This is an abstract about research out of the University of Louisville. Here are the highlights from the abstract: “Although little is known about the etiology of progressive supranuclear palsy (PSP), genetic and epigenetic factors, oxidative injury and inflammation are thought to contribute to its development and/or progression. Evidence for activated glia involvement in PSP has raised the possibility that neuroinflammation may contribute to its pathogenesis. These results…[suggest] that these cytokines may contribute to the pathologic process. If so, the use of cytokine-inhibitors and/or other anti-inflammatory agents may be able to slow disease progression in PSP.”
Sorry but I couldn’t find a list of cytokine inhibitors. From spending a few minutes on the web looking into this, it seems that cytokine research is a rapidly evolving area.
Of course “anti-inflammatory agents” includes NSAIDs (nonsteroidal anti-inflammatory drugs). (Ibuprofen is an example of an NSAID.) The authors refer to a trial of NSAIDs in Alzheimer’s Disease in the final sentence of the article: “Although in the case of AD the evidence from anti-inflammatory clinical trials remains controversial, no such trials have been conducted in PSP patients.”
All of the brain tissue utilized for this study came from Mayo Jax. Tissue samples were used from both frozen brains and formalin-fixed brains. Thanks to all those who donate brain tissue of loved ones to Mayo Jax for making research like this possible.
I’ve copied the abstract below.
Robin
Parkinsonism and Related Disorders. 2011 Jul 6. [Epub ahead of print]
Cytokine expression and microglial activation in progressive supranuclear palsy.
Fernández-Botrán R, Ahmed Z, Crespo FA, Gatenbee C, Gonzalez J, Dickson DW, Litvan I.
Department of Pathology and Laboratory Medicine, School of Medicine, University of Louisville, Louisville, KY.
Abstract
Although little is known about the etiology of progressive supranuclear palsy (PSP), genetic and epigenetic factors, oxidative injury and inflammation are thought to contribute to its development and/or progression.
Evidence for activated glia involvement in PSP has raised the possibility that neuroinflammation may contribute to its pathogenesis.
To investigate the correlation between neuroinflammation and PSP, a comparative study was conducted on the patterns of cytokine expression in different regions of the brains of PSP, Alzheimer’s disease (AD) patients and normal controls.
Our results show different patterns of cytokine expression in each disease, with the expression of IL-1beta transcripts being significantly higher in the substantia nigra of PSP than in AD and controls, while AD brains had significantly higher IL-1beta expression in the parietal cortex compared to PSP and controls.
In addition, expression of TGFbeta was significantly higher in the cortical areas (particularly frontal and parietal lobes) of AD compared to PSP and controls.
These results show a disease-specific topographical relationship among the expression of certain cytokines (IL-1beta and TGFbeta), microglial activation and neurodegenerative changes, suggesting that these cytokines may contribute to the pathologic process. If so, the use of cytokine-inhibitors and/or other anti-inflammatory agents may be able to slow disease progression in PSP.
Copyright © 2011 Elsevier Ltd. All rights reserved.
PubMed ID#: 21741294 (see pubmed.gov for this abstract only)