ABSTRACT Active forgetting through retrieval suppression can impair memory for information encountered nearby in time (“amnesic shadow”). Whether this collateral effect extends to spatial memory is unclear. Across three experiments, we examined how suppression influences the encoding of new spatial memories. Experiment 1 used a modified hippocampal-modulation paradigm that paired the Think/No-Think task with a spatial location task. Spatial locations encoded between suppression trials were recalled less accurately than those encoded between retrieval trials or a baseline, evidencing an amnesic shadow for spatial memory. Experiment 2 introduced a 24-hour delay and showed that the deficit persisted, indicating durability beyond initial encoding. Experiment 3 manipulated control strategies: direct suppression produced the shadow, whereas thought substitution did not impair nearby spatial learning. Together, the results support systemic-suppression accounts in which prefrontal control transiently down-regulates hippocampal function, broadly weakening hippocampus-dependent processes. By extending the amnesic shadow to spatial memory and isolating it to direct suppression, this work provides a strategy-specific behavioural marker of memory control and clarifies how attempts to contain unwanted thoughts can unintentionally degrade concurrent spatial learning.

Inhibitory control training might be a gateway to enhance fear extinction.

Mild traumatic brain injury (mTBI) is typically associated with transient cognitive disturbance, particularly involving attention and new learning, with most patients demonstrating full recovery within weeks. Memory impairment in uncomplicated mTBI generally reflects reversible neurometabolic dysfunction and is limited to a brief period of post-traumatic amnesia and restricted retrograde loss surrounding the injury. However, a subset of patients develop persistent and disproportionate autobiographical memory disturbance that exceeds expected neuroanatomical limits and lacks structural correlates on neuroimaging. In rare but clinically challenging cases, this presentation may resemble extensive retrograde or identity-related amnesia. This review examines functional (dissociative) amnesia emerging after mTBI and proposes that concussion may act as a gateway condition facilitating the development of Functional Cognitive Disorder (FCD) in vulnerable individuals. We differentiate expected post-traumatic memory patterns from atypical selective impairment of autobiographical retrieval and clarify how distinct memory systems-episodic, autobiographical, semantic, and procedural-are differentially affected. We expand the two-hit hypothesis by integrating contemporary neurobiological evidence. The first hit comprises concussion-induced neurometabolic disturbance, glial activation, oxidative imbalance, and transient fronto-limbic dysregulation. The second hit may involve psychological stress, identity threat, maladaptive metacognitive processes, or persistent neuroinflammatory signalling, collectively resulting in functional inhibition of autobiographical memory retrieval despite preserved memory storage. Functional amnesia is conceptualised as a severe phenotype within the spectrum of functional cognitive disorder. We introduce a structured clinician-administered interview (SIFRA) to operationalise diagnostic features and support systematic assessment. This integrative framework reconciles neurological vulnerability with functional network dysregulation and provides a coherent basis for diagnosis and multidisciplinary management of persistent memory disturbance after mTBI.

Inhibitory control plays a critical role in regulating eating behaviour. While previous research focused primarily on motor inhibition (e.g. go/no-go tasks), the role of memory suppression remains underexplored. This study employed a food-specific think/no-think (TNT) paradigm to investigate two questions: (1) whether individuals can intentionally suppress food-related memories, and whether suppression performance is associated with body mass index (BMI); and (2) whether memory suppression reduces subjective food valuation. Sixty-one young female participants completed a TNT task and subsequently rated food items for liking and wanting. Results showed that recall accuracy for suppressed (No-think) items was significantly lower than for both retrieved (Think) and Baseline items, indicating suppression-induced forgetting. However, food-related memory suppression performance was not associated with BMI. Moreover, memory suppression did not significantly alter subjective ratings of liking or wanting. These findings suggest that food-related memories can be deliberately suppressed regardless of BMI, but such suppression may not influence food valuation directly. Further studies are needed to determine whether such memory suppression has any downstream impact on eating behaviour and to identify mechanisms beyond mere changes in valuation.

