D-047 | Convergence of interoception, emotion, and social cognition in the allostatic interoceptive network across neurodegenerative diseases

D-047 | Convergence of interoception, emotion, and social cognition in the allostatic interoceptive network across neurodegenerative diseases 150 150 SAN 2024 Annual Meeting

Cognition, Behavior, and Memory
Author: Jessica Hazelton | Email: jessica.hazelton@edu.uai.cl


Jessica L. Hazelton1°2°3°, Fábio Carneiro, Marcelo Maito1°2°,  Fabian Richter, Agustina Legaz1°2°, Florencia Altschuler, Leidy Cubillos-Pinilla,  Yu Chen, Colin P Doherty, Prof Sandra Baez,  Agustín Ibáñez1°2°

Latin American Brain Health Institute (BrainLat), Universidad Adolfo Ibáñez, Santiago, Chile
Cognitive Neuroscience Center (CNC), Universidad de San Andres, Buenos Aires, Argentina
The University of Sydney, Brain and Mind Centre, School of Psychology, Sydney, Australia
Laboratory of Neuropsychophysiology, Faculty of Psychology and Education Sciences, University of Porto, Portugal

Deficits in interoception, emotion, and social cognition occur in neurodegeneration. Indirect evidence suggests that allostatic-interoceptive network (AIN) dysfunction underlies these deficits. No study, however, has investigated the convergence of these deficits in neurodegeneration or considered how both structural and functional changes may lead to the cross-domain impairment.
We conducted Activated-Likelihood Estimate (ALE) meta-analyses in studies measuring neural correlates of interoception, emotion, or social cognition (structural: MRI; functional: fMRI and FDG-PET) in neurodegeneration (e.g., behavioral-variant frontotemporal dementia (bvFTD), primary progressive aphasias, Alzheimer’s disease, and Parkinson’s Disease).
From 20,593 studies, 170 reports met inclusion criteria (58 interoception, 65 emotion, and 47 social cognition) involving 7032 participants (4963 patients and 2069 healthy controls). In all patients combined, conjunction analyses revealed cross-domain involvement of the insula, amygdala, orbitofrontal cortex, anterior cingulate, striatum, thalamus, and hippocampus. In bvFTD only, we replicated this result.
Neurodegeneration induces dysfunctional AIN across atrophy, connectivity, and metabolism, with particular relevance for bvFTD. Findings bolster the predictive coding theories of large-scale AIN, calling for more synergistic approaches to understanding interoception, emotion, and social cognition impairments in neurodegeneration.

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