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Does Infection-Induced Immune Activation Contribute to Dementia? Tatiana Barichello 1, 2 ;Jaqueline S. Generoso 2 ;Jessica A. Goularte 2 ;Allan Collodel.

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Presentation on theme: "Does Infection-Induced Immune Activation Contribute to Dementia? Tatiana Barichello 1, 2 ;Jaqueline S. Generoso 2 ;Jessica A. Goularte 2 ;Allan Collodel."— Presentation transcript:

1 Does Infection-Induced Immune Activation Contribute to Dementia? Tatiana Barichello 1, 2 ;Jaqueline S. Generoso 2 ;Jessica A. Goularte 2 ;Allan Collodel 2 ;Meagan R. Pitcher 1 ;Lutiana R. Sim#cod#x000F5;es 2 ;Jo#cod#x000E3;o Quevedo 1, 3 ;Felipe Dal-Pizzol 4 ; 1 Center for Translational Psychiatry, Department of Psychiatry and Behavioral Sciences, The University of Texas Medical School at Houston, Houston, TX, USA ; 2 Laborat#cod#x000F3;rio de Microbiologia Experimental, Programa de P#cod#x000F3;s- Gradua#cod#x000E7;#cod#x000E3;o em Ci#cod#x000EA;ncias da Sa#cod#x000FA;de, Unidade Acad#cod#x000EA;mica de Ci#cod#x000EA;ncias da Sa#cod#x000FA;de, Universidade do Extremo Sul Catarinense, Crici#cod#x000FA;ma, SC, Brazil. ; 3 Laborat#cod#x000F3;rio de Neuroci#cod#x000EA;ncias, Programa de P#cod#x000F3;s-Gradua#cod#x000E7;#cod#x000E3;o em Ci#cod#x000EA;ncias da Sa#cod#x000FA;de, Unidade Acad#cod#x000EA;mica de Ci#cod#x000EA;ncias da Sa#cod#x000FA;de, Universidade do Extremo Sul Catarinense, Crici#cod#x000FA;ma, SC, Brazil. ; 4 Laboratorio de Fisiopatologia Experimental, Programa de Pos-Graduacao em Ciencias da Saude, Unidade Academica de Ciencias da Saude, Universidade do Extremo Sul Catarinense, 88806- 000 Criciuma, SC, Brazil. ; Figure 1. Recognition of pathogens by the innate immune system. Toll-like receptors TLR recognize molecular motifs that are expressed by pathogens or endogenous ligands released from damaged cells. AGE, advanced glycation end products; AP-1, activator protein-1; ASC, apoptosis-associated speck-like protein containing a caspase- recruitment domain; Cdc42, cell division control protein 42 homolog; Csp3, caspase-3; eNOS, endothelial nitric oxide synthase; ERK, extracellular signal regulated; IL, interleukin; IKK, NEMOIKK#cod#x003B1;IKK#cod#x000DF; complex; IRAK-4, interleukin-1 receptor-associated kinase 4; I#cod#x003BA;B, inhibitor of NF-#cod#x003BA;B; IKK, I#cod#x003BA;B kinase; INF, interferon; IRF3, interferon regulatory factor 3; JNK, c-jun N-terminal kinase; MAPK, mitogen-activated protein kinases; MyD88, myeloid differentiation factor 88; MEK, mitogen-activated protein kinase; MKK, MAPK kinase; NADPH, Nicotinamide adenine dinucleotide phosphate; NEMO, NF-#cod#x003BA;B essential modulator, IKK#cod#x003B3;; NF-#cod#x003BA;B, nuclear transcription factor kappa B; NLRP3, nucleotide-binding domain and leucine-rich repeat protein 3; NO, nitric oxide; NODs, nucleotide binding oligomerisation domains; PI3K, phosphatidylinositide 3-kinase; PKB, protein kinase A; RAGE; receptor for advanced glycation endproducts; PKR, protein kinase RNA-activated; ROS, reactive oxygen species; TAB, TGF-#cod#x003B2;-activated kinase 1-binding protein 1; TAK1, TGF#cod#x000DF; activated kinase 1; TIRAP, TIR-containing protein; TLRs, toll-like receptors; TRAF, receptor-associated factor; TRAM, TRIF-related adaptor molecule; TRIF, TIR-domain- containing adapter-inducing interferon-#cod#x003B2; Aging and Disease,null,6(5),342-348. Doi:10.14336/AD.2015.0521


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