Querfurth HW, LaFerla FM. Alzheimer’s disease. N Engl J Med. 2010;362:329–44.
Scheltens P, De Strooper B, Kivipelto M, Holstege H, Chetelat G, Teunissen CE, et al. Alzheimer’s disease. Lancet. 2021;397:1577–90.
Kunkle BW, Grenier-Boley B, Sims R, Bis JC, Damotte V, Naj AC, et al. Genetic meta-analysis of diagnosed Alzheimer’s disease identifies new risk loci and implicates Abeta, tau, immunity and lipid processing. Nat Genet. 2019;51:414–30.
Jansen IE, Savage JE, Watanabe K, Bryois J, Williams DM, Steinberg S, et al. Genome-wide meta-analysis identifies new loci and functional pathways influencing Alzheimer’s disease risk. Nat Genet. 2019;51:404–13.
Wightman DP, Jansen IE, Savage JE, Shadrin AA, Bahrami S, Holland D, et al. A genome-wide association study with 1,126,563 individuals identifies new risk loci for Alzheimer’s disease. Nat Genet. 2021;53:1276–82.
Bellenguez C, Küçükali F, Jansen IE, Kleineidam L, Moreno-Grau S, Amin N, et al. New insights into the genetic etiology of Alzheimer’s disease and related dementias. Nat Genet. 2022;54:412–36.
Jia L, Li F, Wei C, Zhu M, Qu Q, Qin W, et al. Prediction of Alzheimer’s disease using multi-variants from a Chinese genome-wide association study. Brain. 2021;144:924–37.
Guerreiro R, Wojtas A, Bras J, Carrasquillo M, Rogaeva E, Majounie E, et al. TREM2 variants in Alzheimer’s disease. N Engl J Med. 2013;368:117–27.
Zhang DF, Fan Y, Xu M, Wang G, Wang D, Li J, et al. Complement C7 is a novel risk gene for Alzheimer’s disease in Han Chinese. Natl Sci Rev. 2019;6:257–74.
Zhou X, Chen Y, Mok KY, Zhao Q, Chen K, Chen Y, et al. Identification of genetic risk factors in the Chinese population implicates a role of immune system in Alzheimer’s disease pathogenesis. Proc Natl Acad Sci U S A. 2018;115:1697–706.
Heneka MT, Carson MJ, El Khoury J, Landreth GE, Brosseron F, Feinstein DL, et al. Neuroinflammation in Alzheimer’s disease. Lancet Neurol. 2015;14:388–405.
Koelink PJ, Overbeek SA, Braber S, de Kruijf P, Folkerts G, Smit MJ, et al. Targeting chemokine receptors in chronic inflammatory diseases: an extensive review. Pharmacol Ther. 2012;133:1–18.
Su F, Bai F, Zhang Z. Inflammatory cytokines and Alzheimer’s disease: a review from the perspective of genetic polymorphisms. Neurosci Bull. 2016;32:469–80.
Savarin-Vuaillat C, Ransohoff RM. Chemokines and chemokine receptors in neurological disease: raise, retain, or reduce? Neurotherapeutics. 2007;4:590–601.
Bajetto A, Bonavia R, Barbero S, Florio T, Schettini G. Chemokines and their receptors in the central nervous system. Front Neuroendocrinol. 2001;22:147–84.
Réaux-Le Goazigo A, Van Steenwinckel J, Rostène W, Mélik PS. Current status of chemokines in the adult CNS. Prog Neurobiol. 2013;104:67–92.
Dziembowska M, Tham TN, Lau P, Vitry S, Lazarini F, Dubois-Dalcq M. A role for CXCR4 signaling in survival and migration of neural and oligodendrocyte precursors. Glia. 2005;50:258–69.
Tsai HH, Frost E, To V, Robinson S, Ffrench-Constant C, Geertman R, et al. The chemokine receptor CXCR2 controls positioning of oligodendrocyte precursors in developing spinal cord by arresting their migration. Cell. 2002;110:373–83.
Padovani-Claudio DA, Liu L, Ransohoff RM, Miller RH. Alterations in the oligodendrocyte lineage, myelin, and white matter in adult mice lacking the chemokine receptor CXCR2. Glia. 2006;54:471–83.
Bertollini C, Ragozzino D, Gross C, Limatola C, Eusebi F. Fractalkine/CX3CL1 depresses central synaptic transmission in mouse hippocampal slices. Neuropharmacology. 2006;51:816–21.
Da Mesquita S, Herz J, Wall M, Dykstra T, de Lima KA, Norris GT, et al. Aging-associated deficit in CCR7 is linked to worsened glymphatic function, cognition, neuroinflammation, and beta-amyloid pathology. Sci Adv. 2021;7:eabe4601.
Zhou L, Kong G, Palmisano I, Cencioni MT, Danzi M, De Virgiliis F, et al. Reversible CD8 T cell-neuron cross-talk causes aging-dependent neuronal regenerative decline. Science. 2022;376:eabd5926.
