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Current Alzheimer Research

Editor-in-Chief

ISSN (Print): 1567-2050
ISSN (Online): 1875-5828

Review Article

Inflammation in the CNS: Understanding Various Aspects of the Pathogenesis of Alzheimer's Disease

Author(s): Julia Doroszkiewicz*, Piotr Mroczko and Agnieszka Kulczyńska-Przybik*

Volume 19, Issue 1, 2022

Published on: 11 February, 2022

Page: [16 - 31] Pages: 16

DOI: 10.2174/1567205018666211202143935

open access plus

Abstract

Alzheimer’s disease is a progressive and deadly neurodegenerative disorder and one of the most common causes of dementia globally. Current, insufficiently sensitive and specific methods of early diagnosing and monitoring this disease prompt a search for new tools. Numerous literature data have indicated that the pathogenesis of Alzheimer’s disease (AD) is not limited to the neuronal compartment but involves various immunological mechanisms. Neuroinflammation has been recognized as a very important process in AD pathology. It seems to play pleiotropic roles, both neuroprotective and neurodegenerative, in the development of cognitive impairment depending on the stage of the disease. Mounting evidence demonstrates that inflammatory proteins could be considered biomarkers of disease progression. Therefore, the present review summarizes the role of some inflammatory molecules and their potential utility in detecting and monitoring dementia severity. This paper also provides a valuable insight into new mechanisms leading to the development of dementia, which might be useful in discovering possible anti-inflammatory treatment.

Keywords: neuroinflammation, Alzheimer's disease, dementia disorders, biomarkers, neurodegeneration, chemokines, interleukins

