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Multimodal mechanisms of human sociallyreinforced learning across neurodegenerative diseases

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dc.contributor.authorLegaz, Agustina
dc.contributor.authorAbrevaya, Sofía
dc.contributor.authorDottori, Martín
dc.contributor.authorGonzález, Cecilia
dc.contributor.authorBirba, Agustina
dc.contributor.authorMartorell, Miguel
dc.contributor.authorAguirre, Julieta
dc.contributor.authorSlachevsky Chonchol, Andrea
dc.contributor.authorAranguiz, Rafael
dc.contributor.authorSerrano, Cecilia
dc.contributor.authorGillan, Claire
dc.contributor.authorLeroi, Iracema
dc.contributor.authorGarcía, Adolfo
dc.contributor.authorFittipaldi, Sol
dc.contributor.authorIbañez, Agustín
dc.date.accessioned2023-12-14T19:55:22Z
dc.date.available2023-12-14T19:55:22Z
dc.date.issued2022
dc.description.abstractSocial feedback can selectively enhance learning in diverse domains. Relevant neurocognitive mechanisms have been studied mainly in healthy persons, yielding correlational findings. Neurodegenerative lesion models, coupled with multimodal brain measures, can complement standard approaches by revealing direct multidimensional correlates of the phenomenon. To this end, we assessed socially reinforced and non-socially reinforced learning in 40 healthy participants as well as persons with behavioural variant frontotemporal dementia (n = 21), Parkinson's disease (n = 31) and Alzheimer's disease (n = 20). These conditions are typified by predominant deficits in social cognition, feedback-based learning and associative learning, respectively, although all three domains may be partly compromised in the other conditions. We combined a validated behavioural task with ongoing EEG signatures of implicit learning (medial frontal negativity) and offline MRI measures (voxel-based morphometry). In healthy participants, learning was facilitated by social feedback relative to non-social feedback. In comparison with controls, this effect was specifically impaired in behavioural variant frontotemporal dementia and Parkinson's disease, while unspecific learning deficits (across social and non-social conditions) were observed in Alzheimer's disease. EEG results showed increased medial frontal negativity in healthy controls during social feedback and learning. Such a modulation was selectively disrupted in behavioural variant frontotemporal dementia. Neuroanatomical results revealed extended temporo-parietal and fronto-limbic correlates of socially reinforced learning, with specific temporo-parietal associations in behavioural variant frontotemporal dementia and predominantly fronto-limbic regions in Alzheimer's disease. In contrast, non-socially reinforced learning was consistently linked to medial temporal/hippocampal regions. No associations with cortical volume were found in Parkinson's disease. Results are consistent with core social deficits in behavioural variant frontotemporal dementia, subtle disruptions in ongoing feedback-mechanisms and social processes in Parkinson's disease and generalized learning alterations in Alzheimer's disease. This multimodal approach highlights the impact of different neurodegenerative profiles on learning and social feedback. Our findings inform a promising theoretical and clinical agenda in the fields of social learning, socially reinforced learning and neurodegeneration.
dc.description.versionVersión Publicada
dc.identifier.citationLegaz A, Abrevaya S, Dottori M, González Campo C, Birba A, Martorell Caro M, Aguirre J, Slachevsky A, Aranguiz R, Serrano C, Gillan CM, Leroi I, García AM, Fittipaldi S, Ibañez A. Multimodal mechanisms of human socially reinforced learning across neurodegenerative diseases. Brain. 2022 Apr 29;145(3):1052-1068. doi: 10.1093/brain/awab345
dc.identifier.doihttps://doi.org/10.1093/brain/awab345
dc.identifier.urihttps://repositorio.udd.cl/handle/11447/8195
dc.language.isoen
dc.subjectAlzheimer’s disease
dc.subjectParkinson’s disease
dc.subjectBehavioural variant frontotemporal dementia
dc.subjectLearning
dc.subjectSocial reinforcement
dc.titleMultimodal mechanisms of human sociallyreinforced learning across neurodegenerative diseases
dc.typeArticle
dcterms.accessRightsAcceso Abierto
dcterms.sourceBrain : a journal of neurology
dspace.entity.typePublication
relation.isAuthorOfPublicatione25c3d3e-63b5-4e04-951a-12a4989aa772
relation.isAuthorOfPublication.latestForDiscoverye25c3d3e-63b5-4e04-951a-12a4989aa772

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