| Objective:To quantitatively analyze the A?(1-42),p-tau(181P)and tau proteins within the cerebrospinal fluid(CSF)of patients with Huntington's disease in Chinese Han population and pursuit the biomarkers reflecting the pathophysiological changes of the patients,so that to provide the basis for monitoring disease progression and therapeutic effect of Huntington's disease.Methods:Fifty-eight subjects from Chinese Han ethnic origin were enrolled in this study,including 15 patients with HD(HD group),15 negative controls(CON group)and 28Alzheimer's Disease positive patients(AD group);negative controls were individuals without mental disorders or central nervous system degenerative diseases.All subjects were collected for venous and CSF.Polymerase chain reaction(PCR)was used to amplify the HTT gene fragment,molecular diagnosis completed,and then the numbers of(CAG)n repeats within HD patients were determined by Sanger sequencing;All subjects completed the assessment of the MMSE scale on cognitive aspects,and HD patients the UHDRS.In addition to related clinical data,clinical assessment and grouping finished.The levels of A?(1-42),p-tau(181P)and tau protein in the CSF of the individuals were determined by enzyme-linked immunosorbent assay(ELISA).Results:We measured the levels of A?(1-42),p-tau(181P)and tau in the cerebrospinal fluid of the tested individuals,and grouped them with 50 years old to compare.According to the TCF score,HD patients were divided into Early group(TFC: 7-13),Middle and Late group(TFC: 0-6.9),and then compared with group.1.There was no significant difference(p =.294)in the CSF of A?(1-42)between theselected HD patients(1216.52±220.00 ng/L)and the negative control group(1135.04±192.92 ng/L).Compared with the positive AD group(669.72±214.72ng/L),A?(1-42)of HD group was significantly higher(p =.000).2.The concentrations of p-tau(181P)protein in the CSF between the two age groupof HD(32.14±14.28 ng/L and 33.64±8.04 ng/L,respectively)and the negativecontrol(26.15±5.04 ng/L and 29.71±8.31 ng/L,respectively)were different,andthe statistical results were not significantly different(p =.076 and p =.603,respectively).3.The quantitative test results of tau protein in CSF of HD patients(150.48±85.94ng/L and 165.37±57.35 ng/L in the younger and older subgroups,respectively)were compared with those in the negative control group(114.18±76.90 ng/L and107.39±70.67 ng/L,respectively),and the statistical results showed no significantdifferences(p =.571 and p =.185,respectively).4.At the same time,there was no significant difference in the A?(1-42),p-tau(181P),tau and the ratio of tau with p-tau(181P)between the Early-HD,the Middle andLate-HD and control group(p =.175,.352,.159 and.283,respectively).5.There is a linear correlation between two proteins among A?(1-42)?p-tau(181P)and tau in CSF of HD patients.Conclusion:1.ELISA can be used to quantitatively detect A?,p-tau and tau in CSF accurately.2.There was no significant difference in the A? protein in the CSF between the HDpatients and the negative control group,but the protein of HD group wassignificantly higher than that of the AD patients.The kit was reliable and stable.3.A?(1-42)in CSF couldn't be a biomarker to detect different stage of HDcondition.4.The protein measurement of p-tau(181P)and tau failed to support the conclusion"HD is tau-related disease". |
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