Semantic memory retrieval is essential for language, thought, and adaptive behavior. Although both the prefrontal cortex (PFC) and the cerebellum have been implicated in this function, the role of the PFC remains poorly understood and the contribution of the cerebellum largely overlooked in current neurocognitive models. To address these gaps, we conducted a double-blind, randomized, placebo-controlled experiment in which healthy adults received anodal transcranial direct current stimulation (tDCS) targeting the left lateral PFC, the right posterior cerebellum, or sham stimulation. Participants completed a novel process-sensitive paradigm comprising lexical decision, free-associative (FA; automatic) retrieval, dissociative (DA; controlled) retrieval, and intrusion monitoring, while manipulating response predictability and rule switching. Cerebellar tDCS selectively impaired FA performance, particularly for cues evoking predictable responses, supporting its role in automatic access to overlearned associations. In contrast, prefrontal tDCS disrupted DA performance and increased associative intrusions, implicating the PFC in retrieval inhibition. Importantly, mediation analysis showed that the reduction in DA fluency was largely explained by higher probability of intrusions, indicating a perturbation of proactive inhibitory control that normally prevents irrelevant memory activations from entering working memory. Further exploratory analyses ruled out several alternative accounts of these stimulation effects, underscoring their process specificity. Together, these findings advance models of semantic cognition by demonstrating complementary contributions of the cerebellum to automatic retrieval and of the PFC to inhibitory control over intrusions.

Extensive research has demonstrated that people can intentionally forget by inhibiting the retrieval of unwanted memories, a phenomenon known as suppression-induced forgetting (SIF). Although neuroimaging studies have linked retrieval suppression to the right lateral prefrontal cortex (LPFC), direct evidence for the causal role this region plays in supporting SIF is still lacking. In this registered report, our aim is putting to a strong empirical test such an idea by using cathodal transcranial direct current stimulation in a standard think/no-think procedure. Across two experiments, we will compare the SIF achieved by participants receiving cathodal transcranial direct current stimulation over the right LPFC-which has been shown to disrupt prefrontally mediated inhibitory control-with those receiving sham stimulation or cathodal stimulation over a control site. In addition, we will examine the lateralization of this effect by comparing stimulation of the right and left LPFC. Our results will provide novel and critical insights into the brain mechanisms of inhibitory control.

Sleep disturbances are associated with intrusive memories, but the neurocognitive mechanisms underpinning this relationship are poorly understood. Here, we show that sleep deprivation disrupts prefrontal inhibition of memory retrieval, and that the overnight restoration of this inhibitory mechanism is associated with time spent in rapid eye movement (REM) sleep. The functional impairments arising from sleep deprivation are linked to a behavioral deficit in the ability to downregulate unwanted memories, and coincide with a deterioration of deliberate patterns of self-generated thought. We conclude that sleep deprivation gives rise to intrusive memories via the disruption of neural circuits governing mnemonic inhibitory control, which may rely on REM sleep.

The mechanisms underlying generalized forms of dissociative ('psychogenic') amnesia are poorly understood. One theory suggests that memory retrieval is inhibited via prefrontal control. Findings from cognitive neuroscience offer a candidate mechanism for this proposed retrieval inhibition. By applying predictions based on these experimental findings, we examined the putative role of retrieval suppression in dissociative amnesia. We analyzed fMRI data from two previously reported cases of dissociative amnesia. Patients had been shown reminders from forgotten and remembered time periods (colleagues and school friends). We examined the neuroanatomical overlap between regions engaged in the unrecognized compared to the recognized condition, and the regions engaged during retrieval suppression in laboratory-based tasks. Effective connectivity analyses were performed to test the hypothesized modulatory relationship between the right anterior dorsolateral prefrontal cortex (raDLPFC) and the hippocampus. Both patients were scanned again following treatment, and analyses were repeated. We observed substantial functional alignment between the inhibitory regions engaged during laboratory-based retrieval suppression tasks, and those engaged when patients failed to recognize their current colleagues. This included significant activation in the raDLPFC and right ventrolateral prefrontal cortex, and a corresponding deactivation across autobiographical memory regions (hippocampus, medial PFC). Dynamic causal modeling confirmed the hypothesized modulatory relationship between the raDLPFC and the hippocampus. This pattern was no longer evident following memory recovery in the first patient, but persisted in the second patient who remained amnesic. Findings are consistent with an inhibitory mechanism driving down activity across core memory regions to prevent the recognition of personally relevant stimuli.

When reminded of an unpleasant experience, people often try to exclude the unwanted memory from awareness, a process known as retrieval suppression. Here we used multivariate decoding (MVPA) and representational similarity analyses on EEG data to track how suppression unfolds in time and to reveal its impact on item-specific cortical patterns. We presented reminders to aversive scenes and asked people to either suppress or to retrieve the scene. During suppression, mid-frontal theta power within the first 500ms distinguished suppression from passive viewing of the reminder, indicating that suppression rapidly recruited control. During retrieval, we could discern EEG cortical patterns relating to individual memories-initially, based on theta-driven visual perception of the reminders (0 to 500ms) and later, based on alpha-driven reinstatement of the aversive scene (500 to 3000ms). Critically, suppressing retrieval weakened (during 360 to 600ms) and eventually abolished item-specific cortical patterns, a robust effect that persisted until the reminder disappeared (780 to 3000ms). Representational similarity analyses provided converging evidence that retrieval suppression weakened the representation of target scenes during the 500 to 3000ms reinstatement window. Together, rapid top-down control during retrieval suppression abolished cortical patterns of individual memories, and precipitated later forgetting. These findings reveal a precise chronometry on the voluntary suppression of individual memories.

