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• W2890168785 abstract "Aberrant inflammatory signaling between neuronal and glial cells can develop into a persistent sickness behavior-related disorders, negatively impacting learning, memory and neurogenesis. While there is an abundance of literature describing these interactions, there still lacks a comprehensive mathematical model describing the complex feed-forward and feedback mechanisms of neural-glial interaction. Here we compile molecular and cellular signaling information from various studies and reviews in the literature to create a logically-consistent, theoretical model of neural-glial interaction in the brain to explore the role of neuron-glia homeostatic regulation in the perpetuation of neuroinflammation. Logic rules are applied to this connectivity diagram to predict the system’s homeostatic behavior. We validate our model predicted homeostatic profiles against RNAseq gene expression profiles in a mouse model of stress primed neuroinflammation. A meta-analysis was used to calculate the significance of similarity between the inflammatory profiles of mice exposed to diisopropyl fluorophostphate (DFP) (with and without prior priming by the glucocorticoid stress hormone corticosterone (CORT)), with the equilibrium states predicted by the model, and to provide estimates of the degree of the neuroinflammatory response. Beyond normal homeostatic regulation, our model predicts an alternate self-perpetuating condition consistent with chronic neuroinflammation. RNAseq gene expression profiles from the cortex of mice exposed to DFP and CORT+DFP align with this predicted state of neuroinflammation, whereas the alignment to CORT alone was negligible. Simulations of putative treatment strategies post-exposure were shown to be theoretically capable of returning the system to a state of typically healthy regulation with broad-acting anti-inflammatory agents showing the highest probability of success. The results support a role for the brain’s own homeostatic drive in perpetuating the chronic neuroinflammation associated with exposure to the organophosphate DFP, with and without CORT priming. The deviation of illness profiles from exact model predictions suggests the presence of additional factors or of lasting changes to the brain’s regulatory circuitry specific to each exposure." @default.
• W2890168785 created "2018-09-27" @default.
• W2890168785 creator A5003877429 @default.
• W2890168785 creator A5011861328 @default.
• W2890168785 creator A5015262975 @default.
• W2890168785 creator A5015576193 @default.
• W2890168785 creator A5030536201 @default.
• W2890168785 creator A5040688985 @default.
• W2890168785 creator A5041794756 @default.
• W2890168785 creator A5073925608 @default.
• W2890168785 creator A5089175484 @default.
• W2890168785 date "2018-10-15" @default.
• W2890168785 modified "2023-10-15" @default.
• W2890168785 title "A Logic Model of Neuronal-Glial Interaction Suggests Altered Homeostatic Regulation in the Perpetuation of Neuroinflammation" @default.
• W2890168785 cites W1033942775 @default.
• W2890168785 cites W1558100964 @default.
• W2890168785 cites W1587164985 @default.
• W2890168785 cites W1617668199 @default.
• W2890168785 cites W1847890422 @default.
• W2890168785 cites W1886819223 @default.
• W2890168785 cites W1964334511 @default.
• W2890168785 cites W1964744961 @default.
• W2890168785 cites W1965604886 @default.
• W2890168785 cites W1965666333 @default.
• W2890168785 cites W1966338898 @default.
• W2890168785 cites W1967375281 @default.
• W2890168785 cites W1967720787 @default.
• W2890168785 cites W1971224531 @default.
• W2890168785 cites W1975177900 @default.
• W2890168785 cites W1977773662 @default.
• W2890168785 cites W1977807607 @default.
• W2890168785 cites W1979871839 @default.
• W2890168785 cites W1988092837 @default.
• W2890168785 cites W1989284002 @default.
• W2890168785 cites W1989369404 @default.
• W2890168785 cites W1990043489 @default.
• W2890168785 cites W1993637512 @default.
• W2890168785 cites W1996024251 @default.
• W2890168785 cites W1996588072 @default.
• W2890168785 cites W2003123811 @default.
• W2890168785 cites W2007217012 @default.
• W2890168785 cites W2009277428 @default.
• W2890168785 cites W2009478129 @default.
• W2890168785 cites W2015070234 @default.
• W2890168785 cites W2015541518 @default.
• W2890168785 cites W2015851283 @default.
• W2890168785 cites W2016575029 @default.
• W2890168785 cites W2021688937 @default.
• W2890168785 cites W2025026106 @default.
• W2890168785 cites W2035036667 @default.
• W2890168785 cites W2036956824 @default.
• W2890168785 cites W2038655472 @default.
• W2890168785 cites W2041796079 @default.
• W2890168785 cites W2042991023 @default.
• W2890168785 cites W2045683532 @default.
• W2890168785 cites W2048259921 @default.
• W2890168785 cites W2051947267 @default.
• W2890168785 cites W2052285428 @default.
• W2890168785 cites W2057871265 @default.
• W2890168785 cites W2058221907 @default.
• W2890168785 cites W2059844545 @default.
• W2890168785 cites W2061576298 @default.
• W2890168785 cites W2061653274 @default.
• W2890168785 cites W2063388001 @default.
• W2890168785 cites W2063579231 @default.
• W2890168785 cites W2065669632 @default.
• W2890168785 cites W2067267561 @default.
• W2890168785 cites W2073170210 @default.
• W2890168785 cites W2073295417 @default.
• W2890168785 cites W2074661552 @default.
• W2890168785 cites W2078090509 @default.
• W2890168785 cites W2079394030 @default.
• W2890168785 cites W2084566588 @default.
• W2890168785 cites W2086697336 @default.
• W2890168785 cites W2086854638 @default.
• W2890168785 cites W2087146795 @default.
• W2890168785 cites W2088747855 @default.
• W2890168785 cites W2088882360 @default.
• W2890168785 cites W2090804892 @default.
• W2890168785 cites W2092933011 @default.
• W2890168785 cites W2093202085 @default.
• W2890168785 cites W2094660330 @default.
• W2890168785 cites W2094905802 @default.
• W2890168785 cites W2095369231 @default.
• W2890168785 cites W2095547457 @default.
• W2890168785 cites W2099516158 @default.
• W2890168785 cites W2102093684 @default.
• W2890168785 cites W2110729320 @default.
• W2890168785 cites W2111572664 @default.
• W2890168785 cites W2113617025 @default.
• W2890168785 cites W2113632571 @default.
• W2890168785 cites W2116629441 @default.
• W2890168785 cites W2118450265 @default.
• W2890168785 cites W2119679649 @default.
• W2890168785 cites W2122828560 @default.
• W2890168785 cites W2126795224 @default.
• W2890168785 cites W2127854743 @default.
• W2890168785 cites W2129690840 @default.
• W2890168785 cites W2129771952 @default.
• W2890168785 cites W2132867079 @default.

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