2019
DOI: 10.1016/j.ajpath.2019.03.006
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Abstract: Pathologic inflammation in response to injury, infection, or oxidative stress is a proposed mechanism relating cognitive decline to dementia. The kynurenine pathway and thioredoxin-interacting protein (TXNIP) activity regulate inflammation and neurotoxicity in Alzheimer disease (AD). We examined cognitive deficits, kynurenine pathway mediators, TXNIP, and oxidative damage in the cerebrum and spleen, including inflammatory cytokine production by stimulated splenocytes, from female triple transgenic (3xTg-AD) mi… Show more

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Cited by 21 publications
(28 citation statements)
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“…TRP and its catabolites are well known for their immunosuppressive functions, disease tolerance, and contributions to immune-privileged sites, such as the brain [74]. The relationship among cognitive deficits, KP mediators, and oxidative damage in the brain of an AD mouse model has been recently provided, showing an increase of TRP metabolites in the brain [75].…”
Section: Discussionmentioning
confidence: 99%
“…TRP and its catabolites are well known for their immunosuppressive functions, disease tolerance, and contributions to immune-privileged sites, such as the brain [74]. The relationship among cognitive deficits, KP mediators, and oxidative damage in the brain of an AD mouse model has been recently provided, showing an increase of TRP metabolites in the brain [75].…”
Section: Discussionmentioning
confidence: 99%
“…Even though tryptophan metabolism via the KP seems to be involved in the progression of AD, there are many other mechanisms underlying AD, including cholinergic (dys)function, metabolic deficits, and environmental factors (Grant et al, 2002; Dziewczapolski et al, 2009; Lee et al, 2018). In addition, thioredoxin-interacting protein (TXNIP) is increased by Aβ 42 and increases oxidative stress, thereby increasing the progression of AD (Fertan et al, 2019a). Future studies should investigate the neurobiological mechanisms in which these factors contribute to AD and their interaction with each other and Aβ 42 .…”
Section: Discussionmentioning
confidence: 99%
“…IDO gene expression is stimulated by interferon gamma (INF-ɣ, Taylor and Feng, 1991; Jurgens et al, 2009) and by Aβ 42 (Guillemin et al, 2003). IDO levels are increased in the hippocampus of AD patients (Guillemin et al, 2005a), and INF-ɣ and IDO levels are increased in the cerebrum of female triple transgenic mice (3xTg-AD), a commonly used model of AD (Fertan et al, 2019a). Thus, overactivity of IDO in the KP may integrate the various mechanisms involved in the pathogenesis of AD, leading to neuronal loss and behavioral deficits.…”
Section: Introductionmentioning
confidence: 99%
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“…Frozen cerebrum were weighted and mechanically homogenized in ice‐cold IP buffer: 150 mM NaCl (Cat# J21618, Millipore Sigma, St. Louis, Missouri); 10 mM Tris‐HCL, pH 7.4 (Cat# BP2471‐1, Thermo Fisher Scientific, Waltham, Massachusetts); 1 mM EDTA (Cat# BP118‐500, Thermo Fisher Scientific); 1 mM EGTA, pH 8.0 (Cat# E3889, Millipore Sigma); 0.2 mM sodium orthovanadate (Cat# S6508, Millipore Sigma); 0.2 mM PMSF (Cat# P7626, Millipore Sigma); 1% Triton X‐100 (Cat# X100, Millipore Sigma); 0.5% NP‐40 (Cat# 97063‐298, Amresco, LLC., Solon, Ohio), and centrifuged (10,000 g , 5 min, 4°C). Immunoprecipitations were performed on total protein adjusted to 1 mg/mL with IP buffer, as described by Fertan, et al 105 In brief, samples were precleared with protein A/G magnetic beads (Cat# 88802) and incubated on a nutator (4C, 1 hr) with antibodies specific for NLGN1 (Cat#: MBS9365594), NLGN2 (Cat#: MBS9915356), or MDGA2 (Cat#: MBS9717695) or nonimmune IgG (MyBioSource, San Diego, California). Immuno‐complexes were captured with Protein A beads on a nutator (4C, 1 hr) and the supernatant was discharged.…”
Section: Methodsmentioning
confidence: 99%