[1]
Lane CA, Hardy J, Schott JM. Alzheimer’s disease. Eur J Neurol 2018; 25(1): 59-70.
[http://dx.doi.org/10.1111/ene.13439] [PMID: 28872215]
[2]
WHO. Risk Reduction of cognitive decline and dementia. World Health Organization 2019; p. 96. Available from: https://www.who.int/publications/i/item/risk-reduction-of-cognitive-decline-and-dementia.
[3]
Alzheimer’s Association. Alzheimer’s Facts and Figures Report. Available from: https://www.alz.org/alzheimers-dementia/facts-figures.
[4]
Clarimón J, Djaldetti R, Lleó A, et al. Whole genome analysis in a consanguineous family with early onset Alzheimer’s disease. Neurobiol Aging 2009; 30(12): 1986-91.
[http://dx.doi.org/10.1016/j.neurobiolaging.2008.02.008] [PMID: 18387709]
[5]
Muñoz SS, Garner B, Ooi L. Understanding the role of apoe fragments in alzheimer’s disease. Neurochem Res 2019; 44(6): 1297-305.
[http://dx.doi.org/10.1007/s11064-018-2629-1] [PMID: 30225748]
[6]
Crews L, Masliah E. Molecular mechanisms of neurodegeneration in Alzheimer’s disease. Hum Mol Genet 2010; 19(R1): R12-20.
[http://dx.doi.org/10.1093/hmg/ddq160] [PMID: 20413653]
[7]
Weiner MW, Veitch DP, Aisen PS, et al. 2014 Update of the Alzheimer’s Disease Neuroimaging Initiative: A review of papers published since its inception. Alzheimers Dement 2015; 11(6): e1-e120.
[http://dx.doi.org/10.1016/j.jalz.2014.11.001] [PMID: 26073027]
[8]
Chen GF, Xu TH, Yan Y, et al. Amyloid beta: structure, biology and structure-based therapeutic development. Acta Pharmacol Sin 2017; 38(9): 1205-35.
[http://dx.doi.org/10.1038/aps.2017.28] [PMID: 28713158]
[9]
Kojro E, Fahrenholz F. The Non-Amyloidogenic Pathway: Structure and Function of α-Secretases. Alzheimer’s Disease. Springer US 2005; Vol. 38: pp. 105-27.
[10]
Tarasoff-Conway JM, Carare RO, Osorio RS, et al. Clearance systems in the brain-implications for Alzheimer disease. Nat Rev Neurol 2015; 11(8): 457-70.
[http://dx.doi.org/10.1038/nrneurol.2015.119] [PMID: 26195256]
[11]
Iba M, Guo JL, McBride JD, Zhang B, Trojanowski JQ, Lee VMY. Synthetic tau fibrils mediate transmission of neurofibrillary tangles in a transgenic mouse model of Alzheimer’s-like tauopathy. J Neurosci 2013; 33(3): 1024-37.
[http://dx.doi.org/10.1523/JNEUROSCI.2642-12.2013] [PMID: 23325240]
[12]
Hoskin JL, Sabbagh MN, Al-Hasan Y, Decourt B. Tau immunotherapies for Alzheimer’s disease. Expert Opin Investig Drugs 2019; 28(6): 545-54.
[http://dx.doi.org/10.1080/13543784.2019.1619694] [PMID: 31094578]
[13]
Martin L, Latypova X, Wilson CM, et al. Tau protein kinases: involvement in Alzheimer’s disease. Ageing Res Rev 2013; 12(1): 289-309.
[http://dx.doi.org/10.1016/j.arr.2012.06.003] [PMID: 22742992]
[14]
Naseri NN, Wang H, Guo J, Sharma M, Luo W. The complexity of tau in Alzheimer’s disease. Neurosci Lett 2019; 705: 183-94.
[http://dx.doi.org/10.1016/j.neulet.2019.04.022] [PMID: 31028844]
[15]
Heneka MT, Carson MJ, El Khoury J, et al. NeuroInflammation in Alzheimer’s disease. Lancet Neurol 2015; 14(4): 388-405.
[http://dx.doi.org/10.1016/S1474-4422(15)70016-5] [PMID: 25792098]
[16]
Krstic D, Knuesel I. Deciphering the mechanism underlying late-onset Alzheimer disease. Nat Rev Neurol 2013; 9(1): 25-34.
[http://dx.doi.org/10.1038/nrneurol.2012.236] [PMID: 23183882]
[17]
Nazem A, Sankowski R, Bacher M, Al-Abed Y. Rodent models of neuroinflammation for Alzheimer’s disease. J Neuroinflammation 2015; 12: 74.
[http://dx.doi.org/10.1186/s12974-015-0291-y] [PMID: 25890375]
[18]
Webers A, Heneka MT, Gleeson PA. The role of innate immune responses and neuroinflammation in amyloid accumulation and progression of Alzheimer’s disease. Immunol Cell Biol 2020; 98(1): 28-41.
[http://dx.doi.org/10.1111/imcb.12301] [PMID: 31654430]
[19]
Lee JW, Lee YK, Yuk DY, et al. Neuro-inflammation induced by lipopolysaccharide causes cognitive impairment through enhancement of beta-amyloid generation. J Neuroinflammation 2008; 5: 37.
[http://dx.doi.org/10.1186/1742-2094-5-37] [PMID: 18759972]
[20]
Ransohoff RM, Perry VH. Microglial physiology: unique stimuli, specialized responses. Annu Rev Immunol 2009; 27: 119-45.
[http://dx.doi.org/10.1146/annurev.immunol.021908.132528] [PMID: 19302036]
[21]
Schafer DP, Stevens B. Microglia function in central nervous system development and plasticity. Cold Spring Harb Perspect Biol 2015; 7(10): a020545.
[http://dx.doi.org/10.1101/cshperspect.a020545] [PMID: 26187728]
[22]
Cai Z, Hussain MD, Yan L-J. Microglia, neuroinflammation, and beta-amyloid protein in Alzheimer’s disease. Int J Neurosci 2014; 124(5): 307-21.
[http://dx.doi.org/10.3109/00207454.2013.833510] [PMID: 23930978]
[23]
Tang Y, Le W. Differential roles of M1 and M2 microglia in neurodegenerative diseases. Mol Neurobiol 2016; 53(2): 1181-94.
[http://dx.doi.org/10.1007/s12035-014-9070-5] [PMID: 25598354]
[24]
Jin X, Liu M-YY, Zhang D-FF, et al. Natural products as a potential modulator of microglial polarization in neurodegenerative diseases. Pharmacol Res 2019; 145: 104253.
[http://dx.doi.org/10.1016/j.phrs.2019.104253] [PMID: 31059788]
[25]
Zhang Z, Zhang Z, Lu H, Yang Q, Wu H, Wang J. Microglial polarization and inflammatory mediators after intracerebral hemorrhage. Mol Neurobiol 2017; 54(3): 1874-86.
[http://dx.doi.org/10.1007/s12035-016-9785-6] [PMID: 26894396]
[26]
Chee SEJ, Solito E. The impact of ageing on the CNS immune response in Alzheimer’s disease. Front Immunol 2021; 12: 738511.
[http://dx.doi.org/10.3389/fimmu.2021.738511] [PMID: 34603320]
[27]
Frank S, Burbach GJ, Bonin M, et al. TREM2 is upregulated in amyloid plaque-associated microglia in aged APP23 transgenic mice. Glia 2008; 56(13): 1438-47.
[http://dx.doi.org/10.1002/glia.20710] [PMID: 18551625]
[28]
Hickman SE, El Khoury J. TREM2 and the neuroimmunology of Alzheimer’s disease. Biochem Pharmacol 2014; 88(4): 495-8.
[http://dx.doi.org/10.1016/j.bcp.2013.11.021] [PMID: 24355566]
[29]
Medeiros R, LaFerla FM. Astrocytes: conductors of the Alzheimer disease neuroinflammatory symphony. Exp Neurol 2013; 239: 133-8.
[http://dx.doi.org/10.1016/j.expneurol.2012.10.007] [PMID: 23063604]
[30]
Fakhoury M. Microglia and astrocytes in Alzheimer’s disease: implications for therapy. Curr Neuropharmacol 2018; 16(5): 508-18.
[http://dx.doi.org/10.2174/1570159X15666170720095240] [PMID: 28730967]
[31]
Wyss-Coray T, Rogers J. Inflammation in Alzheimer disease-a brief review of the basic science and clinical literature. Cold Spring Harb Perspect Med 2012; 2(1): a006346-6.
[http://dx.doi.org/10.1101/cshperspect.a006346] [PMID: 22315714]
[32]
Olabarria M, Noristani HN, Verkhratsky A, Rodríguez JJ. Concomitant astroglial atrophy and astrogliosis in a triple transgenic animal model of Alzheimer’s disease. Glia 2010; 58(7): 831-8.
[http://dx.doi.org/10.1002/glia.20967]
[33]
