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Paper text:
peroxisome proliferator - activated receptors ( ppars ) are a class of nuclear transcription factors that are activated by fatty acids and their derivatives .
one of these , ppar , regulates responsiveness to insulin in adipose cells , and ppar-activating drugs such as pioglitazone are used in the treatment of type 2 diabetes .
ppar acts in myeloid - lineage cells , including t - cells and macrophages , to suppress their activation and their elaboration of inflammatory molecules .
ppar activation also suppresses the activated phenotype in microglia , suggesting that ppar-activating drugs may be of benefit in chronic neuroinflammatory diseases .
some , but not all , nonsteroidal anti - inflammatory agents ( indomethacin and ibuprofen in particular ) also have activating effects on ppar.
these observations suggest on the one hand a role for ppar-activating drugs in the treatment of chronic neuroinflammatory diseases - as shown for a patient with secondary progressive multiple sclerosis by pershadsingh et al . in this issue of the journal of neuroinflammation - and
suggest on the other hand a possible explanation for confusing and contradictory results in trials of nonsteroidal anti - inflammatory agents in alzheimer 's disease .
there are still times in modern medicine when a single patient can enlighten our understanding of a disease or disease process , and can serve as an impetus for further discovery . in this issue of journal of neuroinflammation , harrihar pershadsingh and his colleagues  
describe stabilization and , indeed , clinical improvement in a patient with progressive secondary multiple sclerosis who was treated with pioglitazone over a three - year period .
the possible connection between pioglitazone and multiple sclerosis is a fascinating story in itself , and one that not only provides interesting parallels between chronic cns inflammatory diseases and chronic peripheral diseases , but also illuminates an area of current interest for diseases such as alzheimer 's disease as well .
the mechanism of action involves activation of a nuclear transcription factor known as the peroxisome proliferator - activated receptor gamma , or ppar , that controls lipid metabolism in adipocytes , and sensitizes these cells to insulin .
ppar agonists also suppress t - cell activation suggesting that they may be useful in treating inflammatory diseases .
moreover , activation of ppar in microglia ( as well as in macrophages ) results in decreased activation of these cells , with decreased expression of pro - inflammatory cytokines and related molecules .
this suggests that ppar agonists might be useful in a number of central nervous system diseases with inflammatory components .
peroxisomes , or microbodies as they were originally known , were discovered by early electron microscopists in the 1950s .
christian de duve , in brussels , belgium , subsequently isolated these structures , demonstrated hydrogen peroxide generation , and renamed them peroxisomes .
a class of drugs was identified that promoted cancer - like growths in animals , but that did not cause dna damage .
what these drugs did do was to stimulate proliferation of peroxisomes in target cells . at the time , this suggested a specific genetic trigger for tumorigenesis , and there ensued two decades of attempts to identify the receptor for these peroxisome proliferation - activating drugs . by the 1990s , when ppars were identified and shown to be transcription factors , interest had waned in cancer circles .
ppars are a class of transcription factors that are activated by fatty acids and their derivatives .
they were found to control a number of genes , most of which have little or nothing to do with peroxisomes .
ppar is important both in fat cell metabolism and in modulating cellular responsiveness to insulin - hence the connection with diabetes .
ppar-activating drugs were subsequently found to regulate t - cell responsiveness   and to suppress macrophage and microglia activation [ 9 - 11 ] .
both of these actions are relevant to multiple sclerosis , and may have implications for other chronic neurodegenerative diseases as well .
in addition to pioglitazone , some ( but not all ) nonsteroidal anti - inflammatory drugs ( in particular indomethacin and ibuprofen ) have activating effects on ppar in addition to their effects on cyclooxygenase .
nsaid use has been linked with decreased risk of alzheimer 's disease in epidemiological studies [ 13 - 15 ] , but prospective trials of nsaids in alzheimer patients have yielded contradictory and inconclusive results [ 16 - 18 ] .
the nsaid - ppar connection might explain some of these contradictions , as the only one of these clinical trials that reported a benefit was also the only one that used a ppar-activating drug .
there are currently two clinical trials in progress testing the efficacy of ppar agonists in ad patients .
pioglitazone and related drugs activate ppar , and activation of ppar suppresses t - cell , macrophage , and microglial immune responses . if suppression of these immune responses is of potential benefit for inflammatory diseases of the brain , then pioglitazone should provide therapeutic benefit in multiple sclerosis .
multiple sclerosis , of course , is notoriously variable in its course , but the secondary progressive variant is an exception to this .
show clinical stabilization in such a patient , treated for three years with the ppar-activating drug pioglitazone .
this single clinical case thus provides support for a link between ppar activation and suppression of neuroinflammation , and suggests avenues of research for the further treatment of multiple sclerosis as well as other chronic neuroinflammatory diseases .
supported in part by nih po1 ag 12411 , nih p30 ag19606 , and nih ro1 ag 37989
backgroundperoxisome proliferator - activated receptors ( ppars ) are a class of nuclear transcription factors that are activated by fatty acids and their derivatives . 
 one of these , ppar , regulates responsiveness to insulin in adipose cells , and ppar-activating drugs such as pioglitazone are used in the treatment of type 2 diabetes . 
 ppar acts in myeloid - lineage cells , including t - cells and macrophages , to suppress their activation and their elaboration of inflammatory molecules . 
 ppar activation also suppresses the activated phenotype in microglia , suggesting that ppar-activating drugs may be of benefit in chronic neuroinflammatory diseases . 
 some , but not all , nonsteroidal anti - inflammatory agents ( indomethacin and ibuprofen in particular ) also have activating effects on ppar.discussion and conclusionsthese observations suggest on the one hand a role for ppar-activating drugs in the treatment of chronic neuroinflammatory diseases - as shown for a patient with secondary progressive multiple sclerosis by pershadsingh et al . in this issue of the journal of neuroinflammation - and 
 suggest on the other hand a possible explanation for confusing and contradictory results in trials of nonsteroidal anti - inflammatory agents in alzheimer 's disease .