Abstract

The neuroimmune-neuroplasticity interface and brain pathology.

Highlights

  • It is well-established that the brain, immune privileged, has fundamental interactions with elements of the immune system

  • All psychiatric and neurological [e.g., Parkinson’s (PD) and Alzheimer’s disease (AD)] disorders have been associated with changes in neuroplasticity and neuroinflammatory processes (Frank-Cannon et al, 2009; Hayley, 2011)

  • Papers in the present special topic discuss evidence that the pro-inflammatory factors [e.g., interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α)] provoke neuroplastic deficits, whereas anti-inflammatory and neurotrophic cytokines enhance neuroplasticity and might even have neuroprotective or regenerative effects (e.g., Hayley and Litteljohn, 2013). This Frontiers Research Topic is comprised of a series of articles that deal with how brain-immune system interactions occur and their influence on neuroplasticity

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Summary

Introduction

It is well-established that the brain, immune privileged, has fundamental interactions with elements of the immune system. Papers in the present special topic discuss evidence that the pro-inflammatory factors [e.g., interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α)] provoke neuroplastic deficits, whereas anti-inflammatory and neurotrophic cytokines enhance neuroplasticity and might even have neuroprotective or regenerative effects (e.g., Hayley and Litteljohn, 2013).

Results
Conclusion

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