作者: Franc Llorens , Saima Zafar , Belén Ansoleaga , Mohsin Shafiq , Rosi Blanco
DOI: 10.1111/NAN.12175
关键词:
摘要: Aims Creutzfeldt–Jakob disease (CJD) is a rapid progressive neurological leading to dementia and death. Prion biomarkers are altered in the cerebrospinal fluid (CSF) of CJD patients, but pathogenic mechanisms underlying these alterations still unknown. The present study examined prion biomarker levels brain CSF sporadic (sCJD) cases their correlation with neuropathological lesion profiles. Methods The expression 14-3-3, Tau, phospho-Tau α-synuclein were measured sCJD subtype- region-specific manner. In addition, activity kinases, hallmarks most frequent findings analysed. Results Prion increased patients; however, correlations between mRNA, total protein phosphorylated forms different. observed downregulation main Tau kinase, GSK3, samples may help explain differential phospho-Tau/Tau ratios other dementias CSF. Importantly, do not necessarily correlate findings. Interpretation Present indicate that tissues release into differentially regulated following specific modulated responses, suggest functional role for proteins pathogenesis.