[1] Ginhoux F, Greter M, Leboeuf M, et al. Fate mapping analysis reveals that adult microglia derive from primitive macrophages[J]. Science, 2010, 330(6005):841-845.
[2] Ajami B, Bennett J L, Krieger C, et al. Local self-renewal can sustain CNS microglia maintenance and function throughout adult life[J]. Nature Neuroscience, 2007, 10(12):1538-1543.
[3] Hammond T R, Robinton D, Stevens B. Microglia and the Brain:Complementary partners in development and disease[J]. Annual Review of Cell Development Biology, 2018, 34:523-44.
[4] Fourgeaud L, Través P G, Tufail Y, et al. TAM receptors regulate multiple features of microglial physiology[J]. Nature, 2016, 532(7598):240-244.
[5] Parkhurst C N, Yang G, Ninan I, et al. Microglia promote learning-dependent synapse formation through brain-derived neurotrophic factor[J]. Cell, 2013, 155(7):1596-1609.
[6] Leng F, Edison P. Neuroinflammation and microglial activation in Alzheimer disease:Where do we go from here[J]. Nature Reviews:Neurology, 2021, 17:157-172.
[7] Colonna M, Butovsky O. Microglia function in the central nervous system during health and neurodegeneration[J]. Annual Review of Immunology, 2017, 35:441-468.
[8] Villa A, Vegeto E, Poletti A, et al. Estrogens, Neuroinflammation, and Neurodegeneration[J]. Endocrine Reviews, 2016, 37(4):372-402.
[9] Nimmerjahn A, Kirchhoff F, Helmchen F. Resting microglial cells are highly dynamic surveillants of brain parenchyma in vivo[J]. Science, 2005, 308(5726):1314-1318.
[10] Heneka M T, Carson M J, El Khoury J, et al. Neuroinflammation in Alzheimer's disease[J]. Lancet Neurology, 2015, 14(4):388-405.
[11] Davalos D, Grutzendler J, Yang G, et al. ATP mediates rapid microglial response to local brain injury in vivo[J]. Nature Neuroscience, 2005, 8(6):752-758.
[12] Freeman L, Guo H, David C N, et al. NLR members NLRC4 and NLRP3 mediate sterile inflammasome activation in microglia and astrocytes[J]. Journal of Experimental Medicine, 2017, 214(5):1351-1370.
[13] Labzin L I, Heneka M T, Latz E. Innate Immunity and Neurodegeneration[J]. Annual Review of Medicine, 2018, 69:437-49.
[14] Sweeney M D, Sagare A P, Zlokovic B V. Blood-brain barrier breakdown in Alzheimer disease and other neurodegenerative disorders[J]. Nature Reviews:Neurology, 2018, 14(3):133-50.
[15] Cheng Y, Wang Y J. Meningeal lymphatic vessels:A drain of the brain involved in neurodegeneration[J]. Neuroscience Bulletin, 2020, 36(5):557-560.
[16] Schain M, Kreisl W C. Neuroinflammation in neurodegenerative disorders:A review[J]. Current Neurology and Neuroscience Reports, 2017, 17(3):25.
[17] Fiebich B L, Batista C R A, Saliba S W, et al. Role of microglia TLRs in neurodegeneration[J]. Frontiers in Cellular Neuroscience, 2018, 12:329.
[18] De Nardo D. Toll-like receptors:Activation, signalling and transcriptional modulation[J]. Cytokine, 2015, 74(2):181-189.
[19] Broz P, Dixit V M. Inflammasomes:Mechanism of assembly, regulation and signalling[J]. Nature Reviews:Immunology, 2016, 16(7):407-420.
[20] Voet S, Srinivasan S, Lamkanfi M, et al. Inflammasomes in neuroinflammatory and neurodegenerative diseases[J]. EMBO Molecular Medicine, 2019, 11(6):e10248.
[21] Tohidpour A, Morgun A V, Boitsova E B, et al. Neuroinflammation and infection:Molecular mechanisms associated with dysfunction of neurovascular unit[J]. Frontiers in cellular and infection microbiology, 2017, 7:276.
[22] Calsolaro V, Edison P. Neuroinflammation in Alzheimer's disease:Current evidence and future directions[J]. Alzheimers Dement, 2016, 12(6):719-732.
