AIM: : The aim of this study is to check the ability of cerebrospinal fluid biomarkers of Alzheimer disease (CSF-BMK-AD) to make a discrimination checklist within a healthy group, according to their cognitive development at 2 years of obtaining the sample. MATERIALS AND METHODS: Between 2008 and 2010, 67 subjects without cognitive or behavioral disorders were included as a control group in a study on CSF-AD-BMK. Neuropsychological assessment at baseline and at follow-up had been carried out 2 years later. CSF was obtained at the inclusion. It was analyzed by Innotest reagents to measure amyloid-β (Aβ1-42), total-τ (T-τ), and phosphorylated τ181 (P-τ181p) protein levels, as well as T-τ/Aβ1-42 and P-τ181p/Aβ1-42 ratios. RESULTS: Two years after inclusion, 28 subjects were not able to be checked for cognitive evolution. Of those who were seen for follow-up (n=39), 29 were cognitively stable and 10 showed cognitive impairment. We found significant differences in Aβ1-42 protein level (820 vs. 1359 pg/mL, P<0.003), in the T-τ/Aβ1-42 ratio (0.40 vs. 0.19, P<0.009), and in the P-τ181p/Aβ1-42 ratio (0.09 vs. 0.04, P<0.003) when both groups were compared. CONCLUSIONS: CSF-BMK-AD are able to discriminate between subjects in a group initially asymptomatic depending on their cognitive evolution at the 2 years' follow-up. These results are consistent with the decrease of CSF Aβ1-42 protein levels as the first finding in preclinical AD showed.
AIM: : The aim of this study is to check the ability of cerebrospinal fluid biomarkers of Alzheimer disease (CSF-BMK-AD) to make a discrimination checklist within a healthy group, according to their cognitive development at 2 years of obtaining the sample. MATERIALS AND METHODS: Between 2008 and 2010, 67 subjects without cognitive or behavioral disorders were included as a control group in a study on CSF-AD-BMK. Neuropsychological assessment at baseline and at follow-up had been carried out 2 years later. CSF was obtained at the inclusion. It was analyzed by Innotest reagents to measure amyloid-β (Aβ1-42), total-τ (T-τ), and phosphorylated τ181 (P-τ181p) protein levels, as well as T-τ/Aβ1-42 and P-τ181p/Aβ1-42 ratios. RESULTS: Two years after inclusion, 28 subjects were not able to be checked for cognitive evolution. Of those who were seen for follow-up (n=39), 29 were cognitively stable and 10 showed cognitive impairment. We found significant differences in Aβ1-42 protein level (820 vs. 1359 pg/mL, P<0.003), in the T-τ/Aβ1-42 ratio (0.40 vs. 0.19, P<0.009), and in the P-τ181p/Aβ1-42 ratio (0.09 vs. 0.04, P<0.003) when both groups were compared. CONCLUSIONS: CSF-BMK-AD are able to discriminate between subjects in a group initially asymptomatic depending on their cognitive evolution at the 2 years' follow-up. These results are consistent with the decrease of CSF Aβ1-42 protein levels as the first finding in preclinical AD showed.
Authors: Jon B Toledo; Henrik Zetterberg; Argonde C van Harten; Lidia Glodzik; Pablo Martinez-Lage; Luisella Bocchio-Chiavetto; Lorena Rami; Oskar Hansson; Reisa Sperling; Sebastiaan Engelborghs; Ricardo S Osorio; Hugo Vanderstichele; Manu Vandijck; Harald Hampel; Stefan Teipl; Abhay Moghekar; Marilyn Albert; William T Hu; Jose A Monge Argilés; Ana Gorostidi; Charlotte E Teunissen; Peter P De Deyn; Bradley T Hyman; Jose L Molinuevo; Giovanni B Frisoni; Gurutz Linazasoro; Mony J de Leon; Wiesje M van der Flier; Philip Scheltens; Kaj Blennow; Leslie M Shaw; John Q Trojanowski Journal: Brain Date: 2015-07-27 Impact factor: 13.501
Authors: William Charles Kreisl; Peng Jin; Seonjoo Lee; Ezra R Dayan; Shankar Vallabhajosula; Gregory Pelton; José A Luchsinger; Gnanavalli Pradhaban; D P Devanand Journal: J Alzheimers Dis Date: 2018 Impact factor: 4.472
Authors: J A Monge-Argilés; R Gasparini-Berenguer; M Gutierrez-Agulló; C Muñoz-Ruiz; J Sánchez-Payá; C Leiva-Santana Journal: Biomed Res Int Date: 2016-03-22 Impact factor: 3.411