID: 23514872]
[86]
Sun, Y.; Chen, H.; Dai, J.; Wan, Z.; Xiong, P.; Xu, Y.; Han, Z.; Chai, W.; Gong, F.; Zheng, F. Glycyrrhizin protects mice against experi-mental autoimmune encephalomyelitis by inhibiting high-mobility group box 1 (HMGB1) expression and neuronal HMGB1 release. Front. Immunol., 2018, 9, 1518.
[http://dx.doi.org/10.3389/fimmu.2018.01518] [PMID: 30013568]
[87]
Sun, Y.; Chen, H.; Dai, J.; Zou, H.; Gao, M.; Wu, H.; Ming, B.; Lai, L.; Xiao, Y.; Xiong, P.; Xu, Y.; Gong, F.; Zheng, F. HMGB1 expres-sion patterns during the progression of experimental autoimmune encephalomyelitis. J. Neuroimmunol., 2015, 280, 29-35.
[http://dx.doi.org/10.1016/j.jneuroim.2015.02.005] [PMID: 25773152]
[88]
Uzawa, A.; Mori, M.; Masuda, H.; Ohtani, R.; Uchida, T.; Kuwabara, S. Recombinant thrombomodulin ameliorates experimental autoim-mune encephalomyelitis by suppressing high mobility group box 1 and inflammatory cytokines. Clin. Exp. Immunol., 2018, 193(1), 47-54.
[http://dx.doi.org/10.1111/cei.13123] [PMID: 29509323]
[89]
Uzawa, A.; Mori, M.; Taniguchi, J.; Masuda, S.; Muto, M.; Kuwabara, S. Anti-high mobility group box 1 monoclonal antibody ameliorates experimental autoimmune encephalomyelitis. Clin. Exp. Immunol., 2013, 172(1), 37-43.
[http://dx.doi.org/10.1111/cei.12036] [PMID: 23480183]
[90]
Ito, H.; Fujita, K.; Tagawa, K.; Chen, X.; Homma, H.; Sasabe, T.; Shimizu, J.; Shimizu, S.; Tamura, T.; Muramatsu, S.; Okazawa, H. HMGB1 facilitates repair of mitochondrial DNA damage and extends the lifespan of mutant ataxin-1 knock-in mice. EMBO Mol. Med., 2015, 7(1), 78-101.
[http://dx.doi.org/10.15252/emmm.201404392] [PMID: 25510912]
[91]
Lee, L.C.; Chen, C.M.; Wang, P.R.; Su, M.T.; Lee-Chen, G.J.; Chang, C.Y. Role of high mobility group box 1 (HMGB1) in SCA17 patho-genesis. PLoS One, 2014, 9(12), e115809.
[http://dx.doi.org/10.1371/journal.pone.0115809] [PMID: 25549101]
[92]
Abu El-Asrar, A.M.; Nawaz, M.I.; Siddiquei, M.M.; Al-Kharashi, A.S.; Kangave, D.; Mohammad, G. High-mobility group box-1 induces decreased brain-derived neurotrophic factor-mediated neuroprotection in the diabetic retina. Mediators Inflamm., 2013, 2013, 863036.
[http://dx.doi.org/10.1155/2013/863036] [PMID: 23766563]
[93]
Busch, S.; Wu, L.; Feng, Y.; Gretz, N.; Hoffmann, S.; Hammes, H.P. Alzheimer’s disease and retinal neurodegeneration share a consistent stress response of the neurovascular unit. Cell. Physiol. Biochem., 2012, 30(6), 1436-1443.
[http://dx.doi.org/10.1159/000343331] [PMID: 23171816]
[94]
Böhm, M.R.; Schallenberg, M.; Brockhaus, K.; Melkonyan, H.; Thanos, S. The pro-inflammatory role of high-mobility group box 1 pro-tein (HMGB-1) in photoreceptors and retinal explants exposed to elevated pressure. Lab. Invest., 2016, 96(4), 409-427.
[http://dx.doi.org/10.1038/labinvest.2015.156] [PMID: 26779828]
[95]
Ross, B.X.; Choi, J.; Yao, J.; Hager, H.M.; Abcouwer, S.F.; Zacks, D.N. Loss of high-mobility group box 1 (HMGB1) protein in rods ac-celerates rod photoreceptor degeneration after retinal detachment. Invest. Ophthalmol. Vis. Sci., 2020, 61(5), 50.
