BRAIN AREAS RELATED TO REDUCED SERIAL DEPENDENCE IN ANTI-NMDAR ENCEPHALITIS AND SCHIZOPHRENIA: AN FMRI STUDY
Fundació de Recerca Clínic Barcelona-Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS)
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PS04-08PM-008
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The neural reactivation of recent memories supports the integration of past and present information and underlies serial dependence effects in perception and decision-making. Previous EEG studies have reported reduced memory reactivations during working memory in patients with anti-NMDAR encephalitis and schizophrenia. Understanding the neural basis of these reactivation deficits is essential to understand how impaired serial dependence affects cognitive dysfunction in clinical populations. In this study, we investigated the brain network substrates of memory reactivation deficits in patients using fMRI.
Healthy controls and patient groups performed a delayed-response visual working memory task while fMRI data were acquired. Brain activity during the fixation and delay periods was analyzed using a GLM framework to identify neural correlates of memory reactivation and memory maintenance in the absence or sensory input. Group-level contrasts were computed to compare activation patterns between healthy controls and patient groups to identify regions showing reduced reactivation-related activity.
The control cohort exhibited robust maintenance-related activation across frontoparietal and temporal regions, consistent with sustained internal memory representations. In the fixation period, anti-NMDAR encephalitis patients showed reduced activation in key memory-related regions, including the fronto-parietal network, particularly during early recovery stages. Additionally, both patient groups showed reduced reactivation-related signals across sensorimotor and subcortical networks, indicating widespread network disruption.
These findings support network-based and dynamical models of working memory in which stable, distributed neural states during delay periods enable memory-guided prediction and serial dependence. Our results indicate a distributed neurobiological basis for memory reactivation deficits in neuropsychiatric disorders characterized by persistent cognitive dysfunction.
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