PPARs in Neuroinflammation
Call for Papers
A variety of central nervous system disorders including Alzheimer's disease, ALS, brain abscess, multiple scleroses, Parkinson's disease, spinal cord injury, and stroke are characterized by neuroinflammation and neurodegeneration. Peroxisome proliferator-activated receptors (PPARs) and the related liver-X-receptors (LXRs) are members of the nuclear hormone receptor family of proteins. The role of these receptors in modulating lipid and glucose metabolism is well established. More recently, PPARs and LXRs have been demonstrated to modulate inflammation, including in the central nervous system (CNS). PPARs and LXRs are transcription factors capable of regulating gene expression through multiple mechanisms. These receptors generally function as heterodimers in association with retinoid-X-receptors (RXRs) and regulate gene expression through binding to peroxisome-proliferator-activated response elements (PPREs) or LXREs, respectively, found in the promoters of specific target genes. PPARs are also capable of regulating gene expression independent of PPREs. For example, PPARs are capable of suppressing NF-κB-mediated gene activation of proinflammatory genes through receptor-dependent transrepression. PPARs and LXRs agonists inhibit the production of proinflammatory molecules by peripheral immune cells as well as resident CNS glia. These agonists also alter T-cell phenotype and function. Furthermore, PPAR receptor agonists have proven effective in animal models of many of the CNS inflammatory and neurodegenerative disorders described above. This suggests that modulation of PPARs and LXRs may be effective in treating the related human diseases.
This special issue of PPAR Research will be focused on the role of PPARs in modulating inflammation in the CNS. We invite authors to present original research articles, reviews, and minireviews that discuss the potential role of PPARs and/or RXRs in molecular, cellular, and clinical aspects of neuroinflammation and neurodegeneration.
Potential topics include but are not limited to the role of PPAR and LXRs in:
- Glial cell function
- T-cell function and phenotype
- Chemotaxis
- Neuroinflammation and neurodegeneration
- CNS disease
Authors should follow the PPAR Research manuscript format described at http://www.hindawi.com/journals/ppar/. Prospective authors should submit an electronic copy of their complete manuscript through the journal Manuscript Tracking System at http://mts.hindawi.com/, according to the following timetable:
| Manuscript Due | December 1, 2007 |
| First Round of Reviews | March 1, 2008 |
| Publication Date | June 1, 2008 |
Guest Editors
- Michael K. Racke, Department of Neurology, The Ohio State University Medical Center, 1654 Upham Drive, 445 Means Hall, Columbus, OH 43210-1228, USA
- Paul D. Drew, Department of Neurobiology and Developmental Sciences, University of Arkansas for Medical Sciences, Slot 846, 4301 W. Markham Street, Little Rock, AR 72205, USA