[23] Hussain R, Zubair H, Pursell S, et al. Neurodegenerative diseases:Regenerative mechanisms and novel therapeutic approaches[J]. Brain Sciences, 2018, 8(9):177.
[24] Colpo G D, Ribeiro F M, Rocha N P, et al. Animal models for the study of human neurodegenerative diseases[M]//Conn P M. Animal Models for the Study of Human Disease. 2nd ed. London:Academic Press, 2017:1109-1129.
[25] Hammond T R, Marsh S E, Stevens B. Immune signaling in neurodegeneration[J]. Immunity, 2019, 50(4):955-974.
[26] Alzheimer A. Uber eine eigenartige Erkrankung der Hirnrinde[J]. Zentralbl Nervenh Psych, 1907, 18:177-179.
[27] Alzheimer A. Über eigenartige Krankheitsfälle des späteren Alters[J]. Zeitschrift für die gesamte Neurologie und Psychiatrie, 1911, 4(1):356.
[28] Prince M J. World Alzheimer report 2015:The global impact of dementia[M]. Alzheimer's Disease International, 2015.
[29] Selkoe D J. Soluble oligomers of the amyloid β-protein impair synaptic plasticity and behavior[J]. Behavioural Brain Research, 2008, 192(1):106-113.
[30] Wang Y, Mandelkow E. Tau in physiology and pathology[J]. Nature Reviews:Neuroscience, 2016, 17(1):5-21.
[31] Iqbal K, Liu F, Gong C X. Tau and neurodegenerative disease:The story so far[J]. Nature Reviews:Neurology, 2016, 12(1):15-27.
[32] McGeer P L, Itagaki S, Tago H, et al. Reactive microglia in patients with senile dementia of the Alzheimer type are positive for the histocompatibility glycoprotein HLADR[J]. Neuroscience Letters, 1987, 79(1/2):195-200.
[33] Sarlus H, Heneka M T. Microglia in Alzheimer's disease[J]. Journal of Clinical Investigation, 2017, 127(9):3240-3249.
[34] Sheedy F J, Grebe A, Rayner K J, et al. CD36 coordinates NLRP3 inflammasome activation by facilitating intracellular nucleation of soluble ligands into particulate ligands in sterile inflammation[J]. Nature Immunology, 2013, 14(8):812-820.
[35] Halle A, Hornung V, Petzold G C, et al. The NALP3 inflammasome is involved in the innate immune response to amyloid-β[J]. Nature Immunology, 2008, 9(8):857-865.
[36] Heneka M T, Kummer M P, Stutz A, et al. NLRP3 is activated in Alzheimer's disease and contributes to pathology in APP/PS1 mice[J]. Nature, 2013, 493(7434):674-678.
[37] Dunn N, Mullee M, Perry V H, et al. Association between dementia and infectious disease:Evidence from a case-control study[J]. Alzheimer Disease and Associated Disorders, 2005, 19(2):91-94.
[38] Tischer J, Krueger M, Mueller W, et al. Inhomogeneous distribution of Iba-1 characterizes microglial pathology in Alzheimer's disease[J]. Glia, 2016, 64(9):1562-1572.
[39] Swardfager W, Lanctôt K, Rothenburg L, et al. A meta-analysis of cytokines in Alzheimer's disease[J]. Biological Psychiatry, 2010, 68(10):930-941.
[40] Misra A, Chakrabarti S S, Gambhir I S. New genetic players in late-onset Alzheimer's disease:Findings of genome-wide association studies[J]. Indian Journal of Medical Research, 2018, 148(2):135-144.
[41] Philippens I H, Ormel P R, Baarends G, et al. Acceleration of amyloidosis by inflammation in the amyloid-beta marmoset monkey model of Alzheimer's disease[J]. Journal of Alzheimer's Disease, 2017, 55(1):101-113.
[42] Hur J Y, Frost G R, Wu X, et al. The innate immunity protein IFITM3 modulates γ-secretase in Alzheimer's disease[J]. Nature, 2020, 586(7831):735-740.
[43] Soscia S J, Kirby J E, Washicosky K J, et al. The Alzheimer's disease-associated amyloid beta-protein is an antimicrobial peptide[J]. PloS One, 2010, 5(3):e9505.
[44] Dempsey C, Rubio Araiz A, Bryson K J, et al. Inhibiting the NLRP3 inflammasome with MCC950 promotes nonphlogistic clearance of amyloid-β and cognitive function in APP/PS1 mice[J]. Brain, Behavior, and Immunity, 2017, 61:306-316.
