Please use this identifier to cite or link to this item: https://hdl.handle.net/10216/155830
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dc.creatorMaturana-Candelas, A
dc.creatorGómez, C
dc.creatorPoza, J
dc.creatorRodríguez-González, V
dc.creatorPablo, VGd
dc.creatorLopes, AM
dc.creatorPinto, N
dc.creatorHornero, R
dc.date.accessioned2023-12-15T12:31:22Z-
dc.date.available2023-12-15T12:31:22Z-
dc.date.issued2021
dc.identifier.issn2045-2322
dc.identifier.urihttps://hdl.handle.net/10216/155830-
dc.description.abstractPICALM and CLU genes have been linked to alterations in brain biochemical processes that may have an impact on Alzheimer’s disease (AD) development and neurophysiological dynamics. The aim of this study is to analyze the relationship between the electroencephalographic (EEG) activity and the PICALM and CLU alleles described as conferring risk or protective effects on AD patients and healthy controls. For this purpose, EEG activity was acquired from: 18 AD patients and 12 controls carrying risk alleles of both PICALM and CLU genes, and 35 AD patients and 12 controls carrying both protective alleles. Relative power (RP) in the conventional EEG frequency bands (delta, theta, alpha, beta, and gamma) was computed to quantify the brain activity at source level. In addition, spatial ent+N364ropy (SE) was calculated in each band to characterize the regional distribution of the RP values throughout the brain. Statistically significant differences in global RP and SE at beta band (p-values < 0.05, Mann–Whitney U-test) were found between genotypes in the AD group. Furthermore, RP showed statistically significant differences in 58 cortical regions out of the 68 analyzed in AD. No statistically significant differences were found in the control group at any frequency band. Our results suggest that PICALM and CLU AD-inducing genotypes are involved in physiological processes related to disruption in beta power, which may be associated with physiological disturbances such as alterations in beta-amyloid and neurotransmitter metabolism.
dc.description.sponsorshipThis research was supported by ‘Ministerio de Ciencia, Innovación y Universidades - Agencia Estatal de Investi-gación’ and ‘European Regional Development Fund’ (FEDER) under project PGC2018-098214-A-I00, by ‘European Commission’ and ‘FEDER’ under projects ‘Análisis y correlación entre el genoma completo y la actividad cerebral para la ayuda en el diagnóstico de la enfermedad de Alzheimer’ and ‘Análisis y correlación entre la epigenética y la actividad cerebral para evaluar el riesgo de migraña crónica y episódica en mujeres’ (‘Cooperation Programme Interreg V-A Spain-Portugal POCTEP 2014–2020’), by ‘CIBER de Bioingeniería, Biomateriales y Nanomedicina (CIBER-BBN)’ through ‘Instituto de Salud Carlos III’ co-funded with FEDER funds, and by Portuguese funds through FCT-Fundação para a Ciência e a Tecnologia/Ministério da Ciência, Tecnologia e Ino-vação and the projects ‘Institute for Research and Innovation in Health Sciences’ (POCI-01-0145-FEDER-007274) and ‘Center of Mathematics of the University of Porto’ (UID/MAT/00144/2013). V.R.-G. was in receipt of a PIF-UVa grant from the University of Valladolid. A.L. and N.P. are funded by FCT: IF/01262/2014, and through the Decreto-Lei n◦ 57/2016 de 29 de Agosto, respectively. The genotyping service was carried out at CEGEN-PRB3-ISCIII; it is supported by grant PT17/0019, of the PE I+D+i 2013-2016, funded by ISCIII and ERDF.
dc.language.isoeng
dc.publisherNature Publishing Group
dc.relationinfo:eu-repo/grantAgreement/FCT/6817 - DCRRNI ID/UID%2FMAT%2F00144%2F2013/PT
dc.relation.ispartofScientific Reports, vol.11(1):20465
dc.rightsopenAccess
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.subject.meshAged
dc.subject.meshAged, 80 and over
dc.subject.meshAlzheimer Disease / genetics
dc.subject.meshAlzheimer Disease / physiopathology
dc.subject.meshBrain
dc.subject.meshClusterin / genetics
dc.subject.meshElectroencephalography
dc.subject.meshFemale
dc.subject.meshGenetic Predisposition to Disease
dc.subject.meshGenotype
dc.subject.meshHumans
dc.subject.meshMale
dc.subject.meshMonomeric Clathrin Assembly Proteins / genetics
dc.titleInfluence of PICALM and CLU risk variants on beta EEG activity in Alzheimer’s disease patients
dc.typeArtigo em Revista Científica Internacional
dc.contributor.uportoInstituto de Investigação e Inovação em Saúde
dc.identifier.doi10.1038/s41598-021-99589-y
dc.relation.publisherversionhttps://www.nature.com/articles/s41598-021-99589-y
Appears in Collections:I3S - Artigo em Revista Científica Internacional

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