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;19:392–8.
Tripathy D, Thirumangalakudi L, Grammas P. RANTES upregulation in the Alzheimer’s disease brain: a possible neuroprotective role. Neurobiol Aging. 2010;31:8–16.
Kauwe JS, Bailey MH, Ridge PG, Perry R, Wadsworth ME, Hoyt KL, et al. Genome-wide association study of CSF levels of 59 alzheimer’s disease candidate proteins: significant associations with proteins involved in amyloid processing and inflammation. PLoS Genet. 2014;10:e1004758.
Perea JR, Lleo A, Alcolea D, Fortea J, Avila J, Bolos M. Decreased CX3CL1 levels in the cerebrospinal fluid of patients with Alzheimer’s disease. Front Neurosci. 2018;12:609.
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;8:1280.
Goldeck D, Larbi A, Pellicano M, Alam I, Zerr I, Schmidt C, et al. Enhanced chemokine receptor expression on leukocytes of patients with Alzheimer’s disease. PLoS ONE. 2013;8:e66664.
Iarlori C, Gambi D, Gambi F, Lucci I, Feliciani C, Salvatore M, et al. Expression and production of two selected beta-chemokines in peripheral blood mononuclear cells from patients with Alzheimer’s disease. Exp Gerontol. 2005;40:605–11.
Jorda A, Cauli O, Santonja JM, Aldasoro M, Aldasoro C, Obrador E, et al. Changes in chemokines and chemokine receptors expression in a mouse model of Alzheimer’s disease. Int J Biol Sci. 2019;15:453–63.
Guedes JR, Santana I, Cunha C, Duro D, Almeida MR, Cardoso AM, et al. MicroRNA deregulation and chemotaxis and phagocytosis impairment in Alzheimer’s disease. Alzheimers Dement (Amst). 2016;3:7–17.
Guedes JR, Lao T, Cardoso AL, El Khoury J. Roles of microglial and monocyte chemokines and their receptors in regulating Alzheimer’s disease-associated amyloid-beta and tau pathologies. Front Neurol. 2018;9:549.
Subbarayan MS, Joly-Amado A, Bickford PC, Nash KR. CX3CL1/CX3CR1 signaling targets for the treatment of neurodegenerative diseases. Pharmacol Ther. 2022;231:107989.
Bhaskar K, Konerth M, Kokiko-Cochran ON, Cardona A, Ransohoff RM, Lamb BT. Regulation of tau pathology by the microglial fractalkine receptor. Neuron. 2010;68:19–31.
Liu Z, Condello C, Schain A, Harb R, Grutzendler J. CX3CR1 in microglia regulates brain amyloid deposition through selective protofibrillar amyloid-beta phagocytosis. J Neurosci. 2010;30:17091–101.
Kiyota T, Gendelman HE, Weir RA, Higgins EE, Zhang G, Jain M. CCL2 affects beta-amyloidosis and progressive neurocognitive dysfunction in a mouse model of Alzheimer’s disease. Neurobiol Aging. 2013;34:1060–8.
Vendramini AA, de Labio RW, Rasmussen LT, Minett T, Bertolucci PH, de Arruda Cardoso Smith M, et al. Interleukin-8 gene polymorphism -251T>A and Alzheimer’s disease. J Alzheimers Dis. 2007;12:221–2.
Villa C, Venturelli E, Fenoglio C, Clerici F, Marcone A, Benussi L, et al. CCL8/MCP-2 association analysis in patients with Alzheimer’s disease and frontotemporal lobar degeneration. J Neurol. 2009;256:1379–81.
Balistreri CR, Grimaldi MP, Vasto S, Listi F, Chiappelli M, Licastro F, et al. Association between the polymorphism of CCR5 and Alzheimer’s disease: results of a study performed on male and female patients from Northern Italy. Ann N Y Acad Sci. 2006;1089:454–61.
Lalli MA, Bettcher BM, Arcila ML, Garcia G, Guzman C, Madrigal L, et al. Whole-genome sequencing suggests a chemokine gene cluster that modifies age at onset in familial Alzheimer’s disease. Mol Psychiatry. 2015;20:1294–300.
Xu M, Zhang DF, Luo R, Wu Y, Zhou H, Kong LL, et al. A systematic integrated analysis of brain expression profiles reveals YAP1 and other prioritized hub genes as important upstream regulators in Alzheimer’s disease. Alzheimers Dement. 2018;14:215–29.
Sood S, Gallagher IJ, Lunnon K, Rullman E, Keohane A, Crossland H, et al. A novel multi-tissue RNA diagnostic of healthy ageing relates to cognitive health status. Genome Biol. 2015;16:185.
Matarin M, Salih DA, Yasvoina M, Cummings DM, Guelfi S, Liu W, et al. A genome-wide gene-expression analysis and database in transgenic mice during development of amyloid or tau pathology. Cell Rep. 2015;10:633–44.
留言 (0)