Van Eldik LJ, Carrillo MC, Cole PE, et al. The roles of inflammation and immune mechanisms in Alzheimer’s disease. Alzheimers Dement (N Y) 2016; 2(2): 99-109.
[http://dx.doi.org/10.1016/j.trci.2016.05.001] [PMID: 29067297]
[34]
Lian H, Yang L, Cole A, et al. NFκB-activated astroglial release of complement C3 compromises neuronal morphology and function associated with Alzheimer’s disease. Neuron 2015; 85(1): 101-15.
[http://dx.doi.org/10.1016/j.neuron.2014.11.018] [PMID: 25533482]
[35]
Dong Y, Lagarde J, Xicota L, et al. Neutrophil hyperactivation correlates with Alzheimer’s disease progression. Ann Neurol 2018; 83(2): 387-405.
[http://dx.doi.org/10.1002/ana.25159] [PMID: 29369398]
[36]
Vitte J, Michel BF, Bongrand P, Gastaut JL. Oxidative stress level in circulating neutrophils is linked to neurodegenerative diseases. J Clin Immunol 2004; 24(6): 683-92.
[http://dx.doi.org/10.1007/s10875-004-6243-4] [PMID: 15622453]
[37]
Zenaro E, Pietronigro E, Della Bianca V, et al. Neutrophils promote Alzheimer’s disease-like pathology and cognitive decline via LFA-1 integrin. Nat Med 2015; 21(8): 880-6.
[http://dx.doi.org/10.1038/nm.3913] [PMID: 26214837]
[38]
Stock AJ, Kasus-Jacobi A, Pereira HA. The role of neutrophil granule proteins in neuroinflammation and Alzheimer’s disease. J Neuroinflammation 2018; 15(1): 240.
[http://dx.doi.org/10.1186/s12974-018-1284-4] [PMID: 30149799]
[39]
Kowalski K, Mulak A. Brain-gut-microbiota axis in Alzheimer’s disease. J Neurogastroenterol Motil 2019; 25(1): 48-60.
[http://dx.doi.org/10.5056/jnm18087] [PMID: 30646475]
[40]
Kim M-S, Kim Y, Choi H, et al. Transfer of a healthy microbiota reduces amyloid and tau pathology in an Alzheimer’s disease animal model. Gut 2020; 69(2): 283-94.
[http://dx.doi.org/10.1136/gutjnl-2018-317431] [PMID: 31471351]
[41]
Park J-C, Han S-H, Mook-Jung I. Peripheral inflammatory biomarkers in Alzheimer’s disease: A brief review. BMB Rep 2020; 53(1): 10-9.
[http://dx.doi.org/10.5483/BMBRep.2020.53.1.309] [PMID: 31865964]
[42]
Megur A, Baltriukienė D, Bukelskienė V, Burokas A. The microbiota-gut-brain axis and alzheimer’s disease: neuroinflammation is to blame? Nutrients 2020; 13(1): 37.
[http://dx.doi.org/10.3390/nu13010037] [PMID: 33374235]
[43]
Friedland RP, Chapman MR. The role of microbial amyloid in neurodegeneration. PLoS Pathog 2017; 13(12): e1006654.
[http://dx.doi.org/10.1371/journal.ppat.1006654] [PMID: 29267402]
[44]
Cattaneo A, Cattane N, Galluzzi S, et al. Association of brain amyloidosis with pro-inflammatory gut bacterial taxa and peripheral inflammation markers in cognitively impaired elderly. Neurobiol Aging 2017; 49: 60-8.
[http://dx.doi.org/10.1016/j.neurobiolaging.2016.08.019] [PMID: 27776263]
[45]
Bonfili L, Cecarini V, Berardi S, et al. Microbiota modulation counteracts Alzheimer’s disease progression influencing neuronal proteolysis and gut hormones plasma levels. Sci Rep 2017; 7(1): 2426.
[http://dx.doi.org/10.1038/s41598-017-02587-2] [PMID: 28546539]
[46]
Bradburn S, Murgatroyd C, Ray N. Neuroinflammation in mild cognitive impairment and Alzheimer’s disease: A meta-analysis. Ageing Res Rev 2019; 50: 1-8.
[http://dx.doi.org/10.1016/j.arr.2019.01.002] [PMID: 30610927]
[47]
Pedrero-Prieto CM, García-Carpintero S, Frontiñán-Rubio J, et al. A comprehensive systematic review of CSF proteins and peptides that define Alzheimer’s disease. Clin Proteomics 2020; 17: 21.
[http://dx.doi.org/10.1186/s12014-020-09276-9] [PMID: 32518535]
[48]
Brosseron F, Traschütz A, Widmann CN, et al. Characterization and clinical use of inflammatory cerebrospinal fluid protein markers in Alzheimer’s disease. Alzheimers Res Ther 2018; 10(1): 25.
[http://dx.doi.org/10.1186/s13195-018-0353-3] [PMID: 29482610]
[49]
El Naqa I, Murphy MJ. What Is Machine Learning? Machine Learning in Radiation Oncology. Cham: Springer International Publishing 2015; pp. 3-11.
[http://dx.doi.org/10.1007/978-3-319-18305-3_1]
[50]
Chang C-H, Lin C-H, Lane H-Y. Machine learning and novel biomarkers for the diagnosis of Alzheimer’s disease. Int J Mol Sci 2021; 22(5): 2761.
[http://dx.doi.org/10.3390/ijms22052761] [PMID: 33803217]
[51]
Abate G, Vezzoli M, Polito L, et al. A conformation variant of p53 combined with machine learning identifies Alzheimer disease in preclinical and prodromal stages. J Pers Med 2020; 11(1): 14.
[http://dx.doi.org/10.3390/jpm11010014] [PMID: 33375220]
[52]
Choi H, Jin KH. Predicting cognitive decline with deep learning of brain metabolism and amyloid imaging. Behav Brain Res 2018; 344: 103-9.
[http://dx.doi.org/10.1016/j.bbr.2018.02.017] [PMID: 29454006]
[53]
Italiani P, Puxeddu I, Napoletano S, et al. Circulating levels of IL-1 family cytokines and receptors in Alzheimer’s disease: new markers of disease progression? J Neuroinflammation 2018; 15(1): 342.
[http://dx.doi.org/10.1186/s12974-018-1376-1] [PMID: 30541566]
[54]
Forlenza OV, Diniz BS, Talib LL, et al. Increased serum IL-1β level in Alzheimer’s disease and mild cognitive impairment. Dement Geriatr Cogn Disord 2009; 28(6): 507-12.
[http://dx.doi.org/10.1159/000255051] [PMID: 19996595]
[55]
Blum-Degen D, Müller T, Kuhn W, Gerlach M, Przuntek H, Riederer P. Interleukin-1 β and interleukin-6 are elevated in the cerebrospinal fluid of Alzheimer’s and de novo Parkinson’s disease patients. Neurosci Lett 1995; 202(1-2): 17-20.
[http://dx.doi.org/10.1016/0304-3940(95)12192-7] [PMID: 8787820]
[56]
Lai KSP, Liu CS, Rau A, et al. Peripheral inflammatory markers in Alzheimer’s disease: A systematic review and meta-analysis of 175 studies. J Neurol Neurosurg Psychiatry 2017; 88(10): 876-82.
[http://dx.doi.org/10.1136/jnnp-2017-316201] [PMID: 28794151]
[57]
Gezen-Ak D, Dursun E, Hanağası H, et al. BDNF, TNFα, HSP90, CFH, and IL-10 serum levels in patients with early or late onset Alzheimer’s disease or mild cognitive impairment. J Alzheimers Dis 2013; 37(1): 185-95.
[http://dx.doi.org/10.3233/JAD-130497] [PMID: 23948885]
[58]
Taipa R, das Neves SP, Sousa AL, et al. Proinflammatory and anti-inflammatory cytokines in the CSF of patients with Alzheimer’s disease and their correlation with cognitive decline. Neurobiol Aging 2019; 76: 125-32.
[http://dx.doi.org/10.1016/j.neurobiolaging.2018.12.019] [PMID: 30711675]
[59]
Lee WJ, Liao YC, Wang YF, Lin IF, Wang SJ, Fuh JL. Plasma MCP-1 and cognitive decline in patients with Alzheimer’s disease and mild cognitive impairment: A two-year follow-up study. Sci Rep 2018; 8(1): 1280.
[http://dx.doi.org/10.1038/s41598-018-19807-y] [PMID: 29352259]
[60]
Kulczyńska-Przybik A, Słowik A, Mroczko P, et al. Cerebrospinal fluid and blood CX3Cl1 as a potential biomarker in early diagnosis and prognosis of dementia. Curr Alzheimer Res 2020; 17(8): 709-21.
[http://dx.doi.org/10.2174/1567205017666201109095657] [PMID: 33167838]
