Area:
Pharmacology, Neuroscience Biology
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High-probability grants
According to our matching algorithm, Thad A. Rosenberger is the likely recipient of the following grants.
| Years |
Recipients |
Code |
Title / Keywords |
Matching
score |
| 2008 — 2011 |
Rosenberger, Thad Allen |
P20Activity Code Description:
To support planning for new programs, expansion or modification of existing resources, and feasibility studies to explore various approaches to the development of interdisciplinary programs that offer potential solutions to problems of special significance to the mission of the NIH. These exploratory studies may lead to specialized or comprehensive centers. |
Lipid-Mediated Signaling and Neuroinflammation @ University of North Dakota
1-Phosphatidylinositol 3-Kinase; ATP[{..}]1-phosphatidyl-1D-myo-inositol 3-phosphotransferase; Amentia; Assay; Behavioral; Bioassay; Biochemical; Biologic Assays; Biological Assay; Brain; CRISP; Cell Communication and Signaling; Cell Death; Cell Signaling; Cells; Common Rat Strains; Computer Retrieval of Information on Scientific Projects Database; Cytosolic Phospholipase A2; Cytosolic Phospholipase A2 Group IV; Cytosolic Phospholipase A2G4; Cytosolic Phospholipase A2IV; Degenerative Diseases, Nervous System; Degenerative Neurologic Disorders; Dementia; EC 3.1.1.4; Eicosanoids; Encephalon; Encephalons; Enzyme Activation; Enzymes; Event; Funding; G Protein-Complex Receptor; G-Protein-Coupled Receptors; Gene Expression; Glutamates; Goals; Grant; Histocytochemistry; Human; Human, General; Inflammatory; Injury; Institution; Intervention; Intervention Strategies; Intracellular Communication and Signaling; Intracellular Second Messengers; Investigators; Ion Channel; Ionic Channels; Kinetic; Kinetics; L-Glutamate; Lecithinase A2; Lecithinase C; Lecithinases; Lipids; Mammals, Rats; Man (Taxonomy); Man, Modern; Mediating; Membrane; Membrane Channels; Modeling; NIH; National Institutes of Health; National Institutes of Health (U.S.); Nerve Cells; Nerve Unit; Nervous System, Brain; Neural Cell; Neurocyte; Neurodegenerative Diseases; Neurodegenerative Disorders; Neurologic Degenerative Conditions; Neurologic Diseases, Degenerative; Neurons; Numbers; PI 3K Isotype p110 gamma; PI-3 Kinase; PI-3K; PI3-Kinase; PI3-Kinase p110 Subunit Gamma; PI3KGamma; PIK3CG; PLA(2)-IV; PLA2; PLA2-IV; PTDINS-3-Kinase; Pathogenesis; Pathway interactions; Phosphatides; Phosphatidylinositol 3 Kinase Gamma, p110 Gamma; Phosphatidylinositol 3-Kinase; Phosphatidylinositol 3-Kinase Catalytic 110-kD Gamma; Phosphatidylinositol 3-Kinase, Catalytic, Gamma Polypeptide; Phosphatidylinositol-3-OH Kinase; Phosphatidylinositol-4,5-Bisphosphate 3-Kinase Catalytic Subunit, Gamma Isoform; Phosphoinositide 3-Hydroxykinase; Phosphoinositide-3-Kinase Gamma Catalytic Subunit; Phosphoinositide-3-Kinase, Catalytic, Gamma Polypeptide; Phospholipase; Phospholipase A2; Phospholipase A2G4; Phospholipase A2IV; Phospholipase C; Phospholipids; PtdIns 3-Kinase; PtdIns-3-Kinase p110; RNA, Small Interfering; Rat; Rattus; Reaction; Research; Research Personnel; Research Resources; Researchers; Resources; Second Messenger Systems; Second Messengers; Signal Pathway; Signal Transduction; Signal Transduction Systems; Signaling; Small Interfering RNA; Source; Technology; Testing; Type I Phosphatidylinositol Kinase; Type III Phosphoinositide 3-Kinase; United States National Institutes of Health; biological signal transduction; brain metabolism; cPLA2; histochemistry; histochemistry/cytochemistry; in vivo; inhibitor; inhibitor/antagonist; interventional strategy; lecithinase A; lipophosphodiesterase I; membrane structure; necrocytosis; neurodegenerative illness; neuroinflammation; neuronal; p110 gamma; pathway; phosphatidase; phosphatidolipase; phosphatidylcholine 2 acylhydrolase; phosphatidylcholine cholinephosphohydrolase; phospholipase A2 IV; radiolabel; radiotracer; second messenger; siRNA
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| 2020 — 2021 |
Rosenberger, Thad Allen |
R03Activity Code Description:
To provide research support specifically limited in time and amount for studies in categorical program areas. Small grants provide flexibility for initiating studies which are generally for preliminary short-term projects and are non-renewable. |
Epigenetic Modulation of Purinergic Signaling in Microglia @ University of North Dakota
In the brain, the innate immune response is initiated by microglia and amplified by astrocytes, which through glial communication act to propagate the neuroinflammatory response. It is well known that adenosinergic signaling is ubiquitous to the brain yet is immerging as a key regulatory mechanism that can be utilized to disrupt neuroglial communication and reduce neuroinflammation. Both microglia and astrocytes possess adenosinergic receptors and express the enzymes that metabolize extracellular ATP and adenosine which in turn modulate adenosinergic and inflammatory signaling. Because adenosine can influence neuronal activity and modulate neuroinflammation, being able to modulate adenosine levels or the receptors involved in adenosinergic signaling has a broad therapeutic potential. However, the link between acetate-induced epigenetic changes in purinergic protein expression is not well understood. Based on these studies we propose the hypothesis that increasing acetate metabolism, via increases in histone acetylation, will modulate purinergic signaling in microglia promoting an anti-inflammatory phenotype. To test this hypothesis we will complete following two aims (1) to determine the mechanism(s) by which acetate alters purine metabolism and (2) to determine the functional effect that acetate-induced changes in purinergic signaling have on inflammatory phenotype. Our working hypothesis is that acetate-induced changes in purinergic signaling will confer an anti-inflammatory phenotype my modulating histone acetylation. By describing how energy supplementation can influence the expression of enzymes and receptors involved in purinergic signaling is important to understand the therapeutic mechanism of acetate supplementation. The innovative of this study is to determine the epigenetic link between an increase in acetyl-CoA metabolism, alterations in purinergic signaling, and its functional effect on inflammatory phenotype.
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