Krebs Cycle Starting Molecule

Glial fibrillary acidic pro te in message was depleted in the cen terofthe largest lesions, butincreased at the peripheryof the lesions.These studies therefore show th atchron ic lowdose adm inistrationof NP can replicate Beta-Sitosterol mostof the characteristic neurochemical and neuropathologic featuresof HD. Beal and coworkers recently ex tended their studies to non hum an primates.Theneu ro an a tomyof the pr ima te basal ganglia mu ch more closely resembles th atofman, a nd it is possible to produce chorea, the cardinal clinical feature of HD. Ch ron ic adm in istrationof NP topr ima tes re sulted in an apomo rph ine induc ib le mov em entdisorder which closely resembles th atseen in HD. The an ima ls showed orifacial dyskinesia, dystonia, dyskinesiaof the extremities, and choreiform movemen ts. H is to log ic ev a lu ation showed th atthelesions werestr ik inglyrem iniscentoftho se wh ichoc curin HD. Therewas a depletionofbo th N issls ta ined andca lb ind in st a in ed neu rons. In contr astmedium sized a sp inyneuronssta in edwi th NADPH diaphorase and largestria taln eu ronswere spa red, simil arto findings wh ichoccurin HD. Thep atch m a se rved in HD, was a lso spa red by thelesions.These findings the re fo re show th atch ronic NP lesions in pr im atesc anproduce bo th an apomo rph ine inducible mov em entdisorder andhistologic findings wh ich replica te thoseof HD. Thesestud iesshow th attherea rema rk ed increases in lac rebral cort ex. Thesefindingsprov idedi rectev idence for imp airm entofene rgymetaboli sm in HD andthe re fo re suggest th at NP neu ro tox icity wh ich ac ts th ro ughse cond a ry excito tox icme ch anismsm aybe a re levantmodel for thed isease process.During cy an idein toxic ationtheappe aranceofneuro log ical dysfunct ionoc curswi th in seconds. Ithasbe en assum ed th atthe extr emesensit ivity to cy an ideresultsfrom thebr a in slow an aerobic capacity andl imit ed ene rgy reserve.L evodop a ther apypro duced variab le imp rov em ent.Also, chroniccy anideexpo sure has been assoc ia tedwi th mo torneuron disease,heredit a ry optic atrophy, and tob acco am nidemetaboli smmaypred isposeto motorn euron disease. Cy an ideinteractswith severalcentr altran smittersys temsand alte redneu rotr an smitterfunct ionmayplay a ro le incy anidetox icity. Cy an idedep le tes am inobu tyricac id andeleva tesglutam ate in Colistimethate Sodium ratbrain. Dop aminergic systemsappe arto be highly susceptib leto cyan ide. A le thaldo seof cy an idedep le tesstr ia taldop am ine and local perfusion of cy an idein thestria tumst imulatesreleaseof DA asme a. In thePC cell model, cyan ideproduces acalc ium d ep en dentrelease anddepletionof DA and alte red DA syn thes is andmetaboli sm have been described. In rats, le thaldosesof cy an idepart ially inh ibitbr a in DOPA deca rboxy la se asme a suredby inc reased levelsof DOPA. Theroleof this comp ound in thecy an ide inducedneu ro tox ic synd romer em a insto bedete rm in ed. A recently ch aracteriz ed mousemodelof cy an ide in duced dop am inergic tox icitymayprove useful inst udy ing thede layedneurod egener ationproduced by cy an ide.

Leave a Reply