[61]
Rentzos M, Zoga M, Paraskevas GP, et al. IL-15 is elevated in cerebrospinal fluid of patients with Alzheimer’s disease and frontotemporal dementia. J Geriatr Psychiatry Neurol 2006; 19(2): 114-7.
[http://dx.doi.org/10.1177/0891988706286226] [PMID: 16690997]
[62]
Janelidze S, Mattsson N, Stomrud E, et al. CSF biomarkers of neuroinflammation and cerebrovascular dysfunction in early Alzheimer disease. Neurology 2018; 91(9): e867-77.
[http://dx.doi.org/10.1212/WNL.0000000000006082] [PMID: 30054439]
[63]
King E, O’Brien JT, Donaghy P, et al. Peripheral inflammation in prodromal Alzheimer’s and Lewy body dementias. J Neurol Neurosurg Psychiatry 2018; 89(4): 339-45.
[http://dx.doi.org/10.1136/jnnp-2017-317134] [PMID: 29248892]
[64]
D’Anna L, Abu-Rumeileh S, Fabris M, et al. Serum interleukin-10 levels correlate with cerebrospinal fluid amyloid beta deposition in alzheimer disease patients. Neurodegener Dis 2017; 17(4-5): 227-34.
[http://dx.doi.org/10.1159/000474940] [PMID: 28719891]
[65]
Laske C, Stellos K, Eschweiler GW, Leyhe T, Gawaz M. Decreased CXCL12 (SDF-1) plasma levels in early Alzheimer’s disease: A contribution to a deficient hematopoietic brain support? J Alzheimers Dis 2008; 15(1): 83-95.
[http://dx.doi.org/10.3233/JAD-2008-15107] [PMID: 18780969]
[66]
Ewers M, Franzmeier N, Suárez-Calvet M, et al. Increased soluble TREM2 in cerebrospinal fluid is associated with reduced cognitive and clinical decline in Alzheimer’s disease. Sci Transl Med 2019; 11(507): eaav6221.
[http://dx.doi.org/10.1126/scitranslmed.aav6221] [PMID: 31462511]
[67]
Wang L, Gao T, Cai T, Li K, Zheng P, Liu J. Cerebrospinal fluid levels of YKL-40 in prodromal Alzheimer’s disease. Neurosci Lett 2020; 715: 134658.
[http://dx.doi.org/10.1016/j.neulet.2019.134658] [PMID: 31794792]
[68]
Festoff BW, Sajja RK, van Dreden P, Cucullo L. HMGB1 and thrombin mediate the blood-brain barrier dysfunction acting as biomarkers 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]
[69]
Hüttenrauch M, Ogorek I, Klafki H, et al. Glycoprotein NMB: A novel Alzheimer’s disease associated marker expressed in a subset of activated microglia. Acta Neuropathol Commun 2018; 6(1): 108.
[http://dx.doi.org/10.1186/s40478-018-0612-3] [PMID: 30340518]
[70]
Zheng C, Zhou X-W, Wang J-Z. The dual roles of cytokines in Alzheimer’s disease: update on interleukins, TNF-α, TGF-β and IFN-γ. Transl Neurodegener 2016; 5: 7.
[http://dx.doi.org/10.1186/s40035-016-0054-4] [PMID: 27054030]
[71]
Griffin WST. Alzheimer’s - Looking beyond plaques. F1000 Med Rep 2011; 3: 24.
[http://dx.doi.org/10.3410/M3-24] [PMID: 22162727]
[72]
Sheng JG, Jones RA, Zhou XQ, et al. Interleukin-1 promotion of MAPK-p38 overexpression in experimental animals and in Alzheimer’s disease: potential significance for tau protein phosphorylation. Neurochem Int 2001; 39(5-6): 341-8.
[http://dx.doi.org/10.1016/S0197-0186(01)00041-9] [PMID: 11578769]
[73]
Gorska-Ciebiada M, Saryusz-Wolska M, Borkowska A, Ciebiada M, Loba J. Adiponectin, leptin and IL-1 β in elderly diabetic patients with mild cognitive impairment. Metab Brain Dis 2016; 31(2): 257-66.
[http://dx.doi.org/10.1007/s11011-015-9739-0] [PMID: 26432692]
[74]
Rizzi L, Roriz-Cruz M. Cerebrospinal fluid inflammatory markers in amnestic mild cognitive impairment. Geriatr Gerontol Int 2017; 17(2): 239-45.
[http://dx.doi.org/10.1111/ggi.12704] [PMID: 26818250]
[75]
Swardfager W, Lanctôt K, Rothenburg L, et al. A meta-analysis of cytokines in Alzheimer’s disease. Biol Psychiatry 2010; 68(10): 930-41.
[http://dx.doi.org/10.1016/j.biopsych.2010.06.012] [PMID: 20692646]
[76]
Hampel H, Haslinger A, Scheloske M, et al. Pattern of interleukin-6 receptor complex immunoreactivity between cortical regions of rapid autopsy normal and Alzheimer’s disease brain. Eur Arch Psychiatry Clin Neurosci 2005; 255(4): 269-78.
[http://dx.doi.org/10.1007/s00406-004-0558-2] [PMID: 15565298]
[77]
Keegan AP, Paris D, Luis CA, et al. Plasma cytokine IL-6 levels and subjective cognitive decline: preliminary findings. Int J Geriatr Psychiatry 2018; 33(2): 358-63.
[http://dx.doi.org/10.1002/gps.4752] [PMID: 28639714]
[78]
Erta M, Quintana A, Hidalgo J. Interleukin-6, a major cytokine in the central nervous system. Int J Biol Sci 2012; 8(9): 1254-66.
[http://dx.doi.org/10.7150/ijbs.4679] [PMID: 23136554]
[79]
Del Bo R, Angeretti N, Lucca E, De Simoni MG, Forloni G. Reciprocal control of inflammatory cytokines, IL-1 and IL-6, and β-amyloid production in cultures. Neurosci Lett 1995; 188(1): 70-4.
[http://dx.doi.org/10.1016/0304-3940(95)11384-9] [PMID: 7783982]
[80]
Domingues C, da Cruz E Silva OAB, Henriques AG. Impact of cytokines and chemokines on Alzheimer’s disease neuropathological hallmarks. Curr Alzheimer Res 2017; 14(8): 870-82.
[http://dx.doi.org/10.2174/1567205014666170317113606] [PMID: 28317487]
[81]
Quintanilla RA, Orellana DI, González-Billault C, Maccioni RB. Interleukin-6 induces Alzheimer-type phosphorylation of tau protein by deregulating the cdk5/p35 pathway. Exp Cell Res 2004; 295(1): 245-57.
[http://dx.doi.org/10.1016/j.yexcr.2004.01.002] [PMID: 15051507]
[82]
Wennberg AMV, Hagen CE, Machulda MM, Knopman DS, Petersen RC, Mielke MM. The cross-sectional and longitudinal associations between IL-6, IL-10, and TNFα and cognitive outcomes in the mayo clinic study of aging. J Gerontol Ser A 2019; 74(8): 1289-95.
[http://dx.doi.org/10.1093/gerona/gly217] [PMID: 30256904]
[83]
Wang Y, Emre C, Gyllenhammar-Schill H, et al. Cerebrospinal fluid inflammatory markers in alzheimer’s disease: influence of comorbidities. Curr Alzheimer Res 2021; 18(2): 157-70.
[http://dx.doi.org/10.2174/1567205018666210330162207] [PMID: 33784960]
[84]
Bishnoi RJ, Palmer RF, Royall DR. Serum interleukin (IL)-15 as a biomarker of Alzheimer’s disease. PLoS One 2015; 10(2): e0117282.
[http://dx.doi.org/10.1371/journal.pone.0117282] [PMID: 25710473]
[85]
Takano M, Nishimura H, Kimura Y, et al. Protective roles of γ δ T cells and interleukin-15 in Escherichia coli infection in mice. Infect Immun 1998; 66(7): 3270-8.
[http://dx.doi.org/10.1128/IAI.66.7.3270-3278.1998] [PMID: 9632595]
[86]
Asby D, Boche D, Allan S, Love S, Miners JS. Systemic infection exacerbates cerebrovascular dysfunction in Alzheimer’s disease. Brain 2021; 144(6): 1869-83.
[http://dx.doi.org/10.1093/brain/awab094] [PMID: 33723589]
[87]
te Velde AA, Huijbens RJ, Heije K, de Vries JE, Figdor CG. Interleukin-4 (IL-4) inhibits secretion of IL-1 beta, tumor necrosis factor alpha, and IL-6 by human monocytes. Blood 1990; 76(7): 1392-7.
[http://dx.doi.org/10.1182/blood.V76.7.1392.1392] [PMID: 2119829]
[88]
Leung R, Proitsi P, Simmons A, et al. Inflammatory proteins in plasma are associated with severity of Alzheimer’s disease. PLoS One 2013; 8(6): e64971.
