2019, Number 3
<< Back Next >>
Rev Mex Neuroci 2019; 20 (3)
Immunology of Alzheimer’s disease
Sosa-García LI, Hernández-Jiménez J, Del Moral-Huerta DI, Duyckaerts C, Calderón-Garcidueñas AL
Language: English
References: 59
Page: 162-170
PDF size: 141.99 Kb.
ABSTRACT
Alzheimer’s disease (AD) is a multifactorial neurodegenerative pathology. Neuroinflammation is an early event of the presymptomatic
stages in AD and contributes to its progression. We review the participation of astrocytes, microglia and blood-brain
barrier cells, the mechanisms of cell death and the inflammatory factors such as chemokines, interferons and Toll-like receptors
involved in progression and perpetuation of AD. Some of its prognostic and therapeutic possibilities are also mentioned.
Identifying the different actors involved in inflammation and the main mechanisms of damage might allow the development
of preventive strategies and treatments to fight against this devastating disease.
REFERENCES
Lewis J, Dickson DW. Propagation of tau pathology: hypotheses, discoveries, and yet unresolved questions from experimental and human brain studies. Acta Neuropathol. 2016;131:27-48.
Balin BJ, Hudson AP. Etiology and pathogenesis of late-onset alzheimer’s disease. Curr Allergy Asthma Rep. 2014;14:417.
Gatz M, Reynolds CA, Fratiglioni L, et al. Role of genes and environments for explaining alzheimer disease. Arch Gen Psychiatry. 2006;63:168-74.
International Genomics of Alzheimer’s Disease Consortium (IGAP). Convergent genetic and expression data implicate immunity in alzheimer’s disease. Alzheimers Dement. 2015;11:658-71.
Heppner FL, Ransohoff RM, Becher B. Immune attack: the role of inflammation in alzheimer disease. Nat Rev Neurosci. 2015;16:358-72.
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;7:8342-55.
Birch AM. The contribution of astrocytes to alzheimer’s disease. Biochem Soc Trans. 2014;42:1316-20.
Lee WJ, Liao YC, Wang YF, et al. 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.
Zhao H, Wang Q, Cheng X, et al. Inhibitive effect of resveratrol on the inflammation in cultured astrocytes and microglia induced by Aβ1-42. Neuroscience. 2018;379:390-404.
Bahniwal M, Little JP, Klegeris A. High glucose enhances neurotoxicity and inflammatory cytokine secretion by stimulated human astrocytes. Curr Alzheimer Res. 2017;14:731-41.
Parkhurst CN, Yang G, Ninan I, et al. Microglia promote learning-dependent synapse formation through brain-derived neurotrophic factor. Cell. 2013;155:1596-609.
Melchior B, Puntambekar SS, Carson MJ. Microglia and the control of autoreactive T cell responses. Neurochem Int. 2006;49:145-53.
Kierdorf K, Erny D, Goldmann T, et al. Microglia emerge from erythromyeloid precursors via pu.1-and irf8-dependent pathways. Nat Neurosci. 2013;16:273-80.
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-β and tau pathologies. Front Neurol. 2018; 9:549.
Lanni C, Fagiani F, Racchi M, et al. Beta-amyloid short-and long-term synaptic entanglement. Pharmacol Res. 2019;139:243-60.
Gay M, Evrard C, Descamps F, et al. A phenotypic approach to the discovery of compounds that promote non-amyloidogenic processing of the amyloid precursor protein: toward a new profile of indirect β-secretase inhibitors. Eur J Med Chem. 2018;159:104-25.
Kirouac L, Rajic AJ, Cribbs DH, Padmanabhan J. Activation of ras-ERK signaling and GSK-3 by amyloid precursor protein and amyloid beta facilitates neurodegeneration in alzheimer’s disease. ENeuro. 2017; 4:ENEURO.0149-16.2017.
Kim Y, Kim C, Jang HY, Mook-Jung I. Inhibition of cholesterol biosynthesis reduces γ-secretase activity and amyloid-β generation. J Alzheimers Dis. 2016;51:1057-68.
Neumann U, Ufer M, Jacobson LH, et al. The BACE-1 inhibitor CNP520 for prevention trials in alzheimer’s disease. EMBO Mol Med. 2018; 10:e9316.