[http://dx.doi.org/10.1167/iovs.61.5.50] [PMID: 32460314]
[96]
Sakamoto, K.; Okuwaki, T.; Ushikubo, H.; Mori, A.; Nakahara, T.; Ishii, K. Activation inhibitors of nuclear factor kappa B protect neurons against the NMDA-induced damage in the rat retina. J. Pharmacol. Sci., 2017, S1347-8613(17), 30162-30167.
[http://dx.doi.org/10.1016/j.jphs.2017.09.031] [PMID: 29110956]
[97]
Das, S.; Mishra, K.P.; Ganju, L.; Singh, S.B. Andrographolide - A promising therapeutic agent, negatively regulates glial cell derived neu-rodegeneration of prefrontal cortex, hippocampus and working memory impairment. J. Neuroimmunol., 2017, 313, 161-175.
[http://dx.doi.org/10.1016/j.jneuroim.2017.11.003] [PMID: 29146293]
[98]
Das, S.; Mishra, K.P.; Chanda, S.; Ganju, L.; Singh, S.B. CXCR7: A key neuroprotective molecule against alarmin HMGB1 mediated CNS pathophysiology and subsequent memory impairment. Brain Behav. Immun., 2019, 82, 319-337.
[http://dx.doi.org/10.1016/j.bbi.2019.09.003] [PMID: 31505255]
[99]
Das, S.; Mishra, K.P.; Ganju, L.; Singh, S.B. Intranasally delivered small interfering RNA-mediated suppression of scavenger receptor Mac-1 attenuates microglial phenotype switching and working memory impairment following hypoxia. Neuropharmacology, 2018, 137, 240-255.
[http://dx.doi.org/10.1016/j.neuropharm.2018.05.002] [PMID: 29738851]
[100]
Gasparotto, J.; Girardi, C.S.; Somensi, N.; Ribeiro, C.T.; Moreira, J.C.F.; Michels, M.; Sonai, B.; Rocha, M.; Steckert, A.V.; Barichello, T.; Quevedo, J.; Dal-Pizzol, F.; Gelain, D.P. Receptor for advanced glycation end products mediates sepsis-triggered amyloid-β accumulation, Tau phosphorylation, and cognitive impairment. J. Biol. Chem., 2018, 293(1), 226-244.
[http://dx.doi.org/10.1074/jbc.M117.786756] [PMID: 29127203]
[101]
Chang, C.F.; Cho, S.; Wang, J. (-)-Epicatechin protects hemorrhagic brain via synergistic Nrf2 pathways. Ann. Clin. Transl. Neurol., 2014, 1(4), 258-271.
[http://dx.doi.org/10.1002/acn3.54] [PMID: 24741667]
[102]
Faraco, G.; Fossati, S.; Bianchi, M.E.; Patrone, M.; Pedrazzi, M.; Sparatore, B.; Moroni, F.; Chiarugi, A. High mobility group box 1 protein is released by neural cells upon different stresses and worsens ischemic neurodegeneration in vitro and in vivo. J. Neurochem., 2007, 103(2), 590-603.
[http://dx.doi.org/10.1111/j.1471-4159.2007.04788.x] [PMID: 17666052]
[103]
Qi, L.; Sun, X.; Li, F.E.; Zhu, B.S.; Braun, F.K.; Liu, Z.Q.; Tang, J.L.; Wu, C.; Xu, F.; Wang, H.H.; Velasquez, L.A.; Zhao, K.; Lei, F.R.; Zhang, J.G.; Shen, Y.T.; Zou, J.X.; Meng, H.M.; An, G.L.; Yang, L.; Zhang, X.D. HMGB1 promotes mitochondrial dysfunction-triggered striatal neurodegeneration via autophagy and apoptosis activation. PLoS One, 2015, 10(11), e0142901.
[http://dx.doi.org/10.1371/journal.pone.0142901] [PMID: 26565401]
[104]
Tajuddin, N.; Kim, H.Y.; Collins, M.A. PARP Inhibition Prevents Ethanol-Induced Neuroinflammatory Signaling and Neurodegeneration in Rat Adult-Age Brain Slice Cultures. J. Pharmacol. Exp. Ther., 2018, 365(1), 117-126.
[http://dx.doi.org/10.1124/jpet.117.245290] [PMID: 29339456]
[105]
Coleman, L.G., Jr; Zou, J.; Crews, F.T. Microglial-derived miRNA let-7 and HMGB1 contribute to ethanol-induced neurotoxicity via TLR7. J. Neuroinflammation, 2017, 14(1), 22.
