LAUSR

TNF is a signaling molecule whose study and characterization have transformed modern medicine [1]. Drugs bioengineered to selectively reduce TNF’s biological activity have proven effective for a variety of inflammatory disorders that could not be adequately controlled with conventional therapeutics [1]. During the past two decades, there has been increasing scientific recognition that TNF plays a pivotal role in the nervous system, modulating both synaptic transmission and neuronal network function [2–7]. To describe TNF as simply a pro-inflammatory cytokine omits the fundamental role that TNF plays in regulating neuronal function [2–9]. TNF, in fact, is an essential neuromodulator. TNF is produced by both glia and neurons and participates in the normal physiology of the tripartite synapse [2–7]. When in excess, TNF interferes with neurotransmission, perturbs brain function, and mediates neuropathic pain [2–9]. Excess TNF is centrally involved in the initiation and maintenance of neuroinflammation, an area of accelerating interest in the field of neurology [1–20]. Bioengineered TNF inhibitors are natural candidates for study in clinical trials of neuroinflammatory disorders [1–21].