Zhang H, Liu D, Huang H, Zhao Y, Zhou H. Characteristics of insulin-degrading enzyme in alzheimer’s disease: a meta-analysis. Curr Alzheimer Res. 2018;15:610-7.
Kazkayasi I, Burul-Bozkurt N, Ismail MA, et al. Insulin deprivation decreases insulin degrading enzyme levels in primary cultured cortical neurons and in the cerebral cortex of rats with streptozotocin-induced diabetes. Pharmacol Rep. 2018;70:677-83.
Shi Y, Holtzman DM. Interplay between innate immunity and alzheimer disease: APOE and TREM2 in the spotlight. Nat Rev Immunol. 2018; 18:759-72.
Arboleda-Bustos CE, Ortega-Rojas J, Mahecha MF, et al. The p.R47H variant of TREM2 gene is associated with late-onset alzheimer disease in colombian population. Alzheimer Dis Assoc Disord. 2018;32:305-8.
Wang Y, Ulland TK, Ulrich JD, et al. TREM2-mediated early microglial response limits diffusion and toxicity of amyloid plaques. J Exp Med. 2016;213:667-75.
Li JT, Zhang Y. TREM2 regulates innate immunity in alzheimer’s disease. J Neuroinflammation. 2018;15:107.
Zheng H, Jia L, Liu CC, et al. TREM2 promotes microglial survival by activating wnt/β-catenin pathway. J Neurosci. 2017;37:1772-84.
Jendresen C, Årskog V, Daws MR, Nilsson LN. The alzheimer’s disease risk factors apolipoprotein E and TREM2 are linked in a receptor signaling pathway. J Neuroinflammation. 2017;14:59.
Tam WY, Ma CH. Bipolar/rod-shaped microglia are proliferating microglia with distinct M1/M2 phenotypes. Sci Rep. 2014;4:7279.
Krbot K, Hermann P, Skorić MK, et al. Distinct microglia profile in creutzfeldt- jakob disease and alzheimer’s disease is independent of disease kinetics. Neuropathology. 2018;38:591-600.
Streit WJ, Braak H, Xue QS, Bechmann I. Dystrophic (senescent) rather than activated microglial cells are associated with tau pathology and likely precede neurodegeneration in alzheimer’s disease. Acta Neuropathol. 2009;118:475-85.
Medeiros R, Kitazawa M, Passos GF, et al. Aspirin-triggered lipoxin A4 stimulates alternative activation of microglia and reduces alzheimer disease- like pathology in mice. Am J Pathol. 2013;182:1780-9.
Kirkland JL, Tchkonia T. Cellular senescence: a translational perspective. EBioMedicine. 2017;21:21-8.
Bussian TJ, Aziz A, Meyer CF, et al. Clearance of senescent glial cells prevents tau-dependent pathology and cognitive decline. Nature. 2018; 562:578-82.
Snyder HM, Corriveau RA, Craft S, et al. Vascular contributions to cognitive impairment and dementia including alzheimer’s disease. Alzheimers Dement. 2015;11:710-7.
McFadyen JD, Kiefer J, Braig D, et al. Dissociation of C-reactive protein localizes and amplifies inflammation: evidence for a direct biological role of C-reactive protein and its conformational changes. Front Immunol. 2018;9:1351.
Shibata M, Yamada S, Kumar SR, et al. Clearance of alzheimer’s amyloid-ss(1-40) peptide from brain by LDL receptor-related protein-1 at the blood-brain barrier. J Clin Invest. 2000;106:1489-99.
Jeynes B, Provias J. Evidence for altered LRP/RAGE expression in alzheimer lesion pathogenesis. Curr Alzheimer Res. 2008;5:432-7.
Erickson MA, Banks WA. Blood-brain barrier dysfunction as a cause and consequence of alzheimer’s disease. J Cereb Blood Flow Metab. 2013;33:1500-13.
Liu C, Chen K, Lu Y, Fang Z, Yu G. Catalpol provides a protective effect on fibrillary Aβ1-42 -induced barrier disruption in an in vitro model of the blood-brain barrier. Phytother Res. 2018;32:1047-55.
Wong WB, Lin VW, Boudreau D, Devine EB. Statins in the prevention of dementia and alzheimer’s disease: a meta-analysis of observational studies and an assessment of confounding. Pharmacoepidemiol Drug Saf. 2013;22:345-58.
