The major produc tsof this prot eolyt iccleavage process conta ineither or residues. Ab is continuously produc ed in a soluble form by cultu redcel ls and is a lso found in CSF, suggest ing that itsproduction andsec retion are partofa physiological pro cess, both invivoand invitro.The refore, assoon as specic antibodiesb ecame available, studieswe re performed a imed at the quant icat ionof the se prote ins in biologicalu ids,especially in CSF from AD patients.Qu ite ex tens ive ove rlap be twe en controls and aec ted ind ividualsoc cur red, hampering us efu lne ss whendiagnosing ind iv idua ls.It is not clear how this may have a ected re su ltsofthe various stud ie s.Polypropylene tubesa re re commended for collect ionof CSF.A Amiodarone hydrochloride lthough this as say waspropos ed as a potent ialdiagno sticte st for AD, itsapplicat ion wi ll be seve rely hampe red by the ne ed for high ly specializ ed equipment.The se latter gu res we re calculated in a study in wh ich theclinicaluse fulnessof thesetests wasinve stigated.A posit ive pred ictive value of and a negat ive predictive va lue of for AD wasreached at a prevalenceofof Losartan probable AD.One major concern of the se stud iesis that cla ssi cation is bas ed on a cl inicaldiagnos is ofdement ia syndrome s, wh ich a re known to suer frommiscla ssication in up to of cases.Incorrectclinicaldiagnosis in the study groupsobviously aectssens it iv ityand specic ity gu re s.Anotherunexplo red issue in the se studiesis how much such labo ratory as se ss mentsadd to a diagnost ic judgement that has already be enestabl ished on the ba sisof clin ical examinat ion and imag ing studie s.Ab levels in AD patientsdid not change during a month fol lowuppe riod. The re su ltsofth is latt er study are in cont rast with the above mentioned data, the refore addit ional stud iesne ed to be pe rformed before nalconclusions can be drawn.Effects of apolipoprotein E A lthoughseve ral formsof familialAD due to mutat ions in the APP or thepre senil in geneshavebeen identi ed, most ca sesof AD occursporad icall y.Howeve r, one major genet ic risk fac tor for spo rad ic AD is now we llestablished the apol ipoprote in E gene.Th is was con rmed in two otherstud ieswith AD patients. In fac t, the most va luable applicat ion of CSF stud iesmay be in the die rent iationof thesedisorde rs.In LBD patient s, tau conc entrationsaresimilarto those in controlgroups.Ab conc ent rat ions in CSF have be en syst ematica lly inve st igated in dement ingdisorde rs otherthan AD in only a few studies. Test ing for prote in in CSF is even pa rtof the diagnost iccriteria for probable CJD.It hasbe en demonst rated, howeve r, that conc ent rat ionsof tau in CSF from CJD patients are ve ry high and may reach a fold inc reaseoverno rmal level s.By using a cut o va lueof pg mL, a diagnost ic sensitiv ityof, with specic ity, was ach ieved, with a po sit ive pred ictive va lueof. In anotherstudy, by using a cut o va lue of pg mL, combined sensit iv ityand spec ic ity of CSF tau analysis we re calcu lated as and ford iscriminat ionbetwe en CJD and AD, re spec tively.