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Cognitive training modulates brain hypersynchrony in a population at risk for Alzheimer’s disease

dc.contributor.authorSuárez Méndez, Isabel
dc.contributor.authorBruña Fernández, Ricardo
dc.contributor.authorLópez Sanz, David
dc.contributor.authorMontejo, Pedro
dc.contributor.authorMontenegro Peña, María Mercedes
dc.contributor.authorDelgado Losada, María Luisa
dc.contributor.authorMarcos Dolado, Alberto
dc.contributor.authorLópez Sánchez, Ramón
dc.contributor.authorMaestu Unturbe, Fernando
dc.date.accessioned2024-02-08T11:41:49Z
dc.date.available2024-02-08T11:41:49Z
dc.date.issued2022-04-05
dc.description.abstractBackground: Recent studies demonstrated that brain hypersynchrony is an early sign of dysfunction in Alzheimer's disease (AD) that can represent a proxy for clinical progression. Conversely, non-pharmacological interventions, such as cognitive training (COGTR), are associated with cognitive gains that may be underpinned by a neuroprotective effect on brain synchrony. Objective: To study the potential of COGTR to modulate brain synchrony and to eventually revert the hypersynchrony phenomenon that characterizes preclinical AD. Methods: The effect of COGTR was examined in a sample of healthy controls (HC, n = 41, 22 trained) and individuals with subjective cognitive decline (SCD, n = 49, 24 trained). Magnetoencephalographic activity and neuropsychological scores were acquired before and after a ten-week COGTR intervention aimed at improving cognitive function and daily living performance. Functional connectivity (FC) was analyzed using the phase-locking value. A mixed-effects ANOVA model with factors time (pre-intervention/post-intervention), training (trained/non-trained), and diagnosis (HC/SCD) was used to investigate significant changes in FC. Results: We found an average increase in alpha-band FC over time, but the effect was different in each group (trained and non-trained). In the trained group (HC and SCD), we report a reduction in the increase in FC within temporo-parietal and temporo-occipital connections. In the trained SCD group, this reduction was stronger and showed a tentative correlation with improved performance in different cognitive tests. Conclusion: COGTR interventions could mitigate aberrant increases in FC in preclinical AD, promoting brain synchrony normalization in groups at a higher risk of developing dementia.
dc.description.departmentDepto. de Psicología Experimental, Procesos Cognitivos y Logopedia
dc.description.departmentDepto. de Radiología, Rehabilitación y Fisioterapia
dc.description.facultyFac. de Psicología
dc.description.facultyFac. de Medicina
dc.description.refereedFALSE
dc.description.sponsorshipComunidad de Madrid
dc.description.sponsorshipComisión Europea
dc.description.statuspub
dc.identifier.citationSuárez-Méndez, Isabel et al. ‘Cognitive Training Modulates Brain Hypersynchrony in a Population at Risk for Alzheimer’s Disease’. 1 Jan. 2022 : 1185 – 1199.
dc.identifier.doi10.3233/JAD-215406
dc.identifier.essn1875-8908
dc.identifier.issn1387-2877
dc.identifier.officialurlhttps://content.iospress.com/articles/journal-of-alzheimers-disease/jad215406
dc.identifier.pmid35180120
dc.identifier.urihttps://hdl.handle.net/20.500.14352/100357
dc.issue.number3
dc.journal.titleJournal of Alzheimer's Disease
dc.language.isoeng
dc.page.final1199
dc.page.initial1185
dc.publisherIOS Press
dc.relation.projectIDB2017/BMD-3760
dc.relation.projectID826421
dc.rightsAttribution-NonCommercial-ShareAlike 4.0 Internationalen
dc.rights.accessRightsopen access
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/
dc.subject.keywordCognitive decline
dc.subject.keywordFunctional neuroimaging
dc.subject.keywordIntervention study
dc.subject.keywordLongitudinal studies
dc.subject.keywordMagnetoencephalography
dc.subject.ucmNeurociencias (Medicina)
dc.subject.unesco2490 Neurociencias
dc.subject.unesco2402.15 Envejecimiento Somático
dc.titleCognitive training modulates brain hypersynchrony in a population at risk for Alzheimer’s disease
dc.typejournal article
dc.type.hasVersionAM
dc.volume.number86
dspace.entity.typePublication
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