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Article

Relationship between the Presence of the ApoE ε4 Allele and EEG Complexity along the Alzheimer’s Disease Continuum

1
Biomedical Engineering Group, E.T.S.I. de Telecomunicación, Universidad de Valladolid, 47011 Valladolid, Spain
2
Centro de Investigación Biomédica en Red en Bioingeniería, Biomateriales y Nanomedicina, (CIBER-BBN), 28029 Madrid, Spain
3
Instituto de Investigación en Matemáticas (IMUVA), Universidad de Valladolid, 47011 Valladolid, Spain
4
Institute of Molecular Pathology and Immunology of the University of Porto (IPATIMUP), 4200-135 Porto, Portugal
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Institute of Research and Innovation in Health (i3S), University of Porto, 4200-135 Porto, Portugal
6
Center of Mathematics of the University of Porto (CMUP), 4169-007 Porto, Portugal
*
Author to whom correspondence should be addressed.
Sensors 2020, 20(14), 3849; https://doi.org/10.3390/s20143849
Received: 7 June 2020 / Revised: 29 June 2020 / Accepted: 8 July 2020 / Published: 10 July 2020
(This article belongs to the Special Issue Biomedical Signal Processing for Disease Diagnosis)
Alzheimer’s disease (AD) is the most prevalent cause of dementia, being considered a major health problem, especially in developed countries. Late-onset AD is the most common form of the disease, with symptoms appearing after 65 years old. Genetic determinants of AD risk are vastly unknown, though, ε 4 allele of the ApoE gene has been reported as the strongest genetic risk factor for AD. The objective of this study was to analyze the relationship between brain complexity and the presence of ApoE ε 4 alleles along the AD continuum. For this purpose, resting-state electroencephalography (EEG) activity was analyzed by computing Lempel-Ziv complexity (LZC) from 46 healthy control subjects, 49 mild cognitive impairment subjects, 45 mild AD patients, 44 moderate AD patients and 33 severe AD patients, subdivided by ApoE status. Subjects with one or more ApoE ε 4 alleles were included in the carriers subgroups, whereas the ApoE ε 4 non-carriers subgroups were formed by subjects without any ε 4 allele. Our results showed that AD continuum is characterized by a progressive complexity loss. No differences were observed between AD ApoE ε 4 carriers and non-carriers. However, brain activity from healthy subjects with ApoE ε 4 allele (carriers subgroup) is more complex than from non-carriers, mainly in left temporal, frontal and posterior regions (p-values < 0.05, FDR-corrected Mann–Whitney U-test). These results suggest that the presence of ApoE ε 4 allele could modify the EEG complexity patterns in different brain regions, as the temporal lobes. These alterations might be related to anatomical changes associated to neurodegeneration, increasing the risk of suffering dementia due to AD before its clinical onset. This interesting finding might help to advance in the development of new tools for early AD diagnosis. View Full-Text
Keywords: Alzheimer’s disease (AD); apolipoprotein E (ApoE); electroencephalography (EEG); Lempel-Ziv complexity (LZC); mild cognitive impairment (MCI) Alzheimer’s disease (AD); apolipoprotein E (ApoE); electroencephalography (EEG); Lempel-Ziv complexity (LZC); mild cognitive impairment (MCI)
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MDPI and ACS Style

Gutiérrez-de Pablo, V.; Gómez, C.; Poza, J.; Maturana-Candelas, A.; Martins, S.; Gomes, I.; Lopes, A.M.; Pinto, N.; Hornero, R. Relationship between the Presence of the ApoE ε4 Allele and EEG Complexity along the Alzheimer’s Disease Continuum. Sensors 2020, 20, 3849. https://doi.org/10.3390/s20143849

AMA Style

Gutiérrez-de Pablo V, Gómez C, Poza J, Maturana-Candelas A, Martins S, Gomes I, Lopes AM, Pinto N, Hornero R. Relationship between the Presence of the ApoE ε4 Allele and EEG Complexity along the Alzheimer’s Disease Continuum. Sensors. 2020; 20(14):3849. https://doi.org/10.3390/s20143849

Chicago/Turabian Style

Gutiérrez-de Pablo, Víctor, Carlos Gómez, Jesús Poza, Aarón Maturana-Candelas, Sandra Martins, Iva Gomes, Alexandra M. Lopes, Nádia Pinto, and Roberto Hornero. 2020. "Relationship between the Presence of the ApoE ε4 Allele and EEG Complexity along the Alzheimer’s Disease Continuum" Sensors 20, no. 14: 3849. https://doi.org/10.3390/s20143849

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