Exploring the neurocognitive basis of episodic recollection in autism

Abstract

Increasing evidence indicates that the subjective experience of recollection is diminished in autism spectrum disorder (ASD) compared to neurotypical individuals. The neurocognitive basis of this difference in how past events are re-experienced has been debated and various theoretical accounts have been proposed to date. Although each existing theory may capture particular features of memory in ASD, recent research questions whether any of these explanations are alone sufficient or indeed fully supported. This review first briefly considers the cognitive neuroscience of how episodic recollection operates in the neurotypical population, informing predictions about the encoding and retrieval mechanisms that might function atypically in ASD. We then review existing research on recollection in ASD, which has often not distinguished between different theoretical explanations. Recent evidence suggests a distinct difficulty engaging recollective retrieval processes, specifically the ability to consciously reconstruct and monitor a past experience, which is likely underpinned by altered functional interactions between neurocognitive systems rather than brain region-specific or process-specific dysfunction. This integrative approach serves to highlight how memory research in ASD may enhance our understanding of memory processes and networks in the typical brain. We make suggestions for future research that are important for further specifying the neurocognitive basis of episodic recollection in ASD and linking such difficulties to social developmental and educational outcomes.

Atypicalities in sleep and semantic consolidation in autism

“…Instead, these data imply a more rapid decay of the integrity of semantic representations over time in ASD. This is consistent with previous reports that, in contrast to intact item memory, the ‘wheres’ and ‘whens’ of episodic memories are atypical in ASD, with generally poorer recall and reduced hippocampal connectivity during recall for such associations (Cooper et al, ; Cooper & Simons, ).…”

Linking the Puzzle Pieces of the Past: A Study of Relational Memory in Children with Autism Spectrum Disorder

“…We propose that altered relational memory processes in ASD may best be understood by examining the complex interplay between relational binding mechanisms and strategic memory processes served by cognitive control abilities. This corresponds with the current perspective on relational memory in ASD suggesting that the generation of relational binding processes is mediated by the connectivity between hippocampus and prefrontal cortex, rather than one of these regions in isolation [Bowler et al, 2011;Cooper et al, 2017;Cooper & Simons, 2019].…”

“…Accordingly, we would argue that an effect of compromised EF is likely to be more pronounced in a relational memory task than in single-feature tasks (as there was a tendency toward in the present study), since processing of relational information is assumed to rely on cognitive control functions to a greater extent than processing of single features [Johnson, 1992;Lorsbach & Reimer, 2005]. This reasoning is in line with two complementary accounts for altered memory in ASD focusing on atypical processing of complex information: according to the complex information processing model [Minshew & Goldstein, 1998 and Task Support Hypothesis [Bowler et al, 2004;Bowler, Matthews, & Gardiner, 1997], memory performance in ASD disproportionately decreases as task complexity and cognitive control demands increase [Cooper & Simons, 2019]. We propose that altered relational memory processes in ASD may best be understood by examining the complex interplay between relational binding mechanisms and strategic memory processes served by cognitive control abilities.…”

Behavioural and brain ultrastructural changes following the systemic administration of propionic acid in adolescent male rats. Further development of a rodent model of autism

“…In the present research, we utilized behaviour analysis and electron microscopy (EM) in order to evaluate social behaviour, spatial reference memory, locomotor activity and the ultrastructure of the hippocampus and medial prefrontal cortex in PPA‐treated male adolescent rats. Both regions play important role in social and motor behaviour, cognition, anxiety, memory and impulse control (Ariza, Rogers, Hashemi, Noctor, & Martinez‐Cerdeno, ; Cooper et al, ; Cooper & Simons, ; Hashemi, Ariza, Rogers, Noctor, & Martinez‐Cerdeno, ) and are known to be involved in autism pathogenesis. Moreover, in both areas of PPA‐treated brain ASD‐like light microscopic and biochemical alterations were described (MacFabe et al, ).…”