Browsing by Author "Cras, P."
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- Some of the metrics are blocked by yourconsent settingsImproved discrimination of AD patients using β-amyloid(1-42) and tau levels in CSF(2012)
;Hulstaert, F. ;Blennow, Kaj ;Ivanoiu, Adrian ;Schoonderwaldt, H. C. ;Riemenschneider, M. ;Deyn, P. P. D. ;Bancher, C. ;Cras, P.; ;Mehta, P. D. ;Iqbal, K. ;Pottel, H. ;Vanmechelen, EugeenVanderstichele, H.Objective: To evaluate CSF levels of β-amyloid(1-42) (Aβ42) alone and in combination with CSF tau for distinguishing AD from other conditions.Methods: At 10 centers in Europe and the United States, 150 CSF samples from AD patients were analyzed and compared with 100 CSF samples from healthy volunteers or patients with disorders not associated with pathologic conditions of the brain (CON), 84 patients with other neurologic disorders (ND), and 79 patients with non-Alzheimer types of dementia (NAD). Sandwich ELISA techniques were used on site for measuring Aβ42 and tau.Results: Median levels of Aβ42 in CSF were significantly lower in AD (487 pg/mL) than in CON (849 pg/mL; p = 0.001), ND (643 pg/mL; p = 0.001), and NAD (603 pg/mL; p = 0.001). Discrimination of AD from CON and ND was significantly improved by the combined assessment of Aβ42 and tau. At 85% sensitivity, specificity of the combined test was 86% (95%CI: 81% to 91%) compared with 55% (95%CI: 47% to 62%) for Aβ42 alone and 65% (95%CI: 58% to 72%) for tau. The combined test at 85% sensitivity was 58% (95%CI: 47% to 69%) specific for NAD. The APOE e4 gene load was negatively correlated with Aβ42 levels not only in AD but also in NAD.Conclusions: The combined measure of CSF Aβ42 and tau meets the requirements for clinical use in discriminating AD from normal aging and specific neurologic disorders. - Some of the metrics are blocked by yourconsent settingsMRI lesion profiles in sporadic Creutzfeldt-Jakob disease(Lippincott Williams & Wilkins, 2009)
; ; ;Sanchez-Juan, P. ;Collie, D. ;Summers, D. M. ;Almonti, S. ;Collins, S. J. ;Smith, P. ;Cras, P.Zerr, I.Background: With respect to sporadic Creutzfeldt-Jakob disease (sCJD), six molecular subtypes (MM1, MM2, MV1, MV2, VV1, and VV2) have been described, which vary with respect to age at disease onset, disease duration, early symptoms, and neuropathology. MRI signal alterations were reported to correlate with distinct Creutzfeldt-Jakob disease (CJD) subtypes. This multicenter, international study aimed to describe the brain MRI findings associated with each of the sCJD molecular subtypes. Methods: Pathologically confirmed sCJD cases with codon 129 genotype (MM, MV, and VV), PrPSc type, and fluid-attenuated inversion recovery (FLAIR) or diffusion-weighted imaging (DWI) were collected in seven countries. All MRI scans were assessed for signal changes according to a standard protocol encompassing seven cortical regions, basal ganglia, thalamus, and cerebellum. Results: MRI scans were evaluated in 211 CJD patients (98 MM1, 23 MM2, 19 MV1, 30 MV2, 9 VV1, and 32 VV2). Basal ganglia hyperintensities occurred most frequently in MV2, VV2, and MM1 subtypes (79, 77, and 70%). Wide cerebral cortical signal increase was most common in VV1, MM2, and MV1 subtypes (86, 77, and 77%). Thalamic hyperintensities occurred most often in VV2 (45%) and MV2 (43%). The most consistent finding across most subtypes was high signal in basal ganglia, with these abnormalities found in 63% (FLAIR) and 71% (DWI). Conclusion: Cortical signal increase and hyperintensities in the basal ganglia and thalamus are detected by MRI across all molecular sporadic Creutzfeldt-Jakob disease subtypes. Our findings argue that characteristic MRI lesion patterns may occur for each molecular subtype. Neurology (R) 2009; 72: 1994-2001