The understanding that neuroinflammation contributes to neurodegeneration and possibly to an autoimmune disease state is emerging in a growing number of nervous system pathologies such as Alzheimer's disease, Parkinson's disease, multiple sclerosis, amyotrophic lateral sclerosis, demyelinating polyradiculoneuropathies and peripheral neuropathies, Guillain-Barré syndrome, prion disease, depression and psychiatric disorders, stroke, and gliomas as well as for microbial infections such as NeuroAIDS, viral and bacterial encephalitis.

Although some inflammatory stimuli induce beneficial effects that help to limit disease, uncontrolled inflammation may result in the production of neurotoxic factors that amplify underlying disease states. Learning more about how inflammatory responses are induced within the nervous system will aid in designing safe and effective therapies for reversing or slowing the course of disease. We invite investigators to contribute original research articles and review articles that will help to expand the current knowledge of the specific mediators of neuroinflammation including inducers, sensors, transducers, amplifiers, and effectors of neuroinflammation. Potential areas include, but are not limited to:

• Inducers and sensors of infection (pathogen-associated molecular signals, pattern recognition receptors, purinergic receptors, and scavenger receptors)
• Inflammasome signaling at the heart of neuroinflammation
• Transduction systems and regulators of neuroinflammation (signal adaptor proteins, transcription factors, and mitogen-activated protein kinase kinases)
• Amplifiers and effectors of inflammation (cytokines, chemokines, and their receptors)
• Role of prostaglandins and cyclooxygenases
• Mediators of oxidative stress
• Matrix metalloproteinases
• Signaling that alters the integrity of the blood-brain barrier
• Soluble molecules that alter neuroglial, neuron-neuron, and neurovascular communications
• Autoimmunity, obesity, stress, and ageing
• Environmental factors