Beta 3 Agonist

Tauopathies A numb er of neurod egene rat ivedisorde rs a re recognized collect ively asso ca lled tauopathie s; these disorde rs are characte rized by pathological intraneu ronal tau ac cumulation s.Theclinicaldie rentiat ion of the se lattertwodisorde rs, orof PSP with PD, can be complicated.Cons equently, conc entrat ions of CSF tau have be en ana lysed in CBD and PSP pat ie ntgroups to eva luate its diagnost ic potent ial.They obse rvedsign icantly inc reas ed CSF tau conc ent rat ions in CBD pat ients compared with PSP patients. CSF concentrat ions inc rea sed in the following orde r: mode rate;mild; seve re diseasefor both CBD and PSP.A sign i cant dierencewas obse rvedbetwe en mode rateandmild ca sesofeitherd is ea se, but not for seve re ca se s.In the sedisorde rs no abnormal tau ac cumulat ionsoccu r.The refore, it can be antic ipated that CSF tau conc ent rat ions a re simi lar to thosefound in control patients.So far, a ssays have be en de scribedthat det ecttau phosphorylatedat th reon ine, th reon ine, se rine, se rine Carvacrol andser ine or combinat ions the reof. It hasbe en repor ted that NFL is inc reased in CSF ofdementia patients.A lso, in patients with no rmalpre ssure hyd roc epha lus an inc rease in NFL conc entrat ions was observed. Finally, an inc rease in NFL wasobserved in both MSA. A trendsimilarto that wh ich hasdeveloped in the ana lysis of tau prote ins may be env is ioned forNFL.L ike tau, neuro lamentprot eins both the high mole cular we ight sub un its may be come pho sphorylated, and so faron ly one study hasbe en desc ribedin which phosphorylatedneu ro laments we re quantied in CSF.In summa ry, the analysisof NFL in CSF may have some promising clin icalapplications,especial ly in the dierentiat ionof PD and MSA patients, and po ssibly in thedierentialdiagnos isof dementia patients, but th is awa itsfu rtherinve st igations by indep endent re search group s.Furthe rmore, the single report on the quant ication of phospho N F sugge ststhat th is typeof ana lysis holds potent ial forthe die rent ialdiagnos is of dement ia synd rome s.SB is not st rictly a brainspec ic prote in, sinceit is also produc ed by melanomacells.In C JD patients, CSF SB conc ent rations we re st rong ly elevated in compa rison with patients with various neurolog icaldisorde rs, onceagain emphas iz ing the rapidly progre ss ive neu rodegenerat ive natu re of th is diso rde r, which leads to strong ly elevated conc ent rat ionsof various brain spec ic prote ins.Glialbrilla ry ac id ic prote in is a component of inte rmediate lamentsin a strocy tesand itsexpression is strong ly upregulated dur ing ast rogliosis.Re commendations made by an inte rnationalconse nsus group state that the sensitiv ityforthe ideal AD bioma rkershould Fluorescein exceed with a sp ec ic ity of distingu ishing otherdementia syndromesof more than aswell.CSF analysisof tau protein may have some signi cant spin o towardsthedie rent ialdiagnos isof tauopath iesand related disorde rs.Both in th is re spec t, and in thedie rent iation of dement ia synd rome s, it is expected that the more recent ly and le ss ex tens ively stud ied brain sp ec ic prote ins willhavediagnostic potent ial for the se neurodegene rat ivedisorde rs.

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