[45] Yin J, Zhao F, Chojnacki J E, et al. NLRP3 inflammasome inhibitor ameliorates amyloid pathology in a mouse model of Alzheimer's disease[J]. Molecular Neurobiology, 2018, 55(3):1977-1987.
[46] Daniels M J, Rivers-Auty J, Schilling T, et al. Fenamate NSAIDs inhibit the NLRP3 inflammasome and protect against Alzheimer's disease in rodent models[J]. Nature Communications, 2016, 7:12504.
[47] Flores J, Noël A, Foveau B, et al. Caspase-1 inhibition alleviates cognitive impairment and neuropathology in an Alzheimer's disease mouse model[J]. Nature Communications, 2018, 9(1):3916.
[48] Poewe W. Non-motor symptoms in Parkinson's disease[J]. European Journal of Neurology, 2008, 15(Suppl 1):14-20.
[49] Spillantini M G, Crowther R A, Jakes R, et al. α-Synuclein in filamentous inclusions of Lewy bodies from Parkinson's disease and dementia with lewy bodies[J]. PNAS, 1998, 95(11):6469-6473.
[50] Elbaz A, Carcaillon L, Kab S, et al. Epidemiology of Parkinson's disease[J]. Revue Neurologique, 2016, 172(1):14-26.
[51] GBD 2016 Parkinson's disease collaborators global, regional, and national burden of Parkinson's disease, 1990-2016:A systematic analysis for the global burden of disease study 2016[J]. Lancet Neurology, 2018, 17(11):939-953.
[52] Dorsey E R, Bloem B R. The Parkinson pandemic-A call to action[J]. JAMA Neurol, 2018, 75(1):9-10.
[53] Codolo G, Plotegher N, Pozzobon T, et al. Triggering of inflammasome by aggregated α-synuclein, an inflammatory response in synucleinopathies[J]. PloS One, 2013, 8(1):e55375.
[54] Daniele S G, Béraud D, Davenport C, et al. Activation of MyD88-dependent TLR1/2 signaling by misfolded α-synuclein, a protein linked to neurodegenerative disorders[J]. Science Signal, 2015, 8(376):ra45.
[55] Fellner L, Irschick R, Schanda K, et al. Toll-like receptor 4 is required for α-synuclein dependent activation of microglia and astroglia[J]. Glia, 2013, 61(3):349-360.
[56] Wang W, Nguyen L T, Burlak C, et al. Caspase-1 causes truncation and aggregation of the Parkinson's disease-associated protein α-synuclein[J]. PNAS, 2016, 113(34):9587-9592.
[57] Yan Y, Jiang W, Liu L, et al. Dopamine controls systemic inflammation through inhibition of NLRP3 inflammasome[J]. Cell, 2015, 160(1/2):62-73.
[58] Deora V, Albornoz E A, Zhu K, et al. The ketone body β-hydroxybutyrate does not inhibit synuclein mediated inflammasome activation in microglia[J]. Journal of Neuroimmune Pharmacology, 2017, 12(4):568-574.
[59] Terada T, Yokokura M, Yoshikawa E, et al. Extrastriatal spreading of microglial activation in Parkinson's disease:A positron emission tomography study[J]. Annals of Nuclear Medicine, 2016, 30(8):579-587.
[60] Duffy M F, Collier T J, Patterson J R, et al. Lewy bodylike alpha-synuclein inclusions trigger reactive microgliosis prior to nigral degeneration[J]. Journal of Neuroinflammation, 2018, 15(1):129.
[61] Harms A S, Delic V, Thome A D, et al. α-Synuclein fibrils recruit peripheral immune cells in the rat brain prior to neurodegeneration[J]. Acta Neuropathol Communications, 2017, 5(1):85.
[62] Gao H M, Kotzbauer P T, Uryu K, et al. Neuroinflammation and oxidation/nitration of α-synuclein linked to dopaminergic neurodegeneration[J]. Journal of Neuroscience, 2008, 28(30):7687-7698.
[63] Challis C, Hori A, Sampson T R, et al. Gut-seeded α-synuclein fibrils promote gut dysfunction and brain pathology specifically in aged mice[J]. Nature Neuroscience, 2020, 23(3):327-336.
