Journal of Neuroimmune Pharmacology (JNIP)

The Society on NeuroImmune Pharmacology, in conjunction with Springer and Dr. Howard Gendelman, our Chief Editor, launched the Journal of Neuroimmune Pharmacology (JNIP) in 2005. JNIP is the official journal of the society reflecting its interdisciplinary ideals. The journal interfaces the disciplines of immunology, pharmacology, experimental neuroscience and drug development. JNIP provides a peer-reviewed platform for exciting new discoveries. Original and interdisciplinary scientific contributions, concise "opinion," and broader reviews form the core of its contents.

Manuscripts include original research germane 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-1 associated dementia, neuroendocrine and microbial infections, and immunological disorders of the brain, spinal cord, and peripheral nerves.

Topical studies of brain-immune interactions include, but are not limited to:

  • The Role of Metabolomics in Brain Metabolism Research (V10.3)
  • Cannabinoid and Endocannabinoid Modulation of Immune Function (V10.2)
  • Growth factor signaling: Implications for Disease & Therapeutics (V9.2)
  • Biomarkers for NeuroAIDS (V8.5)
  • CNS Diseases and the Immune System (V8.4)
  • Imaging Biomarkers and the Role of Neuroinflammation for Neuropathic Pain (V8.3)
  • Microglial-Neuronal Interactions During Neurodegenerative Diseases (V8.2)
  • Molecular Basis for Neuroimmune Receptor Signaling (V7.4)
  • Animal Models for NeuroAIDS (V7.2)
  • Neuroinflammation and Cognitive dysfunction in Chronic Disease and Aging (V7.1)

JNIP continues to publish 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.