Salech F, Ponce DP, SanMartín CD, et al. PARP-1 and p53 regulate the increased susceptibility to oxidative death of lymphocytes from MCI and AD patients. Front Aging Neurosci. 2017;9:310.
Solleiro-Villavicencio H, Rivas-Arancibia S. Systemic th17/IL-17A response appears prior to hippocampal neurodegeneration in rats exposed to low doses of ozone. Neurologia. 2017. pii: S0213-4853(17) 30194-9.
Derkow K, Rössling R, Schipke C, et al. Distinct expression of the neurotoxic microRNA family let-7 in the cerebrospinal fluid of patients with alzheimer’s disease. PLoS One. 2018;13:e0200602.
Merlini M, Kirabali T, Kulic L, Nitsch RM, Ferretti MT. Extravascular CD3+ T cells in brains of alzheimer disease patients correlate with tau but not with amyloid pathology: an immunohistochemical study. Neurodegener Dis. 2018;18:49-56.
SanMartin CD, Henriquez M, Chacon C, et al. Vitamin D increases aβ140 plasma levels and protects lymphocytes from oxidative death in mild cognitive impairment patients. Curr Alzheimer Res. 2018;15:561-9.
Sommer A, Winner B, Prots I. The trojan horse-neuroinflammatory impact of T cells in neurodegenerative diseases. Mol Neurodegener. 2017;12:78.
Ahmed ME, Iyer S, Thangavel R, et al. Co-localization of glia maturation factor with NLRP3 inflammasome and autophagosome markers in human alzheimer’s disease brain. J Alzheimers Dis. 2017;60:1143-60.
Tammineni P, Cai Q. Defective retrograde transport impairs autophagic clearance in alzheimer disease neurons. Autophagy. 2017;13:982-4.
Navarro V, Sanchez-Mejias E, Jimenez S, et al. Microglia in alzheimer’s disease: activated, dysfunctional or degenerative. Front Aging Neurosci. 2018;10:140.
Shao BZ, Cao Q, Liu C. Targeting NLRP3 inflammasome in the treatment of CNS diseases. Front Mol Neurosci. 2018;11:320.
Raikwar SP, Thangavel R, Dubova I, et al. Targeted gene editing of glia maturation factor in microglia: a novel alzheimer’s disease therapeutic target. Mol Neurobiol. 2019;56:378-93.
Ciaramella A, Salani F, Bizzoni F, et al. The stimulation of dendritic cells by amyloid beta 1-42 reduces BDNF production in alzheimer’s disease patients. Brain Behav Immun. 2013;32:29-32.
Janelidze S, Mattsson N, Stomrud E, et al. CSF biomarkers of neuroinflammation and cerebrovascular dysfunction in early alzheimer disease. Neurology. 2018;91:e867-77.
Lin MS, Hung KS, Chiu WT, et al. Curcumin enhances neuronal survival in N-methyl-d-aspartic acid toxicity by inducing RANTES expression in astrocytes via PI-3K and MAPK signaling pathways. Prog Neuropsychopharmacol Biol Psychiatry. 2011;35:931-8.
Ransohoff RM, El Khoury J. Microglia in health and disease. Cold Spring Harb Perspect Biol. 2015;8:a020560.
Xia MQ, Qin SX, Wu LJ, Mackay CR, Hyman BT. Immunohistochemical study of the beta-chemokine receptors CCR3 and CCR5 and their ligands in normal and alzheimer’s disease brains. Am J Pathol. 1998;153:31-7.
Grimaldi LM, Zappalà G, Iemolo F, et al. A pilot study on the use of interferon beta-1a in early alzheimer’s disease subjects. J Neuroinflammation. 2014;11:30.
Rubio-Araiz A, Finucane OM, Keogh S, Lynch MA. Anti-TLR2 antibody triggers oxidative phosphorylation in microglia and increases phagocytosis of β-amyloid. J Neuroinflammation. 2018;15:247.
Sohrabifar N, Gharesouran J, Talebi M, Ghojazadeh M, Mohaddes Ardebili SM. Association of CLU and TLR2 gene polymorphisms with late- onset alzheimer disease in a Northwestern Iranian population. Turk J Med Sci. 2015;45:1082-6.