[http://dx.doi.org/10.1186/s12974-017-0799-4] [PMID: 28118842]
[106]
Qin, L.; Crews, F.T. Chronic ethanol increases systemic TLR3 agonist-induced neuroinflammation and neurodegeneration. J. Neuroinflammation, 2012, 9, 130.
[http://dx.doi.org/10.1186/1742-2094-9-130] [PMID: 22709825]
[107]
Bhatti, G.K.; Reddy, A.P.; Reddy, P.H.; Bhatti, J.S. Lifestyle Modifications and Nutritional Interventions in Aging-Associated Cognitive Decline and Alzheimer’s Disease. Front. Aging Neurosci., 2020, 11, 369.
[http://dx.doi.org/10.3389/fnagi.2019.00369] [PMID: 31998117]
[108]
Herrero, M-T.; Estrada, C.; Maatouk, L.; Vyas, S. Inflammation in Parkinson’s disease: role of glucocorticoids. Front. Neuroanat., 2015, 9, 32.
[http://dx.doi.org/10.3389/fnana.2015.00032] [PMID: 25883554]
[109]
Williams, A.J.; Paulson, H.L. Polyglutamine neurodegeneration: protein misfolding revisited. Trends Neurosci., 2008, 31(10), 521-528.
[http://dx.doi.org/10.1016/j.tins.2008.07.004] [PMID: 18778858]
[110]
Koeppen, A.H. The pathogenesis of spinocerebellar ataxia. Cerebellum, 2005, 4(1), 62-73.
[http://dx.doi.org/10.1080/14734220510007950] [PMID: 15895563]
[111]
Rashid, K.; Akhtar-Schaefer, I.; Langmann, T. Microglia in retinal degeneration. Front. Immunol., 2019, 10, 1975.
[http://dx.doi.org/10.3389/fimmu.2019.01975] [PMID: 31481963]
[112]
Frisoni, G.B.; Boccardi, M.; Barkhof, F.; Blennow, K.; Cappa, S.; Chiotis, K.; Démonet, J.F.; Garibotto, V.; Giannakopoulos, P.; Gietl, A.; Hansson, O.; Herholz, K.; Jack, C.R., Jr; Nobili, F.; Nordberg, A.; Snyder, H.M.; Ten Kate, M.; Varrone, A.; Albanese, E.; Becker, S.; Bos-suyt, P.; Carrillo, M.C.; Cerami, C.; Dubois, B.; Gallo, V.; Giacobini, E.; Gold, G.; Hurst, S.; Lönneborg, A.; Lovblad, K.O.; Mattsson, N.; Molinuevo, J.L.; Monsch, A.U.; Mosimann, U.; Padovani, A.; Picco, A.; Porteri, C.; Ratib, O.; Saint-Aubert, L.; Scerri, C.; Scheltens, P.; Schott, J.M.; Sonni, I.; Teipel, S.; Vineis, P.; Visser, P.J.; Yasui, Y.; Winblad, B. Strategic roadmap for an early diagnosis of Alzheimer’s disease based on biomarkers. Lancet Neurol., 2017, 16(8), 661-676.
[http://dx.doi.org/10.1016/S1474-4422(17)30159-X] [PMID: 28721928]
[113]
Lansbury, P.T., Jr Back to the future: the ‘old-fashioned’ way to new medications for neurodegeneration. Nat. Med., 2004, 10(Suppl.), S51-S57.
[http://dx.doi.org/10.1038/nrn1435] [PMID: 15298008]
[114]
Ehrenberg, A.J.; Khatun, A.; Coomans, E.; Betts, M.J.; Capraro, F.; Thijssen, E.H.; Senkevich, K.; Bharucha, T.; Jafarpour, M.; Young, P.N.E.; Jagust, W.; Carter, S.F.; Lashley, T.; Grinberg, L.T.; Pereira, J.B.; Mattsson-Carlgren, N.; Ashton, N.J.; Hanrieder, J.; Zetterberg, H.; Schöll, M.; Paterson, R.W. Relevance of biomarkers across different neurodegenerative diseases. Alzheimers Res. Ther., 2020, 12(1), 56.
[http://dx.doi.org/10.1186/s13195-020-00601-w] [PMID: 32404143]
[115]
Smith, J.J.; Dunn, B.K. Biomarkers as molecular targets of drug interventions. Semin. Oncol. Nurs., 2012, 28(2), 109-115.
[http://dx.doi.org/10.1016/j.soncn.2012.03.004] [PMID: 22542318]
[116]
Ray, R.; Juranek, J.K.; Rai, V. RAGE axis in neuroinflammation, neurodegeneration and its emerging role in the pathogenesis of amyo-trophic lateral sclerosis. Neurosci. Biobehav. Rev., 2016, 62, 48-55.
