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-Higes 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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