Neuroinflammation, Neuronal IL-1R1, and Behavior

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Principal Investigator: Ning  Quan
Organization: FLORIDA ATLANTIC UNIVERSITY
Fiscal Year: 2024
Award: $331,903
Funding agency: National Institute of Neurological Disorders and Stroke

Project Summary
Neuroinflammation is a significant contributor to most CNS disorders including neurodegenerative
diseases and psychological disorders. A hallmark of neuroinflammation is the increased expression of the
proinflammatory cytokine interleukin-1 (IL-1) in the brain. How IL-1 causes neuro- and psycho-
pathologies is poorly understood. We have recently discovered that the receptor for IL-1, IL-1R1, is
expressed in specific sets of neurons in the brain. These neuronal IL-1R1s, nIL-1R1, modulate neuronal
activity via non-canonical signaling pathways to alter neuronal function and circuit connectivity. This
application is designed to: 1) map nIL-1R1 distribution in the brain, 2)demonstrate the involvement of
nIL-1R1 in neuroinflammation induced behavioral deficits and neuropathology, and 3) elucidate the
mechanisms of nIL-1R1 mediated neuromodulation.

Terms: <Acute Brain Injuries><Adhesions><Affective Disorders><Aging><Ammon Horn><Anatomic Sites><Anatomic structures><Anatomy><Animal Model><Animal Models and Related Studies><Atlases><Behavior><Behavioral><Binding><Brain><Brain Mapping><Brain Nervous System><CNS Diseases><CNS autoimmune disease><CNS disorder><Causality><Cell Body><Cell Communication and Signaling><Cell Signaling><Cells><Central Nervous System Diseases><Central Nervous System Disorders><Chronic><Cognitive Disturbance><Cognitive Impairment><Cognitive decline><Cognitive function abnormal><Cornu Ammonis><Cytosolic Protein Tyrosine Phosphastase><Data><Degenerative Neurologic Disorders><Development><Disease><Disorder><Disturbance in cognition><Encephalon><Epilepsy><Epileptic Seizures><Epileptics><Etiology><Genetic Polymorphism><Genetic Predisposition><Genetic Predisposition to Disease><Genetic Susceptibility><Genetic propensity><Glutamates><Hippocampus><Human Genetics><IL-1><IL-1 Receptors><IL1><IL1 Receptors><IL1R><IL1R1><IL1R1 gene><IL1RA><Immediate Memory><Impaired cognition><Inflammatory><Inherited Predisposition><Inherited Susceptibility><Interleukin I><Interleukin-1><Interleukin-1 Receptors><Intracellular Communication and Signaling><KI mice><Knock-in><Knock-in Mouse><L-Glutamate><Label><Light><Link><LoxP-flanked allele><Lymphocyte-Stimulating Hormone><Macrophage Cell Factor><Maps><Mediating><Memory Deficit><Memory impairment><Mental disorders><Mental health disorders><Methods><Mice><Mice Mammals><Microscopy><Modeling><Molecular><Molecular Interaction><Mood Disorders><Murine><Mus><Nerve Cells><Nerve Transmitter Substances><Nerve Unit><Nervous System><Nervous System Degenerative Diseases><Neural Cell><Neural Degenerative Diseases><Neural degenerative Disorders><Neurocyte><Neurodegenerative Diseases><Neurodegenerative Disorders><Neurologic><Neurologic Body System><Neurologic Degenerative Conditions><Neurologic Organ System><Neurological><Neurons><Neurotransmitters><PTP Family Gene><PTPase><Pathogenesis><Pathology><Pathway interactions><Phosphotyrosine Phosphatase><Phosphotyrosyl Protein Phosphatase><Photoradiation><Predisposition><Protein Tyrosine Phosphatase><Protein Tyrosine Phosphatase Gene><Psychiatric Disease><Psychiatric Disorder><Psychopathology><Receptor Protein><Receptor Type PTP Gene><Reporter><Role><Seizure Disorder><Short-Term Memory><Shortterm Memory><Signal Pathway><Signal Transduction><Signal Transduction Systems><Signaling><Single cell seq><Stress><Susceptibility><Synapses><Synaptic><System><T Helper Factor><Tracer><Tyrosine Phosphatase><Tyrosyl Phosphoprotein Phosphatase><Withdrawal><abnormal psychology><behavior study><behavioral study><biological signal transduction><causation><cell type><central nervous system autoimmune disease><co-morbid><co-morbidity><cognitive dysfunction><cognitive loss><comorbidity><cytokine><degenerative diseases of motor and sensory neurons><degenerative neurological diseases><design><designing><developmental><disease causation><epilepsia><epileptogenic><fighting><floxed><floxed allele><genetic etiology><genetic mechanism of disease><genetic vulnerability><genetically predisposed><glutamatergic><hippocampal><knockin><knockin mice><lymphocyte activating factor><mRNA Expression><memory dysfunction><mental illness><model of animal><neural control><neural inflammation><neural regulation><neurodegenerative illness><neuroinflammation><neuroinflammatory><neuromodulation><neuromodulatory><neuronal><neuropathologic><neuropathological><neuropathology><neuroregulation><novel><pathway><polymorphism><prevent><preventing><protein expression><protein tyrosine phosphate phosphohydrolase><psychiatric illness><psychologic><psychological><psychological disorder><receptive field><receptor><response><single cell next generation sequencing><single cell sequencing><social><social role><synapse><synapse formation><synaptogenesis><working memory>