[64] Williams-Gray C H, Wijeyekoon R, Yarnall A J, et al. Serum immune markers and disease progression in an incident Parkinson's disease cohort (ICICLE-PD)[J]. Movement Disorders, 2016, 31(7):995-1003.
[65] de Pablo-Fernandez E, Goldacre R, Pakpoor J, et al. Association between diabetes and subsequent Parkinson disease:A record-linkage cohort study[J]. Neurology, 2018, 91(2):e139-e142.
[66] Gordon R, Albornoz E A, Christie D C, et al. Inflammasome inhibition prevents α-synuclein pathology and dopaminergic neurodegeneration in mice[J]. Science Translational Medicine, 2018, 10(465):eaah4066.
[67] Zhou Y, Lu M, Du R H, et al. MicroRNA-7 targets Nod-like receptor protein 3 inflammasome to modulate neuroinflammation in the pathogenesis of Parkinson's disease[J]. Molecular Neurodegeneration, 2016, 11:28.
[68] Li D S, Yang H Q, Ma J J, et al. MicroRNA-30e regulates neuroinflammation in MPTP model of Parkinson's disease by targeting Nlrp3[J]. Human Cell, 2018, 31(2):106-115.
[69] Zeng R, Luo D X, Li H P, et al. MicroRNA-135b alleviates MPP(+)-mediated Parkinson's disease in vitro model through suppressing FoxO1-induced NLRP3 inflammasome and pyroptosis[J]. Journal of Clinical Neuroscience, 2019, 65:125-133.
[70] Rothstein J D. Current hypotheses for the underlying biology of amyotrophic lateral sclerosis[J]. Annals of Neurology, 2009, 65(Suppl 1):S3-S9.
[71] Gurney M E, Pu H, Chiu A Y, et al. Motor neuron degeneration in mice that express a human Cu, Zn superoxide dismutase mutation[J]. Science, 1994, 264(5166):1772-1775.
[72] Dugger B N, Dickson D W. Pathology of neurodegenerative diseases[J]. Cold Spring Harbor Perspectives in Biology, 2017, 9(7):a028035.
[73] Zhao W, Beers D R, Bell S, et al. TDP-43 activates microglia through NF-κB and NLRP3 inflammasome[J]. Experimental Neurology, 2015, 273:24-35.
[74] Meissner F, Molawi K, Zychlinsky A. Mutant superoxide dismutase 1-induced IL-1beta accelerates ALS pathogenesis[J]. PNAS, 2010, 107(29):13046-13050.
[75] Zhao W, Beers D R, Henkel J S, et al. Extracellular mutant SOD1 induces microglial-mediated motoneuron injury[J]. Glia, 2010, 58(2):231-243.
[76] Sargsyan S A, Blackburn D J, Barber S C, et al. Acomparison of in vitro properties of resting SOD1 transgenic microglia reveals evidence of reduced neuroprotective function[J]. BMC Neuroscience, 2011, 12:91.
[77] Nguyen M D, D'Aigle T, Gowing G, et al. Exacerbation of motor neuron disease by chronic stimulation of innate immunity in a mouse model of amyotrophic lateral sclerosis[J]. Journal of Neuroscience, 2004, 24(6):1340-1349.
[78] Schütz B, Reimann J, Dumitrescu-Ozimek L, et al. The oral antidiabetic pioglitazone protects from neurodegeneration and amyotrophic lateral sclerosis-like symptoms in superoxide dismutase-G93A transgenic mice[J]. Journal of Neuroscience, 2005, 25(34):7805-7812.
[79] Maier A, Deigendesch N, Müller K, et al. Interleukin-1 antagonist anakinra in amyotrophic lateral sclerosis——A pilot study[J]. PloS One, 2015, 10(10):e0139684.
[80] Caron N S, Dorsey E R, Hayden M R. Therapeutic approaches to Huntington disease:From the bench to the clinic[J]. Nature Reviews:Drug Discovery, 2018, 17(10):729-750.
[81] Walker F O. Huntington's disease[J]. Lancet, 2007, 369(9557):218-228.
[82] Bates G P, Dorsey R, Gusella J F, et al. Huntington disease[J]. Nature Reviews:Disease Primers, 2015, 1(1):1-21.