[http://dx.doi.org/10.1371/journal.pone.0064971] [PMID: 23762274]
[89]
Lugaresi A, Di Iorio A, Iarlori C, et al. IL-4 in vitro production is upregulated in Alzheimer's disease patients treated with acetylcholinesterase inhibitors. Exp Gerontol 2004; 39(4): 653-7.
[http://dx.doi.org/10.1016/j.exger.2003.08.012]
[90]
Han SH, Park JC, Byun MS, et al. Blood acetylcholinesterase level is a potential biomarker for the early detection of cerebral amyloid deposition in cognitively normal individuals. Neurobiol Aging 2019; 73: 21-9.
[http://dx.doi.org/10.1016/j.neurobiolaging.2018.09.001] [PMID: 30316049]
[91]
Kawahara K, Suenobu M, Yoshida A, et al. Intracerebral microinjection of interleukin-4/interleukin-13 reduces β-amyloid accumulation in the ipsilateral side and improves cognitive deficits in young amyloid precursor protein 23 mice. Neuroscience 2012; 207: 243-60.
[http://dx.doi.org/10.1016/j.neuroscience.2012.01.049] [PMID: 22342341]
[92]
Dionisio-Santos DA, Behrouzi A, Olschowka JA, O’Banion MK. Evaluating the effect of interleukin-4 in the 3xtg mouse model of Alzheimer’s disease. Front Neurosci 2020; 14: 441.
[http://dx.doi.org/10.3389/fnins.2020.00441] [PMID: 32528242]
[93]
Porro C, Cianciulli A, Panaro MA. The regulatory role of IL-10 in neurodegenerative diseases. Biomolecules 2020; 10(7): 1-15.
[http://dx.doi.org/10.3390/biom10071017] [PMID: 32659950]
[94]
Kiyota T, Ingraham KL, Swan RJ, Jacobsen MT, Andrews SJ, Ikezu T. AAV serotype 2/1-mediated gene delivery of anti-inflammatory interleukin-10 enhances neurogenesis and cognitive function in APP+PS1 mice. Gene Ther 2012; 19(7): 724-33.
[http://dx.doi.org/10.1038/gt.2011.126] [PMID: 21918553]
[95]
Zhang Y, Zhang J, Tian C, et al. The -1082G/A polymorphism in IL-10 gene is associated with risk of Alzheimer’s disease: A meta- analysis. J Neurol Sci 2011; 303(1-2): 133-8.
[http://dx.doi.org/10.1016/j.jns.2010.12.005] [PMID: 21255795]
[96]
Decourt B, Lahiri DK, Sabbagh MN. Targeting tumor necrosis factor alpha for alzheimer’s disease. Curr Alzheimer Res 2017; 14(4): 412-25.
[http://dx.doi.org/10.2174/1567205013666160930110551] [PMID: 27697064]
[97]
Zhao M, Cribbs DH, Anderson AJ, et al. The induction of the TNFalpha death domain signaling pathway in Alzheimer’s disease brain. Neurochem Res 2003; 28(2): 307-18.
[http://dx.doi.org/10.1023/A:1022337519035] [PMID: 12608703]
[98]
Brosseron F, Krauthausen M, Kummer M, Heneka MT. Body fluid cytokine levels in mild cognitive impairment and Alzheimer’s disease: A comparative overview. Mol Neurobiol 2014; 50(2): 534-44.
[http://dx.doi.org/10.1007/s12035-014-8657-1] [PMID: 24567119]
[99]
Paouri E, Tzara O, Kartalou G-II, Zenelak S, Georgopoulos S. Peripheral tumor necrosis factor-alpha (tnf-α) modulates amyloid pathology by regulating blood-derived immune cells and glial response in the brain of AD/TNF transgenic mice. J Neurosci 2017; 37(20): 5155-71.
[http://dx.doi.org/10.1523/JNEUROSCI.2484-16.2017] [PMID: 28442538]
[100]
Paouri E, Tzara O, Zenelak S, Georgopoulos S. Genetic deletion of tumor necrosis factor-α attenuates amyloid-β production and decreases amyloid plaque formation and glial response in the 5xfad model of Alzheimer’s disease. J Alzheimers Dis 2017; 60(1): 165-81.
[http://dx.doi.org/10.3233/JAD-170065] [PMID: 28826177]
[101]
Bachstetter AD, Morganti JM, Jernberg J, et al. Fractalkine and CX 3 CR1 regulate hippocampal neurogenesis in adult and aged rats. Neurobiol Aging 2011; 32(11): 2030-44.
[http://dx.doi.org/10.1016/j.neurobiolaging.2009.11.022] [PMID: 20018408]
[102]
Rogers JT, Morganti JM, Bachstetter AD, et al. CX3CR1 deficiency leads to impairment of hippocampal cognitive function and synaptic plasticity. J Neurosci 2011; 31(45): 16241-50.
[http://dx.doi.org/10.1523/JNEUROSCI.3667-11.2011] [PMID: 22072675]
[103]
Xu Y, Zeng K, Han Y, et al. Altered expression of CX3CL1 in patients with epilepsy and in a rat model. Am J Pathol 2012; 180(5): 1950-62.
[http://dx.doi.org/10.1016/j.ajpath.2012.01.024] [PMID: 22464888]
[104]
Donohue MM, Cain K, Zierath D, Shibata D, Tanzi PM, Becker KJ. Higher plasma fractalkine is associated with better 6-month outcome from ischemic stroke. Stroke 2012; 43(9): 2300-6.
[http://dx.doi.org/10.1161/STROKEAHA.112.657411] [PMID: 22798324]
[105]
Bhaskar K, Konerth M, Kokiko-Cochran ON, Cardona A, Ransohoff RM, Lamb BT. Regulation of tau pathology by the microglial fractalkine receptor. Neuron 2010; 68(1): 19-31.
[http://dx.doi.org/10.1016/j.neuron.2010.08.023] [PMID: 20920788]
[106]
Cho SH, Sun B, Zhou Y, et al. CX3CR1 protein signaling modulates microglial activation and protects against plaque-independent cognitive deficits in a mouse model of Alzheimer disease. J Biol Chem 2011; 286(37): 32713-22.
[http://dx.doi.org/10.1074/jbc.M111.254268] [PMID: 21771791]
[107]
Ma Q, Jones D, Borghesani PR, et al. Impaired B-lymphopoiesis, myelopoiesis, and derailed cerebellar neuron migration in CXCR4- and SDF-1-deficient mice. Proc Natl Acad Sci USA 1998; 95(16): 9448-53.
[http://dx.doi.org/10.1073/pnas.95.16.9448] [PMID: 9689100]
[108]
Trousse F, Jemli A, Silhol M, et al. Knockdown of the CXCL12/CXCR7 chemokine pathway results in learning deficits and neural progenitor maturation impairment in mice. Brain Behav Immun 2019; 80: 697-710.
[http://dx.doi.org/10.1016/j.bbi.2019.05.019] [PMID: 31100368]
[109]
Janssens R, Struyf S, Proost P. Pathological roles of the homeostatic chemokine CXCL12. Cytokine Growth Factor Rev 2018; 44: 51-68.
[http://dx.doi.org/10.1016/j.cytogfr.2018.10.004] [PMID: 30396776]
[110]
Tanabe S, Heesen M, Yoshizawa I, et al. Functional expression of the CXC-chemokine receptor-4/fusin on mouse microglial cells and astrocytes. J Immunol 1997; 159(2): 905-11.
[PMID: 9218610]
[111]
Bonham LW, Karch CM, Fan CC, et al. CXCR4 involvement in neurodegenerative diseases. Transl Psychiatry 2018; 8(1): 73.
[http://dx.doi.org/10.1038/s41398-017-0049-7] [PMID: 29636460]
[112]
Sanfilippo C, Castrogiovanni P, Imbesi R, Nunnari G, Di Rosa M. Postsynaptic damage and microglial activation in AD patients could be linked CXCR4/CXCL12 expression levels. Brain Res 2020; 1749: 147127.
[http://dx.doi.org/10.1016/j.brainres.2020.147127] [PMID: 32949560]
[113]
Wang Q, Xu Y, Chen J-CC, et al. Stromal cell-derived factor 1α decreases β-amyloid deposition in Alzheimer’s disease mouse model. Brain Res 2012; 1459: 15-26.
[http://dx.doi.org/10.1016/j.brainres.2012.04.011] [PMID: 22560596]
[114]
Deshmane SL, Kremlev S, Amini S, Sawaya BE. Monocyte chemoattractant protein-1 (MCP-1): An overview. J Interferon Cytokine Res 2009; 29(6): 313-26.
[http://dx.doi.org/10.1089/jir.2008.0027] [PMID: 19441883]
[115]
