Decreased CX3CL1 Levels in the Cerebrospinal Fluid of Patients With Alzheimer’s Disease

Alzheimer’s disease (AD) is a neurodegenerative disease characterized by the presence of neurofibrillary tangles, constituted by tau protein, and plaques formed by amyloid-beta protein. The disease courses with high neural damage, which leads to memory loss and death. Here we analyzed the presence o...

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Autores principales: Perea, Juan R., Lleó, Alberto, Alcolea, Daniel, Fortea, Juan, Ávila, Jesús, Bolós, Marta
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2018
Materias:
Neuroscience
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6137321/
https://www.ncbi.nlm.nih.gov/pubmed/30245615
http://dx.doi.org/10.3389/fnins.2018.00609
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author Perea, Juan R.
Lleó, Alberto
Alcolea, Daniel
Fortea, Juan
Ávila, Jesús
Bolós, Marta
author_facet Perea, Juan R.
Lleó, Alberto
Alcolea, Daniel
Fortea, Juan
Ávila, Jesús
Bolós, Marta
author_sort Perea, Juan R.
collection PubMed
description Alzheimer’s disease (AD) is a neurodegenerative disease characterized by the presence of neurofibrillary tangles, constituted by tau protein, and plaques formed by amyloid-beta protein. The disease courses with high neural damage, which leads to memory loss and death. Here we analyzed the presence of CX3CL1, a chemokine expressed by neurons, in cerebrospinal fluid (CSF) samples from control subjects and patients with mild cognitive impairment and AD dementia. CX3CL1 was decreased in the CSF of AD dementia patients compared to control subjects. However, there was not difference in plasma samples from the same subjects.
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spelling pubmed-61373212018-09-21 Decreased CX3CL1 Levels in the Cerebrospinal Fluid of Patients With Alzheimer’s Disease Perea, Juan R. Lleó, Alberto Alcolea, Daniel Fortea, Juan Ávila, Jesús Bolós, Marta Front Neurosci Neuroscience Alzheimer’s disease (AD) is a neurodegenerative disease characterized by the presence of neurofibrillary tangles, constituted by tau protein, and plaques formed by amyloid-beta protein. The disease courses with high neural damage, which leads to memory loss and death. Here we analyzed the presence of CX3CL1, a chemokine expressed by neurons, in cerebrospinal fluid (CSF) samples from control subjects and patients with mild cognitive impairment and AD dementia. CX3CL1 was decreased in the CSF of AD dementia patients compared to control subjects. However, there was not difference in plasma samples from the same subjects. Frontiers Media S.A. 2018-09-07 /pmc/articles/PMC6137321/ /pubmed/30245615 http://dx.doi.org/10.3389/fnins.2018.00609 Text en Copyright © 2018 Perea, Lleó, Alcolea, Fortea, Ávila and Bolós. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Neuroscience
Perea, Juan R.
Lleó, Alberto
Alcolea, Daniel
Fortea, Juan
Ávila, Jesús
Bolós, Marta
Decreased CX3CL1 Levels in the Cerebrospinal Fluid of Patients With Alzheimer’s Disease
title Decreased CX3CL1 Levels in the Cerebrospinal Fluid of Patients With Alzheimer’s Disease
title_full Decreased CX3CL1 Levels in the Cerebrospinal Fluid of Patients With Alzheimer’s Disease
title_fullStr Decreased CX3CL1 Levels in the Cerebrospinal Fluid of Patients With Alzheimer’s Disease
title_full_unstemmed Decreased CX3CL1 Levels in the Cerebrospinal Fluid of Patients With Alzheimer’s Disease
title_short Decreased CX3CL1 Levels in the Cerebrospinal Fluid of Patients With Alzheimer’s Disease
title_sort decreased cx3cl1 levels in the cerebrospinal fluid of patients with alzheimer’s disease
topic Neuroscience
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6137321/
https://www.ncbi.nlm.nih.gov/pubmed/30245615
http://dx.doi.org/10.3389/fnins.2018.00609
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