<p>Welcome to this 
special issue of PPAR Research dedicated
to “PPARs in Neuroinflammation.” The central nervous system (CNS) was once
thought to be an immune-privileged site void of significant inflammation.
However, it is now clear that activated peripheral immune cells are capable or
entering and functioning within the CNS. In addition, resident immune cells
termed “microglia” protect the CNS through production of molecules which are
toxic to pathogens. However, chronically activated microglia can produce
molecules toxic to host CNS cells, potentially leading to neurodegeneration.
Interestingly, a variety of CNS disorders are characterized by neuroinflammation
and associated neurodegeneration. The role of PPARs in modulating lipid and glucose
metabolism is well established. More recently, PPARs have been demonstrated to
modulate inflammation. For example, PPAR agonists inhibit the production of
proinflammatory molecules by peripheral immune cells as well as resident CNS
glia. Furthermore, PPAR receptor agonists have proven effective in suppressing
the development of animal models of CNS inflammatory and neurodegenerative
disorders. This suggests that modulation of PPARs may be effective in treating
the related human diseases.</p> <p>This special issue of PPAR Research contains a series of
reviews concerning the role of PPARs in neuroinflammatory diseases. We are
fortunate to have received contributions from experts in the fields concerning
the potential role of PPARs in modulating CNS disorders including multiple
sclerosis, Alzheimer’s disease, spinal cord injury, stroke, traumatic brain
injury, amyotrophic lateral sclerosis, and Huntington’s disease. Also included
are reviews concerning the role of PPAR agonists in modulating the function of
resident CNS microglia, and the molecular mechanisms by which PPARs regulate
inflammatory signaling as related to CNS disease.</p> <p>We are pleased that this special issue of PPAR Research
also contains two original research reports. The first report provides a thorough
investigation of the effects of PPAR-γ agonists in modulating the production of
proinflammatory molecules by CNS microglia and astrocytes in response to distinct toll-like
receptor ligands relevant to infections of the CNS. The second report
investigates PPAR-γ agonist effects on amyloid beta-mediated microglial
production of cytokines known to alter T-cell differentiation. This study may
have important implications concerning the use of amyloid beta immunization for
the treatment of Alzheimer’s disease.</p> <p>We hope that you find this special issue of PPAR Research
dedicated to PPARs in neuroinflammation to be informative, and that the special
issue will generate additional interest in this rapidly evolving field of
research.</p> <p content-type="signature-group">
<named-content content-type="signature"><italic>Michael K. Racke</italic>
<italic>Michael K. Racke</italic>
</named-content>
<named-content content-type="signature"><italic>Paul D. Drew</italic>
<italic>Paul D. Drew</italic>
</named-content>
</p>
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PPAR Res. 2008 Aug 3; 2008:638356