Kiyota T, Gendelman HE, Weir RA, Higgins EE, Zhang G, Jain M. CCL2 affects β-amyloidosis and progressive neurocognitive dysfunction in a mouse model of Alzheimer’s disease. Neurobiol Aging 2013; 34(4): 1060-8.
[http://dx.doi.org/10.1016/j.neurobiolaging.2012.08.009] [PMID: 23040664]
[116]
Sokolova A, Hill MD, Rahimi F, Warden LA, Halliday GM, Shepherd CE. Monocyte chemoattractant protein-1 plays a dominant role in the chronic inflammation observed in Alzheimer’s disease. Brain Pathol 2009; 19(3): 392-8.
[http://dx.doi.org/10.1111/j.1750-3639.2008.00188.x] [PMID: 18637012]
[117]
Smits HA, Rijsmus A, van Loon JH, et al. Amyloid-β-induced chemokine production in primary human macrophages and astrocytes. J Neuroimmunol 2002; 127(1-2): 160-8.
[http://dx.doi.org/10.1016/S0165-5728(02)00112-1] [PMID: 12044988]
[118]
Vukic V, Callaghan D, Walker D, et al. Expression of inflammatory genes induced by beta-amyloid peptides in human brain endothelial cells and in Alzheimer’s brain is mediated by the JNK-AP1 signaling pathway. Neurobiol Dis 2009; 34(1): 95-106.
[http://dx.doi.org/10.1016/j.nbd.2008.12.007] [PMID: 19162185]
[119]
Liu C, Cui G, Zhu M, Kang X, Guo H. NeuroInflammation in Alzheimer’s disease: chemokines produced by astrocytes and chemokine receptors. Int J Clin Exp Pathol 2014; 7(12): 8342-55.
[PMID: 25674199]
[120]
Kimura A, Yoshikura N, Hayashi Y, Inuzuka T. Cerebrospinal fluid c-c motif chemokine ligand 2 correlates with brain atrophy and cognitive impairment in Alzheimer’s disease. J Alzheimers Dis 2018; 61(2): 581-8.
[http://dx.doi.org/10.3233/JAD-170519] [PMID: 29171996]
[121]
Shen XN, Niu LD, Wang YJ, et al. Inflammatory markers in Alzheimer’s disease and mild cognitive impairment: A meta-analysis and systematic review of 170 studies. J Neurol Neurosurg Psychiatry 2019; 90(5): 590-8.
[http://dx.doi.org/10.1136/jnnp-2018-319148] [PMID: 30630955]
[122]
Westin K, Buchhave P, Nielsen H, Minthon L, Janciauskiene S, Hansson O. CCL2 is associated with a faster rate of cognitive decline during early stages of Alzheimer’s disease. PLoS One 2012; 7(1): e30525.
[http://dx.doi.org/10.1371/journal.pone.0030525] [PMID: 22303443]
[123]
Flynn G, Maru S, Loughlin J, Romero IA, Male D. Regulation of chemokine receptor expression in human microglia and astrocytes. J Neuroimmunol 2003; 136(1-2): 84-93.
[http://dx.doi.org/10.1016/S0165-5728(03)00009-2] [PMID: 12620646]
[124]
Xia MQ, Bacskai BJ, Knowles RB, Qin SX, Hyman BT. Expression of the chemokine receptor CXCR3 on neurons and the elevated expression of its ligand IP-10 in reactive astrocytes: In vitro ERK1/2 activation and role in Alzheimer’s disease. J Neuroimmunol 2000; 108(1-2): 227-35.
[http://dx.doi.org/10.1016/S0165-5728(00)00285-X] [PMID: 10900358]
[125]
Krauthausen M, Kummer MP, Zimmermann J, et al. CXCR3 promotes plaque formation and behavioral deficits in an Alzheimer’s disease model. J Clin Invest 2015; 125(1): 365-78.
[http://dx.doi.org/10.1172/JCI66771] [PMID: 25500888]
[126]
Galimberti D, Schoonenboom N, Scheltens P, et al. Intrathecal chemokine levels in Alzheimer disease and frontotemporal lobar degeneration. Neurology 2006; 66(1): 146-7.
[http://dx.doi.org/10.1212/01.wnl.0000191324.08289.9d] [PMID: 16401871]
[127]
Koper OM, Kamińska J, Sawicki K, Kemona H. CXCL9, CXCL10, CXCL11, and their receptor (CXCR3) in neuroinflammation and neurodegeneration. Adv Clin Exp Med 2018; 27(6): 849-56.
[http://dx.doi.org/10.17219/acem/68846] [PMID: 29893515]
[128]
Corrêa JD, Starling D, Teixeira AL, Caramelli P, Silva TA. Chemokines in CSF of Alzheimer’s disease patients. Arq Neuropsiquiatr 2011; 69(3): 455-9.
[http://dx.doi.org/10.1590/S0004-282X2011000400009] [PMID: 21755121]
[129]
Su F, Bai F, Zhang Z. Inflammatory cytokines and Alzheimer’s disease: a review from the perspective of genetic polymorphisms. Neurosci Bull 2016; 32(5): 469-80.
[http://dx.doi.org/10.1007/s12264-016-0055-4] [PMID: 27568024]
[130]
Hua Y, Guo X, Huang Q, Kong Y, Lu X. Association between interleukin-6 -174G/C polymorphism and the risk of Alzheimer’s disease: A meta-analysis. Int J Neurosci 2013; 123(9): 626-35.
[http://dx.doi.org/10.3109/00207454.2013.784286] [PMID: 23510010]
[131]
Qin X, Peng Q, Zeng Z, et al. Interleukin-1A -889C/T polymorphism and risk of Alzheimer’s disease: A meta-analysis based on 32 case-control studies. J Neurol 2012; 259(8): 1519-29.
[http://dx.doi.org/10.1007/s00415-011-6381-6] [PMID: 22234841]
[132]
Singhal G, Jaehne EJ, Corrigan F, Toben C, Baune BT. Inflammasomes in neuroinflammation and changes in brain function: A focused review. Front Neurosci 2014; 8: 315.
[http://dx.doi.org/10.3389/fnins.2014.00315] [PMID: 25339862]
[133]
Mrak RE, Griffin WST. Glia and their cytokines in progression of neurodegeneration. Neurobiol Aging 2005; 26(3): 349-54.
[http://dx.doi.org/10.1016/j.neurobiolaging.2004.05.010] [PMID: 15639313]
[134]
Déniz-Naranjo MC, Muñoz-Fernandez C, Alemany-Rodríguez MJ, et al. Cytokine IL-1 beta but not IL-1 alpha promoter polymorphism is associated with Alzheimer disease in a population from the Canary Islands, Spain. Eur J Neurol 2008; 15(10): 1080-4.
[http://dx.doi.org/10.1111/j.1468-1331.2008.02252.x] [PMID: 18717723]
[135]
Di Bona D, Plaia A, Vasto S, et al. Association between the interleukin-1β polymorphisms and Alzheimer’s disease: A systematic review and meta-analysis. Brain Res Brain Res Rev 2008; 59(1): 155-63.
[http://dx.doi.org/10.1016/j.brainresrev.2008.07.003] [PMID: 18675847]
[136]
Lee YH, Choi SJ, Ji JD, Song GG. Association between TNF-α promoter -308 A/G polymorphism and Alzheimer’s disease: A meta-analysis. Neurol Sci 2015; 36(6): 825-32.
[http://dx.doi.org/10.1007/s10072-015-2102-8] [PMID: 25647294]
[137]
Ribizzi G, Fiordoro S, Barocci S, Ferrari E, Megna M. Cytokine polymorphisms and Alzheimer disease: possible associations. Neurol Sci 2010; 31(3): 321-5.
[http://dx.doi.org/10.1007/s10072-010-0221-9] [PMID: 20213229]
[138]
Li W, Qian X, Teng H, Ding Y, Zhang L. Association of interleukin-4 genetic polymorphisms with sporadic Alzheimer’s disease in Chinese Han population. Neurosci Lett 2014; 563: 17-21.
[http://dx.doi.org/10.1016/j.neulet.2014.01.019] [PMID: 24463336]
[139]
Moraes CF, Benedet AL, Souza VC, et al. Cytokine gene polymorphisms and Alzheimer’s disease in Brazil. Neuroimmunomodulation 2013; 20(5): 239-46.
[http://dx.doi.org/10.1159/000350368] [PMID: 23838435]
[140]
Karch CM, Goate AM. Alzheimer’s disease risk genes and mechanisms of disease pathogenesis. Biol Psychiatry 2015; 77(1): 43-51.
[http://dx.doi.org/10.1016/j.biopsych.2014.05.006] [PMID: 24951455]
[141]
Griciuc A, Serrano-Pozo A, Parrado AR, et al. Alzheimer’s disease risk gene CD33 inhibits microglial uptake of amyloid beta. Neuron 2013; 78(4): 631-43.
[http://dx.doi.org/10.1016/j.neuron.2013.04.014] [PMID: 23623698]
[142]