[83] Heneka M T, Kummer M P, Latz E. Innate immune activation in neurodegenerative disease[J]. Nature Reviews:Immunology, 2014, 14(7):463-477.
[84] Björkqvist M, Wild E J, Thiele J, et al. A novel pathogenic pathway of immune activation detectable before clinical onset in Huntington's disease[J]. Journal of Experimental Medicine, 2008, 205(8):1869-1877.
[85] Crotti A, Benner C, Kerman B E, et al. Mutant Huntingtin promotes autonomous microglia activation via myeloid lineage-determining factors[J]. Nature Neuroscience, 2014, 17(4):513-521.
[86] Novellino F, Saccà V, Donato A, et al. Innateimmunity:Acommon denominator between neurodegenerative and neuropsychiatric diseases[J]. International Journal of Molecular Sciences, 2020, 21(3):1115.
[87] Ona V O, Li M, Vonsattel J P, et al. Inhibition of caspase-1 slows disease progression in a mouse model of Huntington's disease[J]. Nature, 1999, 399(6733):263-267.
[88] Chen M, Ona V O, Li M, et al. Minocycline inhibits caspase-1 and caspase-3 expression and delays mortality in a transgenic mouse model of Huntington disease[J]. Nature Medicine, 2000, 6(7):797-801.
[89] Wan M, Ding L, Wang D, et al. Serotonin:A potent immune cell modulator in autoimmune diseases[J]. Front Immunol, 2020, 11:186.
[90] Brück W. Clinical implications of neuropathological findings in multiple sclerosis[J]. Journal of Neurology, 2005, 252(Suppl 3):iii10-iii4.
[91] Zhang J, Markovic-Plese S, Lacet B, et al. Increased frequency of interleukin 2-responsive T cells specific for myelin basic protein and proteolipid protein in peripheral blood and cerebrospinal fluid of patients with multiple sclerosis[J]. Journal of Experimental Medicine, 1994, 179(3):973-984.
[92] Bettelli E. Building different mouse models for human MS[J]. Annals of the New York Academy of Sciences, 2007, 1103:11-18.
[93] Inoue M, Shinohara M L. NLRP3 Inflammasome and MS/EAE[J]. Autoimmune Diseases, 2013, 2013:859145.
[94] Ciraci C, Janczy J R, Jain N, et al. Immunecomplexes indirectly suppress the generation of Th17 responses in vivo[J]. PloS One, 2016, 11(3):e0151252.
[95] Gris D, Ye Z, Iocca H A, et al. NLRP3 plays a critical role in the development of experimental autoimmune encephalomyelitis by mediating Th1 and Th17 responses[J]. Journal of Immunology, 2010, 185(2):974-981.
[96] Jha S, Srivastava S Y, Brickey W J, et al. The inflammasome sensor, NLRP3, regulates CNS inflammation and demyelination via caspase-1 and interleukin-18[J]. Journal of Neuroscience, 2010, 30(47):15811-15820.
[97] McKenzie B A, Mamik M K, Saito L B, et al. Caspase-1 inhibition prevents glial inflammasome activation and pyroptosis in models of multiple sclerosis[J]. PNAS, 2018, 115(26):E6065-E6074.
[98] Coll R C, Robertson A A, Chae J J, et al. A small-molecule inhibitor of the NLRP3 inflammasome for the treatment of inflammatory diseases[J]. Nature Medicine, 2015, 21(3):248-255.
[99] Sánchez-Fernández A, Skouras D B, Dinarello C A, et al. OLT1177(Dapansutrile), a selective NLRP3 inflammasome inhibitor, ameliorates experimental autoimmune encephalomyelitis pathogenesis[J]. Frontiers in Immunology, 2019, 10:2578.
[100] Gao Q, Zhang Y, Han C, et al. Blockade of CD47 ameliorates autoimmune inflammation in CNS by suppressing IL-1-triggered infiltration of pathogenic Th17 cells[J]. Journal of Autoimmunity, 2016, 69:74-85.
[101] Lammert C R, Frost E L, Bellinger C E, et al. AIM2 inflammasome surveillance of DNA damage shapes neurodevelopment[J]. Nature, 2020, 580(7805):647-652.
[102] Ambrosini Y M, Borcherding D, Kanthasamy A, et al. The gut-brain axis in neurodegenerative diseases and relevance of the canine model:A review[J]. Frontiers in Aging Neuroscience, 2019, 11:130.