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CSF in Epileptic Prodromal Alzheimer's Disease: No Diagnostic Contribution but a Pathophysiological One

Objective: To study whether cerebrospinal fluid (CSF) analysis may serve as a diagnostic test for the screening of epilepsy in sporadic prodromal Alzheimer's disease (AD). Methods: A total of 29 patients with epileptic prodromal sporadic AD patients (epADs) were included and were retrospectivel...

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Autores principales: Cretin, Benjamin, Bousiges, Olivier, Hautecloque, Geoffroy, Philippi, Nathalie, Blanc, Frederic, Dibitonto, Laure, Martin-Hunyadi, Catherine, Sellal, François
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8369500/
https://www.ncbi.nlm.nih.gov/pubmed/34413819
http://dx.doi.org/10.3389/fneur.2021.623777
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author Cretin, Benjamin
Bousiges, Olivier
Hautecloque, Geoffroy
Philippi, Nathalie
Blanc, Frederic
Dibitonto, Laure
Martin-Hunyadi, Catherine
Sellal, François
author_facet Cretin, Benjamin
Bousiges, Olivier
Hautecloque, Geoffroy
Philippi, Nathalie
Blanc, Frederic
Dibitonto, Laure
Martin-Hunyadi, Catherine
Sellal, François
author_sort Cretin, Benjamin
collection PubMed
description Objective: To study whether cerebrospinal fluid (CSF) analysis may serve as a diagnostic test for the screening of epilepsy in sporadic prodromal Alzheimer's disease (AD). Methods: A total of 29 patients with epileptic prodromal sporadic AD patients (epADs) were included and were retrospectively compared with 38 non-epileptic prodromal AD patients (nepADs) for demographics, clinical features, Mini-Mental Status Examination (MMSE) results, CSF biomarkers, and electro-radiological features. Results: Our study did not show any significant differences in CSF biomarkers regarding neurodegeneration, albumin levels, and inflammation between epADs and nepADs. The epADs were significantly older at diagnosis (p = 0.001), more hypertensive (p = 0.01), and displayed larger white matter hyperintensities on brain magnetic resonance imaging (MRI; p = 0.05). There was a significant correlation between the CSF Aβ-42 and Aβ-40 levels with interictal epileptiform discharges and delta slowing on EEGs recordings, respectively (p = 0.03). Conclusions: Our study suggests that CSF may not serve as a surrogate marker of epilepsy in prodromal AD and cannot circumvent the operator-dependent and time-consuming interpretation of EEG recordings. In humans, AD-related epileptogenesis appears to involve the Aβ peptides but likely also additional non-amyloid factors such as small-vessel disease (i.e., white matter hyperintensities).
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spelling pubmed-83695002021-08-18 CSF in Epileptic Prodromal Alzheimer's Disease: No Diagnostic Contribution but a Pathophysiological One Cretin, Benjamin Bousiges, Olivier Hautecloque, Geoffroy Philippi, Nathalie Blanc, Frederic Dibitonto, Laure Martin-Hunyadi, Catherine Sellal, François Front Neurol Neurology Objective: To study whether cerebrospinal fluid (CSF) analysis may serve as a diagnostic test for the screening of epilepsy in sporadic prodromal Alzheimer's disease (AD). Methods: A total of 29 patients with epileptic prodromal sporadic AD patients (epADs) were included and were retrospectively compared with 38 non-epileptic prodromal AD patients (nepADs) for demographics, clinical features, Mini-Mental Status Examination (MMSE) results, CSF biomarkers, and electro-radiological features. Results: Our study did not show any significant differences in CSF biomarkers regarding neurodegeneration, albumin levels, and inflammation between epADs and nepADs. The epADs were significantly older at diagnosis (p = 0.001), more hypertensive (p = 0.01), and displayed larger white matter hyperintensities on brain magnetic resonance imaging (MRI; p = 0.05). There was a significant correlation between the CSF Aβ-42 and Aβ-40 levels with interictal epileptiform discharges and delta slowing on EEGs recordings, respectively (p = 0.03). Conclusions: Our study suggests that CSF may not serve as a surrogate marker of epilepsy in prodromal AD and cannot circumvent the operator-dependent and time-consuming interpretation of EEG recordings. In humans, AD-related epileptogenesis appears to involve the Aβ peptides but likely also additional non-amyloid factors such as small-vessel disease (i.e., white matter hyperintensities). Frontiers Media S.A. 2021-08-03 /pmc/articles/PMC8369500/ /pubmed/34413819 http://dx.doi.org/10.3389/fneur.2021.623777 Text en Copyright © 2021 Cretin, Bousiges, Hautecloque, Philippi, Blanc, Dibitonto, Martin-Hunyadi and Sellal. https://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 Neurology
Cretin, Benjamin
Bousiges, Olivier
Hautecloque, Geoffroy
Philippi, Nathalie
Blanc, Frederic
Dibitonto, Laure
Martin-Hunyadi, Catherine
Sellal, François
CSF in Epileptic Prodromal Alzheimer's Disease: No Diagnostic Contribution but a Pathophysiological One
title CSF in Epileptic Prodromal Alzheimer's Disease: No Diagnostic Contribution but a Pathophysiological One
title_full CSF in Epileptic Prodromal Alzheimer's Disease: No Diagnostic Contribution but a Pathophysiological One
title_fullStr CSF in Epileptic Prodromal Alzheimer's Disease: No Diagnostic Contribution but a Pathophysiological One
title_full_unstemmed CSF in Epileptic Prodromal Alzheimer's Disease: No Diagnostic Contribution but a Pathophysiological One
title_short CSF in Epileptic Prodromal Alzheimer's Disease: No Diagnostic Contribution but a Pathophysiological One
title_sort csf in epileptic prodromal alzheimer's disease: no diagnostic contribution but a pathophysiological one
topic Neurology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8369500/
https://www.ncbi.nlm.nih.gov/pubmed/34413819
http://dx.doi.org/10.3389/fneur.2021.623777
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