Reitz C, Mayeux R. TREM2 and neurodegenerative disease. N Engl J Med 2013; 369(16): 1564-5.
[http://dx.doi.org/10.1056/NEJMc1306509] [PMID: 24131184]
[143]
Tejera D, Heneka MT. Microglia in Neurodegenerative Disorders. Methods in Molecular Biology. Humana Press Inc. 2019; Vol. 2034: pp. 57-67.
[144]
Wang Y, Cella M, Mallinson K, et al. TREM2 lipid sensing sustains the microglial response in an Alzheimer’s disease model. Cell 2015; 160(6): 1061-71.
[http://dx.doi.org/10.1016/j.cell.2015.01.049] [PMID: 25728668]
[145]
Fan Z, Brooks DJ, Okello A, Edison P. An early and late peak in microglial activation in Alzheimer’s disease trajectory. Brain 2017; 140(3): 792-803.
[http://dx.doi.org/10.1093/brain/aww349] [PMID: 28122877]
[146]
Yeh FL, Hansen DV, Sheng M. TREM2, Microglia, and Neurodegenerative Diseases. Trends Mol Med 2017; 23(6): 512-33.
[http://dx.doi.org/10.1016/j.molmed.2017.03.008] [PMID: 28442216]
[147]
Lashley T, Schott JM, Weston P, et al. Molecular biomarkers of Alzheimer’s disease: progress and prospects. Dis Model Mech 2018; 11(5): dmm031781.
[http://dx.doi.org/10.1242/dmm.031781] [PMID: 29739861]
[148]
Suárez-Calvet M, Kleinberger G, Araque Caballero MÁ, et al. sTREM2 cerebrospinal fluid levels are a potential biomarker for microglia activity in early-stage Alzheimer’s disease and associate with neuronal injury markers. EMBO Mol Med 2016; 8(5): 466-76.
[http://dx.doi.org/10.15252/emmm.201506123] [PMID: 26941262]
[149]
Piccio L, Deming Y, Del-Águila JL, et al. Cerebrospinal fluid soluble TREM2 is higher in Alzheimer disease and associated with mutation status. Acta Neuropathol 2016; 131(6): 925-33.
[http://dx.doi.org/10.1007/s00401-016-1533-5] [PMID: 26754641]
[150]
Yang J, Fu Z, Zhang X, Xiong M, Meng L, Zhang Z. TREM2 ectodomain and its soluble form in Alzheimer’s disease. J Neuroinflammation 2020; 17(1): 204.
[http://dx.doi.org/10.1186/s12974-020-01878-2] [PMID: 32635934]
[151]
Querol-Vilaseca M, Colom-Cadena M, Pegueroles J, et al. YKL-40 (Chitinase 3-like I) is expressed in a subset of astrocytes in Alzheimer’s disease and other tauopathies. J Neuroinflammation 2017; 14(1): 118.
[http://dx.doi.org/10.1186/s12974-017-0893-7] [PMID: 28599675]
[152]
Craig-Schapiro R, Perrin RJ, Roe CM, et al. YKL-40: A novel prognostic fluid biomarker for preclinical Alzheimer’s disease. Biol Psychiatry 2010; 68(10): 903-12.
[http://dx.doi.org/10.1016/j.biopsych.2010.08.025] [PMID: 21035623]
[153]
Wiley CA, Bonneh-Barkay D, Dixon CE, et al. Role for mammalian chitinase 3-like protein 1 in traumatic brain injury. Neuropathology 2015; 35(2): 95-106.
[http://dx.doi.org/10.1111/neup.12158] [PMID: 25377763]
[154]
Llorens F, Thüne K, Tahir W, et al. YKL-40 in the brain and cerebrospinal fluid of neurodegenerative dementias. Mol Neurodegener 2017; 12(1): 83.
[http://dx.doi.org/10.1186/s13024-017-0226-4] [PMID: 29126445]
[155]
Colton CA, Mott RT, Sharpe H, Xu Q, Van Nostrand WE, Vitek MP. Expression profiles for macrophage alternative activation genes in AD and in mouse models of AD. J Neuroinflammation 2006; 3: 27.
[http://dx.doi.org/10.1186/1742-2094-3-27] [PMID: 17005052]
[156]
Rosén C, Andersson C-H, Andreasson U, et al. Increased levels of chitotriosidase and ykl-40 in cerebrospinal fluid from patients with Alzheimer’s disease. Dement Geriatr Cogn Disord Extra 2014; 4(2): 297-304.
[http://dx.doi.org/10.1159/000362164] [PMID: 25254036]
[157]
Blanco-Palmero VA, Rubio-Fernández M, Antequera D, et al. Increased YKL-40 but not C-reactive protein levels in patients with Alzheimer’s disease. Biomedicines 2021; 9(9): 1094.
[http://dx.doi.org/10.3390/biomedicines9091094] [PMID: 34572280]
[158]
Nishibori M, Wang D, Ousaka D, Wake H. High mobility group box-1 and blood-brain barrier disruption. Cells 2020; 9(12): 2650.
[http://dx.doi.org/10.3390/cells9122650] [PMID: 33321691]
[159]
Venegas C, Heneka MT. Danger-associated molecular patterns in Alzheimer’s disease. J Leukoc Biol 2017; 101(1): 87-98.
[http://dx.doi.org/10.1189/jlb.3MR0416-204R] [PMID: 28049142]
[160]
Takata K, Kitamura Y, Kakimura J, et al. Role of high mobility group protein-1 (HMG1) in amyloid-β homeostasis. Biochem Biophys Res Commun 2003; 301(3): 699-703.
[http://dx.doi.org/10.1016/S0006-291X(03)00024-X] [PMID: 12565837]
[161]
Tsui K-H, Chang Y-L, Feng T-H, Chang P-L, Juang H-H. Glycoprotein transmembrane nmb: An androgen-downregulated gene attenuates cell invasion and tumorigenesis in prostate carcinoma cells. Prostate 2012; 72(13): 1431-42.
[http://dx.doi.org/10.1002/pros.22494] [PMID: 22290289]
[162]
Tanaka H, Shimazawa M, Kimura M, et al. The potential of GPNMB as novel neuroprotective factor in amyotrophic lateral sclerosis. Sci Rep 2012; 2: 573.
[http://dx.doi.org/10.1038/srep00573] [PMID: 22891158]
[163]
Ripoll VM, Irvine KM, Ravasi T, Sweet MJ, Hume DA. Gpnmb is induced in macrophages by IFN-γ and lipopolysaccharide and acts as a feedback regulator of proinflammatory responses. J Immunol 2007; 178(10): 6557-66.
[http://dx.doi.org/10.4049/jimmunol.178.10.6557] [PMID: 17475886]
[164]
Nagahara Y, Shimazawa M, Tanaka H, et al. Glycoprotein nonmetastatic melanoma protein B ameliorates skeletal muscle lesions in a SOD1G93A mouse model of amyotrophic lateral sclerosis. J Neurosci Res 2015; 93(10): 1552-66.
[http://dx.doi.org/10.1002/jnr.23619] [PMID: 26140698]
[165]
Murata K, Yoshino Y, Tsuruma K, et al. The extracellular fragment of GPNMB (Glycoprotein nonmelanosoma protein B, osteoactivin) improves memory and increases hippocampal GluA1 levels in mice. J Neurochem 2015; 132(5): 583-94.
[http://dx.doi.org/10.1111/jnc.13010] [PMID: 25545823]
[166]
Satoh JI, Kino Y, Yanaizu M, Ishida T, Saito Y. Microglia express GPNMB in the brains of Alzheimer’s disease and Nasu-Hakola disease. Intractable Rare Dis Res 2019; 8(2): 120-8.
[http://dx.doi.org/10.5582/irdr.2019.01049] [PMID: 31218162]
[167]
Aichholzer F, Klafki H-W, Ogorek I, et al. Evaluation of cerebrospinal fluid glycoprotein NMB (GPNMB) as a potential biomarker for Alzheimer’s disease. Alzheimers Res Ther 2021; 13(1): 94.
[http://dx.doi.org/10.1186/s13195-021-00828-1] [PMID: 33947460]
[168]
Guzik-Makaruk EM, Pływaczewski EW, Laskowska K, Filipkowski W, Jurgielewicz-Delegacz E, Mroczko P. A comparative analysis of the treatment of decision-making by or for patients with neurodegenerative diseases in four legal jurisdictions. J Alzheimers Dis 2019; 70(1): 1-10.
[http://dx.doi.org/10.3233/JAD-190259] [PMID: 31127787]
[169]
Liu Y, Nguyen M, Robert A, Meunier B. Metal ions in Alzheimer’s disease: a key role or not? Acc Chem Res 2019; 52(7): 2026-35.
[http://dx.doi.org/10.1021/acs.accounts.9b00248] [PMID: 31274278]
[170]
Guo T, Zhang D, Zeng Y, Huang TY, Xu H, Zhao Y. Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease. Mol Neurodegener 2020; 15(1): 40.