[http://dx.doi.org/10.1016/j.neubiorev.2015.12.006] [PMID: 26724598]
[117]
Tian, J.; Dai, H.; Deng, Y.; Zhang, J.; Li, Y.; Zhou, J.; Zhao, M.; Zhao, M.; Zhang, C.; Zhang, Y.; Wang, P.; Bing, G.; Zhao, L. The effect of HMGB1 on sub-toxic chlorpyrifos exposure-induced neuroinflammation in amygdala of neonatal rats. Toxicology, 2015, 338, 95-103.
[http://dx.doi.org/10.1016/j.tox.2015.10.010] [PMID: 26524701]
[118]
Paban, V.; Loriod, B.; Villard, C.; Buee, L.; Blum, D.; Pietropaolo, S.; Cho, Y.H.; Gory-Faure, S.; Mansour, E.; Gharbi, A.; Alescio-Lautier, B. Omics analysis of mouse brain models of human diseases. Gene, 2017, 600, 90-100.
[http://dx.doi.org/10.1016/j.gene.2016.11.022] [PMID: 27871923]
[119]
Fang, F.; Lue, L.F.; Yan, S.; Xu, H.; Luddy, J.S.; Chen, D.; Walker, D.G.; Stern, D.M.; Yan, S.; Schmidt, A.M.; Chen, J.X.; Yan, S.S. RAGE-dependent signaling in microglia contributes to neuroinflammation, Abeta accumulation, and impaired learning/memory in a mouse model of Alzheimer’s disease. FASEB J., 2010, 24(4), 1043-1055.
[http://dx.doi.org/10.1096/fj.09-139634] [PMID: 19906677]
[120]
Yu, M.; Wang, H.; Ding, A.; Golenbock, D.T.; Latz, E.; Czura, C.J.; Fenton, M.J.; Tracey, K.J.; Yang, H. HMGB1 signals through toll-like receptor (TLR) 4 and TLR2. Shock, 2006, 26(2), 174-179.
[http://dx.doi.org/10.1097/01.shk.0000225404.51320.82] [PMID: 16878026]
[121]
Kawai, T.; Akira, S. The role of pattern-recognition receptors in innate immunity: update on Toll-like receptors. Nat. Immunol., 2010, 11(5), 373-384.
[http://dx.doi.org/10.1038/ni.1863] [PMID: 20404851]
[122]
Brudvig, J.J.; Weimer, J.M. X MARCKS the spot: myristoylated alanine-rich C kinase substrate in neuronal function and disease. Front. Cell. Neurosci., 2015, 9, 407.
[http://dx.doi.org/10.3389/fncel.2015.00407] [PMID: 26528135]
[123]
Song, J-X.; Lu, J-H.; Liu, L-F.; Chen, L-L.; Durairajan, S.S.K.; Yue, Z.; Zhang, H.Q.; Li, M. HMGB1 is involved in autophagy inhibition caused by SNCA/α-synuclein overexpression: a process modulated by the natural autophagy inducer corynoxine B. Autophagy, 2014, 10(1), 144-154.
[http://dx.doi.org/10.4161/auto.26751] [PMID: 24178442]
[124]
Paudel, Y.N.; Shaikh, M.F.; Chakraborti, A.; Kumari, Y.; Aledo-Serrano, Á.; Aleksovska, K.; Alvim, M.K.M.; Othman, I. HMGB1: A Common biomarker and potential target for TBI, neuroinflammation, epilepsy, and cognitive dysfunction. Front. Neurosci., 2018, 12, 628.
[http://dx.doi.org/10.3389/fnins.2018.00628] [PMID: 30271319]
[125]
Mazarati, A.; Maroso, M.; Iori, V.; Vezzani, A.; Carli, M. High-mobility group box-1 impairs memory in mice through both toll-like recep-tor 4 and receptor for advanced glycation end products. Exp. Neurol., 2011, 232(2), 143-148.
[http://dx.doi.org/10.1016/j.expneurol.2011.08.012] [PMID: 21884699]
[126]
Bortolotto, V.; Grilli, M. Not only a bad guy: potential proneurogenic role of the RAGE/NF-κB axis in Alzheimer’s disease brain. Neural Regen. Res., 2016, 11(12), 1924-1925.
[http://dx.doi.org/10.4103/1673-5374.197130] [PMID: 28197185]

Rights & Permissions Print Cite
© 2024 Bentham Science Publishers | Privacy Policy