Patients with mild cognitive impairment and a reduced CSF Aβ1-42 protein progress rapidly to Alzheimer's disease
Introduction: Some studies have shown that CSF amyloid-beta 1-42 (Aβ1-42), total tau (T-tau) and tau phosphorylated at threonine 181 (P-tau181p) proteins are useful diagnostic markers for distinguishing between clinically stable mild cognitive impairment (MCI) patients and those who will develop Alz...
| Main Authors: | , , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Elsevier España
2012-01-01
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| Series: | Neurología (English Edition) |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S2173580812000119 |
| _version_ | 1818306677999403008 |
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| author | J.A. Monge-Argilés J. Sánchez-Payá C. Muñoz-Ruiz A. Pampliega-Pérez M.J. Gómez-López E. Rodríguez Borja J. Montoya-Gutiérrez C. Leiva-Santana |
| author_facet | J.A. Monge-Argilés J. Sánchez-Payá C. Muñoz-Ruiz A. Pampliega-Pérez M.J. Gómez-López E. Rodríguez Borja J. Montoya-Gutiérrez C. Leiva-Santana |
| author_sort | J.A. Monge-Argilés |
| collection | DOAJ |
| description | Introduction: Some studies have shown that CSF amyloid-beta 1-42 (Aβ1-42), total tau (T-tau) and tau phosphorylated at threonine 181 (P-tau181p) proteins are useful diagnostic markers for distinguishing between clinically stable mild cognitive impairment (MCI) patients and those who will develop Alzheimer's disease (AD).Our objective was to test the ability of this technique to discriminate in our cohort of MCI patients, according to the clinical outcome, one year after the lumbar puncture. Material and methods: A total of 36 MCI patients were included from the local hospital memory clinic. Using INNO-BIA Alzbio-3 reagents from Innogenetics, we measured CSF Aβ1-42, T-tau and P-tau181p proteins, and calculated the T-tau/Aβ1-42 and P-tau181p/Aβ1-42 ratios. This project was approved by the local ethics committee. Results: One year after the lumbar puncture, 14 MCI patients (38%) developed AD. These patients had lower Aβ1-42 protein levels (285.3 ng/ml vs 377 ng/ml, P < .02) and higher P-tau181p/Aβ1-42 ratio (0.25 vs 0.16, P < .02) than the clinically stable patients. Conclusions: Our MCI patients with lower Aβ1-42 protein levels and an increased P-tau181p/Aβ1-42 ratio progressed quickly to AD. These results may help to identify those MCI patients with a poorer prognosis. Resumen: Introducción: En muchos artículos recientes, el análisis de las proteínas Aβ1-42, tau total (T-tau) y tau fostorilada (P-tau) en LCR puede discriminar entre los pacientes con deterioro cognitivo leve (DCL) estables y aquellos otros que van a progresar a enfermedad de Alzheimer (EA). Nuestro objetivo fue comprobar la capacidad de estas proteínas del LCR para discriminar, entre nuestros pacientes DCL, según la evolución clínica en el año siguiente a la punción lumbar. Material y métodos: Se incluyó a 36 pacientes DCL amnésico (criterios de Petersen 2006) procedentes de la consulta de deterioro cognitivo del Hospital General de Alicante. Usando los reactivos INNO-BIA Alzbio-3 (Innogenetics), cuantificamos las proteínas Aβ1-42, T-tau, P-tau181p en LCR, y calculamos los cocientes T-tau/Aβ1-42 y P-tau181p/Aβ1-42. El estudio fue aprobado por el comité ético de investigación del Hospital General de Alicante. Resultados: En los 12 meses posteriores a la punción lumbar, 14 pacientes DCL (38%) evolucionaron a EA. Estos pacientes, presentaron menores niveles de Aβ1-42 (285,3 vs. 377,7 ng/ml, p < 0,02), y un aumento en el valor del cociente P-tau181p/Aβ1-42 (0,25 vs. 0,16, p < 0,02) que los pacientes que se mantuvieron estables. No hubo diferencias significativas en el resto de variables estudiadas. Conclusiones: Nuestros pacientes DCL que presentaron niveles reducidos de la proteína Aβ1-42 y elevación del cociente P-tau181p/Aβ1-42 en LCR, evolucionaron rápidamente a EA. Estos resultados pueden ayudar a conseguir el objetivo de identificar de forma precoz a los pacientes DCL con peor pronóstico. Keywords: CSF biomarkers, Mild cognitive impairment, Alzheimer's disease, Aβ1-42 protein, T-tau protein, P-tau181p protein, Palabras clave: Biomarcadores en LCR, Deterioro cognitivo leve, Enfermedad de Alzheimer, Proteína Aβ1-42, Proteína T-tau, Proteína P-tau181p |
| first_indexed | 2024-12-13T06:46:18Z |
| format | Article |
| id | doaj.art-2116f8f2667e40d39611be3b2fa08281 |
| institution | Directory Open Access Journal |
| issn | 2173-5808 |
| language | English |
| last_indexed | 2024-12-13T06:46:18Z |
| publishDate | 2012-01-01 |
| publisher | Elsevier España |
| record_format | Article |
| series | Neurología (English Edition) |