[http://dx.doi.org/10.1186/s13024-020-00391-7] [PMID: 32677986]
[171]
Zhao Y, Wang Y, Hu J, Zhang X, Zhang YW, Cut A. CutA divalent cation tolerance homolog (Escherichia coli) (CUTA) regulates β-cleavage of β-amyloid precursor protein (APP) through interacting with β-site APP cleaving protein 1 (BACE1). J Biol Chem 2012; 287(14): 11141-50.
[http://dx.doi.org/10.1074/jbc.M111.330209] [PMID: 22351782]
[172]
Cahill CM, Lahiri DK, Huang X, Rogers JT. Amyloid precursor protein and alpha synuclein translation, implications for iron and inflammation in neurodegenerative diseases. Biochim Biophys Acta 2009; 1790(7): 615-28.
[http://dx.doi.org/10.1016/j.bbagen.2008.12.001] [PMID: 19166904]
[173]
Ayton S, Diouf I, Bush AI. Evidence that iron accelerates Alzheimer’s pathology: A CSF biomarker study. J Neurol Neurosurg Psychiatry 2018; 89(5): 456-60.
[http://dx.doi.org/10.1136/jnnp-2017-316551] [PMID: 28939683]
[174]
Shams M, Martola J, Charidimou A, et al. Cerebrospinal fluid metals and the association with cerebral small vessel disease. J Alzheimers Dis 2020; 78(3): 1229-36.
[http://dx.doi.org/10.3233/JAD-200656] [PMID: 33104030]
[175]
Cummings J, Aisen P, Apostolova LG, Atri A, Salloway S, Weiner M. Aducanumab: appropriate use recommendations. J Prev Alzheimers Dis 2021; 8(4): 398-410.
[http://dx.doi.org/10.14283/jpad.2021.41] [PMID: 34585212]
[176]
Cummings JL, Tong G, Ballard C. Treatment combinations for alzheimer’s disease: current and future pharmacotherapy options. J Alzheimers Dis 2019; 67(3): 779-94.
[http://dx.doi.org/10.3233/JAD-180766] [PMID: 30689575]
[177]
Fakhoury M. Inflammation in Alzheimer’s disease. Curr Alzheimer Res 2020; 17(11): 959-61.
[http://dx.doi.org/10.2174/156720501711210101110513] [PMID: 33509069]
[178]
Ozben T, Ozben S. Neuro-inflammation and anti-inflammatory treatment options for Alzheimer’s disease. Clin Biochem 2019; 72: 87-9.
[http://dx.doi.org/10.1016/j.clinbiochem.2019.04.001] [PMID: 30954437]
[179]
Ray B, Chauhan NB, Lahiri DK. Oxidative insults to neurons and synapse are prevented by aged garlic extract and S-allyl-L-cysteine treatment in the neuronal culture and APP-Tg mouse model. J Neurochem 2011; 117(3): 388-402.
[http://dx.doi.org/10.1111/j.1471-4159.2010.07145.x] [PMID: 21166677]
[180]
Gupta VB, Rao KSJ. Anti-amyloidogenic activity of S-allyl-L-cysteine and its activity to destabilize Alzheimer’s β-amyloid fibrils in vitro. Neurosci Lett 2007; 429(2-3): 75-80.
[http://dx.doi.org/10.1016/j.neulet.2007.09.042] [PMID: 18023978]
[181]
Chauhan NB. Effect of aged garlic extract on APP processing and tau phosphorylation in Alzheimer’s transgenic model Tg2576. J Ethnopharmacol 2006; 108(3): 385-94.
[http://dx.doi.org/10.1016/j.jep.2006.05.030] [PMID: 16842945]
[182]
Ray B, Chauhan NB, Lahiri DK. The “aged garlic extract:” (AGE) and one of its active ingredients S-allyl-L-cysteine (SAC) as potential preventive and therapeutic agents for Alzheimer’s disease (AD). Curr Med Chem 2011; 18(22): 3306-13.
[http://dx.doi.org/10.2174/092986711796504664] [PMID: 21728972]
[183]
Chainoglou E, Hadjipavlou-Litina D. Curcumin in health and diseases: Alzheimer’s disease and curcumin analogues, derivatives, and hybrids. Int J Mol Sci 2020; 21(6): 1975.
[http://dx.doi.org/10.3390/ijms21061975] [PMID: 32183162]
[184]
Fang L, Gou S, Liu X, Cao F, Cheng L. Design, synthesis and anti-Alzheimer properties of dimethylaminomethyl-substituted curcumin derivatives. Bioorg Med Chem Lett 2014; 24(1): 40-3.
[http://dx.doi.org/10.1016/j.bmcl.2013.12.011] [PMID: 24342238]
[185]
Sobenin IA, Pryanishnikov VV, Kunnova LM, Rabinovich YA, Martirosyan DM, Orekhov AN. The effects of time-released garlic powder tablets on multifunctional cardiovascular risk in patients with coronary artery disease. Lipids Health Dis 2010; 9: 119.
[http://dx.doi.org/10.1186/1476-511X-9-119] [PMID: 20958974]
[186]
Millen AE, Subar AF, Graubard BI, et al. Fruit and vegetable intake and prevalence of colorectal adenoma in a cancer screening trial. Am J Clin Nutr 2007; 86(6): 1754-64.
[http://dx.doi.org/10.1093/ajcn/86.5.1754] [PMID: 18065596]
[187]
Gullett NP, Ruhul Amin ARM, Bayraktar S, et al. Cancer prevention with natural compounds. Semin Oncol 2010; 37(3): 258-81.
[http://dx.doi.org/10.1053/j.seminoncol.2010.06.014] [PMID: 20709209]
[188]
Okuda M, Fujita Y, Hijikuro I, et al. PE859, A novel curcumin derivative, inhibits amyloid-β and tau aggregation, and ameliorates cognitive dysfunction in senescence-accelerated mouse prone 8. J Alzheimers Dis 2017; 59(1): 313-28.
[http://dx.doi.org/10.3233/JAD-161017] [PMID: 28598836]
[189]
Khanna S, Park H-A, Sen CK, et al. Neuroprotective and antiinflammatory properties of a novel demethylated curcuminoid. Antioxid Redox Signal 2009; 11(3): 449-68.
[http://dx.doi.org/10.1089/ars.2008.2230] [PMID: 18724833]
[190]
Ray B, Lahiri DK. NeuroInflammation in Alzheimer’s disease: different molecular targets and potential therapeutic agents including curcumin. Curr Opin Pharmacol 2009; 9(4): 434-44.
[http://dx.doi.org/10.1016/j.coph.2009.06.012] [PMID: 19656726]
[191]
Konno H, Endo H, Ise S, et al. Synthesis and evaluation of curcumin derivatives toward an inhibitor of beta-site amyloid precursor protein cleaving enzyme 1. Bioorg Med Chem Lett 2014; 24(2): 685-90.
[http://dx.doi.org/10.1016/j.bmcl.2013.11.039] [PMID: 24360557]
[192]
Bisht S, Khan MA, Bekhit M, et al. A polymeric nanoparticle formulation of curcumin (NanoCurc™) ameliorates CCl4-induced hepatic injury and fibrosis through reduction of pro-inflammatory cytokines and stellate cell activation. Lab Invest 2011; 91(9): 1383-95.
[http://dx.doi.org/10.1038/labinvest.2011.86] [PMID: 21691262]
[193]
Ray B, Bisht S, Maitra A, Maitra A, Lahiri DK. Neuroprotective and neurorescue effects of a novel polymeric nanoparticle formulation of curcumin (NanoCurc™) in the neuronal cell culture and animal model: implications for Alzheimer’s disease. J Alzheimers Dis 2011; 23(1): 61-77.
[http://dx.doi.org/10.3233/JAD-2010-101374] [PMID: 20930270]
[194]
Peck KJ, Girard TA, Russo FA, Fiocco AJ. Music and memory in alzheimer’s disease and the potential underlying mechanisms. J Alzheimers Dis 2016; 51(4): 949-59.
[http://dx.doi.org/10.3233/JAD-150998] [PMID: 26967216]
[195]
García-Casares N, Moreno-Leiva RM, García-Arnés JA. Music therapy as a non-pharmacological treatment in Alzheimer’s disease. A systematic review. Rev Neurol 2017; 65(12): 529-38.
[http://dx.doi.org/10.33588/rn.6512.2017181] [PMID: 29235615]
[196]
Gómez Gallego M, Gómez García J. Musicoterapia en la enfermedad de Alzheimer: efectos cognitivos, psicológicos y conductuales. Neurologia 2017; 32(5): 300-8.
[http://dx.doi.org/10.1016/j.nrl.2015.12.003] [PMID: 26896913]

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