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The Effects of a Novel Inhibitor of Tumor Necrosis Factor (TNF) Alpha on Prepulse Inhibition and Microglial Activation in Two Distinct Rodent Models of SchizophreniaShelton, Heath W., Gabbita, S. P., Gill, W. D., Burgess, Katherine C., Whicker, Wyatt S., Brown, Russell W. 21 May 2021 (has links)
Increased neuroinflammation has been shown in individuals diagnosed with schizophrenia (SCHZ). This study evaluated a novel immune modulator (PD2024) that targets the pro-inflammatory cytokine tumor necrosis factor-alpha (TNFα) to alleviate sensorimotor gating deficits and microglial activation employing two different rodent models of SCHZ. In Experiment 1, rats were neonatally treated with saline or the dopamine D2-like agonist quinpirole (NQ; 1 mg/kg) from postnatal day (P) 1-21 which produces increases of dopamine D2 receptor sensitivity throughout the animal's lifetime. In Experiment 2, rats were neonatally treated with saline or the immune system stimulant polyinosinic:polycytidylic acid (Poly I:C) from P5-7. Neonatal Poly I:C treatment mimics immune system activation associated with SCHZ. In both experiments, rats were raised to P30 and administered a control diet or a novel TNFα inhibitor PD2024 (10 mg/kg) in the diet from P30 until P67. At P45-46 and from P60-67, animals were behaviorally tested on auditory sensorimotor gating as measured through prepulse inhibition (PPI). NQ or Poly I:C treatment resulted in PPI deficits, and PD2024 treatment alleviated PPI deficits in both models. Results also revealed that increased hippocampal and prefrontal cortex microglial activation produced by neonatal Poly I:C was significantly reduced to control levels by PD2024. In addition, a separate group of animals neonatally treated with saline or Poly I:C from P5-7 demonstrated increased TNFα protein levels in the hippocampus but not prefrontal cortex, verifying increased TNFα in the brain produced by Poly I:C. Results from this study suggests that that brain TNFα is a viable pharmacological target to treat the neuroinflammation known to be associated with SCHZ.
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A Systems Approach to Dissecting Immune Gene Regulatory Networks in the Modulation of Brain FunctionXu, Yang 20 October 2017 (has links)
Although the central nervous system was long perceived as the ivory tower without immune entities, there is growing evidence that the immune and nervous systems are intimated connected. These two systems have been shown to communicate both cellularly and molecularly under physiological and pathological conditions. Despite our increasing understanding of the interplay between these two systems, there are still numerous open questions. In this thesis, I address such unanswered questions related to: the role of microglia and their mechanism in contributing to pathologies in Rett syndrome; the beneficial effects of T-cell secreted cytokines in supporting social brain function; the evolutionary link of the interactions between the nervous and immune systems; the transcription regulation of a subset of microglia population in common neurodegenerative diseases.
Collectively, the current thesis is focused on the joint frontier of bioinformatics and experimental work in neuroimmunology. A multifaceted approach, that includes transcriptomics, genomics and other biomolecular modules, was implemented to unearth signaling pathways and mechanisms underlying the presenting biological phenomena. The findings of this thesis can be summarized as follows: 1) MeCP2 acts as a master regulator in the transcriptional repression of inflammatory stimuli in macrophages; 2) T-cell secreted IFN-γ supports social brain function through an evolutionally conserved interaction between the immune and nervous systems; 3) The APOE-TREM2 pathway regulates the microglia phenotype switch in neurodegenerative diseases. Provided that recent technologies allow for readily manipulating the immune system, the findings presented herein may create new vistas for therapeutic interventions in various neurological disorders.
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Environmental enrichment mitigates hypothalamic inflammation and improves metabolic function across the lifespan of miceAli, Seemaab 13 November 2020 (has links)
No description available.
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Preparation and Characterization of Polymersomes for Nose-to-Brain Delivery of Combination Therapeutics in Neuroinflammation TreatmentManickavasagam, Dharani 25 April 2019 (has links)
No description available.
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Alteration to Astrocyte Density and Morphology across Mammalia with Specific Attention to Primate Brain Evolution and AgingMunger, Emily LaRee 14 July 2020 (has links)
No description available.
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THE ROLE OF IL-¿¿1 RECEPTOR-¿¿ASSOCIATED KINASE 4 IN MICROGLIAL ACTIVATION IN ALZHEIMER’S DISEASECameron, Brent D. 07 March 2013 (has links)
No description available.
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Gene regulatory mechanisms underlying microglial dysfunction in Alzheimer’s diseaseDaily, Kylene Patricia 19 September 2022 (has links)
No description available.
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Interleukin-1 signaling in the stressed CNS: From microglial source to neuronal destinationDiSabato, Damon J. January 2021 (has links)
No description available.
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Role of P2X7 Receptors in Immune Responses During NeurodegenerationOliveira-Giacomelli, Ágatha, Petiz, Lyvia Lintzmaier, Andrejew, Roberta, Turrini, Natalia, Silva, Jean Bezerra, Sack, Ulrich, Ulrich, Henning 27 March 2023 (has links)
P2X7 receptors are ion-gated channels activated by ATP. Under pathological conditions,
the extensive release of ATP induces sustained P2X7 receptor activation, culminating
in induction of proinflammatory pathways with inflammasome assembly and cytokine
release. These inflammatory conditions, whether occurring peripherally or in the central
nervous system (CNS), increase blood-brain-barrier (BBB) permeability. Besides its well-known involvement in neurodegeneration and neuroinflammation, the P2X7 receptor
may induce BBB disruption and chemotaxis of peripheral immune cells to the CNS,
resulting in brain parenchyma infiltration. For instance, despite common effects on
cytokine release, P2X7 receptor signaling is also associated with metalloproteinase
secretion and activation, as well as migration and differentiation of T lymphocytes,
monocytes and dendritic cells. Here we highlight that peripheral immune cells mediate
the pathogenesis of Multiple Sclerosis and Parkinson’s and Alzheimer’s disease, mainly
through T lymphocyte, neutrophil and monocyte infiltration. We propose that P2X7
receptor activation contributes to neurodegenerative disease progression beyond its
known effects on the CNS. This review discusses how P2X7 receptor activation
mediates responses of peripheral immune cells within the inflamed CNS, as occurring
in the aforementioned diseases.
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The Role of Neuroinflammation in the Pathogenesis of Amyotrophic Lateral SclerosisFrakes, Ashley E. January 2014 (has links)
No description available.
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