| spelling | doaj.art-2116f8f2667e40d39611be3b2fa082812022-12-21T23:56:16ZengElsevier EspañaNeurología (English Edition)2173-58082012-01-012712833Patients with mild cognitive impairment and a reduced CSF Aβ1-42 protein progress rapidly to Alzheimer's diseaseJ.A. Monge-Argilés0J. Sánchez-Payá1C. Muñoz-Ruiz2A. Pampliega-Pérez3M.J. Gómez-López4E. Rodríguez Borja5J. Montoya-Gutiérrez6C. Leiva-Santana7Servicio de Neurología, Hospital General Universitario de Alicante, Alicante, Spain; Corresponding author.Servicio de Medicina Preventiva, Hospital General Universitario de Alicante, Alicante, SpainLaboratorio de Inmunología, Hospital General Universitario de Alicante, Alicante, SpainServicio de Neurología, Hospital General Universitario de Alicante, Alicante, SpainClínica Neuropsicóloga, Hospital General Universitario de Alicante, Alicante, SpainLaboratorio de Inmunología, Hospital General Universitario de Alicante, Alicante, SpainServicio de Neurología, Hospital General Universitario de Alicante, Alicante, SpainServicio de Neurología, Hospital General Universitario de Alicante, Alicante, SpainIntroduction: Some studies have shown that CSF amyloid-beta 1-42 (Aβ1-42), total tau (T-tau) and tau phosphorylated at threonine 181 (P-tau181p) proteins are useful diagnostic markers for distinguishing between clinically stable mild cognitive impairment (MCI) patients and those who will develop Alzheimer's disease (AD).Our objective was to test the ability of this technique to discriminate in our cohort of MCI patients, according to the clinical outcome, one year after the lumbar puncture. Material and methods: A total of 36 MCI patients were included from the local hospital memory clinic. Using INNO-BIA Alzbio-3 reagents from Innogenetics, we measured CSF Aβ1-42, T-tau and P-tau181p proteins, and calculated the T-tau/Aβ1-42 and P-tau181p/Aβ1-42 ratios. This project was approved by the local ethics committee. Results: One year after the lumbar puncture, 14 MCI patients (38%) developed AD. These patients had lower Aβ1-42 protein levels (285.3 ng/ml vs 377 ng/ml, P < .02) and higher P-tau181p/Aβ1-42 ratio (0.25 vs 0.16, P < .02) than the clinically stable patients. Conclusions: Our MCI patients with lower Aβ1-42 protein levels and an increased P-tau181p/Aβ1-42 ratio progressed quickly to AD. These results may help to identify those MCI patients with a poorer prognosis. Resumen: Introducción: En muchos artículos recientes, el análisis de las proteínas Aβ1-42, tau total (T-tau) y tau fostorilada (P-tau) en LCR puede discriminar entre los pacientes con deterioro cognitivo leve (DCL) estables y aquellos otros que van a progresar a enfermedad de Alzheimer (EA). Nuestro objetivo fue comprobar la capacidad de estas proteínas del LCR para discriminar, entre nuestros pacientes DCL, según la evolución clínica en el año siguiente a la punción lumbar. Material y métodos: Se incluyó a 36 pacientes DCL amnésico (criterios de Petersen 2006) procedentes de la consulta de deterioro cognitivo del Hospital General de Alicante. Usando los reactivos INNO-BIA Alzbio-3 (Innogenetics), cuantificamos las proteínas Aβ1-42, T-tau, P-tau181p en LCR, y calculamos los cocientes T-tau/Aβ1-42 y P-tau181p/Aβ1-42. El estudio fue aprobado por el comité ético de investigación del Hospital General de Alicante. Resultados: En los 12 meses posteriores a la punción lumbar, 14 pacientes DCL (38%) evolucionaron a EA. Estos pacientes, presentaron menores niveles de Aβ1-42 (285,3 vs. 377,7 ng/ml, p < 0,02), y un aumento en el valor del cociente P-tau181p/Aβ1-42 (0,25 vs. 0,16, p < 0,02) que los pacientes que se mantuvieron estables. No hubo diferencias significativas en el resto de variables estudiadas. Conclusiones: Nuestros pacientes DCL que presentaron niveles reducidos de la proteína Aβ1-42 y elevación del cociente P-tau181p/Aβ1-42 en LCR, evolucionaron rápidamente a EA. Estos resultados pueden ayudar a conseguir el objetivo de identificar de forma precoz a los pacientes DCL con peor pronóstico. Keywords: CSF biomarkers, Mild cognitive impairment, Alzheimer's disease, Aβ1-42 protein, T-tau protein, P-tau181p protein, Palabras clave: Biomarcadores en LCR, Deterioro cognitivo leve, Enfermedad de Alzheimer, Proteína Aβ1-42, Proteína T-tau, Proteína P-tau181phttp://www.sciencedirect.com/science/article/pii/S2173580812000119 |
| spellingShingle | J.A. Monge-Argilés J. Sánchez-Payá C. Muñoz-Ruiz A. Pampliega-Pérez M.J. Gómez-López E. Rodríguez Borja J. Montoya-Gutiérrez C. Leiva-Santana Patients with mild cognitive impairment and a reduced CSF Aβ1-42 protein progress rapidly to Alzheimer's disease Neurología (English Edition) |
| title | Patients with mild cognitive impairment and a reduced CSF Aβ1-42 protein progress rapidly to Alzheimer's disease |
| title_full | Patients with mild cognitive impairment and a reduced CSF Aβ1-42 protein progress rapidly to Alzheimer's disease |
| title_fullStr | Patients with mild cognitive impairment and a reduced CSF Aβ1-42 protein progress rapidly to Alzheimer's disease |
| title_full_unstemmed | Patients with mild cognitive impairment and a reduced CSF Aβ1-42 protein progress rapidly to Alzheimer's disease |
| title_short | Patients with mild cognitive impairment and a reduced CSF Aβ1-42 protein progress rapidly to Alzheimer's disease |
| title_sort | patients with mild cognitive impairment and a reduced csf aβ1 42 protein progress rapidly to alzheimer s disease |
| url | http://www.sciencedirect.com/science/article/pii/S2173580812000119 |
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