Journal of Neuroimmune Pharmacology
The Journal of Neuroimmune Pharmacology (JNIP) is the peer-reviewed journal of the Society on NeuroImmune Pharmacology. JNIP interfaces the disciplines of immunology, pharmacology and experimental neuroscience by acting as a platform for research discoveries into the pathogenesis and pharmacology of nervous system disorders affecting the immune system and vice versa. Original interdisciplinary scientific contributions, concise "opinion," and broad reviews are welcome. Research areas reporting in JNIP include receptor cell signaling, the pathobiology, cognitive neuroscience, psychopharmacology and immunity of drugs of abuse, neurodegenerative disorders, neurovirology, neuroimmunology, and neuropharmacology. Manuscripts must include original research linked to the immunology and pharmacology of human neurologic and neuropsychiatric disorders including substance abuse, depression, psychosis, Alzheimer's and Parkinson's disease, Amyotrophic Lateral Sclerosis, Multiple Sclerosis, HIV-associated neurocognitive disorders, neuroendocrine and microbial infections, and immunological, toxic and metabolic disorders of the brain, spinal cord, and peripheral nerves. Topical studies of brain-immune interactions include, but are not limited to: (1) leukocyte trafficking into the nervous system; (2) innate immunity in the nervous system; (3) pathophysiology of neurodegenerative diseases; (4) effects of endogenous ligands on brain-immune interactions (neuronal-peripheral immune; neuronal-glial); (5) effects of drugs of abuse and other pharmacophores on peripheral immune responses, (6) medicinal chemistry and drug development; (7) vaccine approaches for neurologic and neuropsychiatric diseases; (8) bioimaging and proteomics; (9) nanomedicine; and (10) immune surveillance for microbial infections. JNIP will identify novel pharmacologic discoveries (organized action of drug targets, mechanisms, and development) of brain-immune interactions with a potential towards modifying the cellular and systemic responses that affect disease or lead to amelioration of brain injury and immune dysfunction.
Howard E. Gendelman (December 2017)
The Ketone Body β-Hydroxybutyrate Does Not Inhibit Synuclein Mediated Inflammasome Activation in Microglia
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