In this study, we investigated the electrical brain responses in a high-density EEG array (64 electrodes) elicited specifically by the word memory cue in the Think/No-Think paradigm in 46 participants. In a first step, we corroborated previous findings demonstrating sustained and reduced brain electrical frontal and parietal late potentials elicited by memory cues following the No-Think (NT) instructions as compared to the Think (T) instructions. The topographical analysis revealed that such reduction was significant 1000 ms after memory cue onset and that it was long-lasting for 1000 ms. In a second step, we estimated the underlying brain generators with a distributed method (swLORETA) which does not preconceive any localization in the gray matter. This method revealed that the cognitive process related to the inhibition of memory retrieval involved classical motoric cerebral structures with the left primary motor cortex (M1, BA4), thalamus, and premotor cortex (BA6). Also, the right frontal-polar cortex was involved in the T condition which we interpreted as an indication of its role in the maintaining of a cognitive set during remembering, by the selection of one cognitive mode of processing, Think, over the other, No-Think, across extended periods of time, as it might be necessary for the successful execution of the Think/No-Think task.

Memory suppression devalues food reward and can predict long-term changes in emotional eating

Traumatic events result in vivid and enduring fear memories. Suppressing the retrieval of these memories is central to behavioral therapies for pathological fear. The medial prefrontal cortex (mPFC) and hippocampus (HPC) have been implicated in retrieval suppression, but how mPFC-HPC activity is coordinated during extinction retrieval is unclear. Here we show that after extinction training, coherent theta oscillations (6–9 Hz) in the HPC and mPFC are correlated with the suppression of conditioned freezing in male and female rats. Inactivation of the nucleus reuniens (RE), a thalamic hub interconnecting the mPFC and HPC, reduces extinction-related Fos expression in both the mPFC and HPC, dampens mPFC-HPC theta coherence, and impairs extinction retrieval. Conversely, theta-paced optogenetic stimulation of RE augments fear suppression and reduces relapse of extinguished fear. Collectively, these results demonstrate a role for RE in coordinating mPFC-HPC interactions to suppress fear memories after extinction.

Memory encoding and memory retrieval are neurally distinct brain states that can be differentiated on the basis of cortical network activity. However, it is unclear whether sustained engagement of one network or fluctuations between multiple networks give rise to these memory states. The spatiotemporal dynamics of memory states may have important implications for memory behavior and cognition; however, measuring temporally resolved signals of cortical networks poses a challenge. Here, we recorded scalp electroencephalography from participants performing a mnemonic state task in which they were biased toward memory encoding or retrieval. We performed a microstate analysis to measure the temporal dynamics of cortical networks throughout this mnemonic state task. We find that Microstate E, a putative analog of the default mode network, shows temporally sustained dissociations between memory encoding and retrieval, with greater engagement during retrieve compared with encode trials. We further show that decreased engagement of Microstate E is a general property of encoding, rather than a reflection of retrieval suppression. Thus, memory success, as well as cognition more broadly, may be influenced by the ability to engage or disengage Microstate E in a goal-dependent manner.

Suppressing retrieval of unwanted memories can cause forgetting, an outcome often attributed to the recruitment of inhibitory control. This suppression-induced forgetting (SIF) generalizes to different cues used to test the suppressed content (cue-independence), a property taken as consistent with inhibition. But does cue-independent forgetting necessarily imply that a memory has been inhibited? Tomlinson et al. (Proc Natl Acad Sci 106:15588–15593, 2009) reported a surprising finding that pressing a button also led to cue-independent forgetting, which was taken as support for an alternative interference account. Here we investigated the role of inhibition in forgetting due to retrieval suppression and pressing buttons. We modified Tomlinson et al.’s procedure to examine an unusual feature they introduced that may have caused memory inhibition effects in their experiment: the omission of explicit task-cues. When tasks were uncued, we replicated the button-press forgetting effect; but when cued, pressing buttons caused no forgetting. Moreover, button-press forgetting partially reflects output-interference effects at test and not a lasting effect of interference. In contrast, SIF occurred regardless of these procedural changes. Collectively, these findings indicate that simply pressing a button does not induce forgetting, on its own, without confounding factors that introduce inhibition into the task and that inhibition likely underlies SIF.

Subliminal backdoors to forgetting emotional memories.

Growing evidence indicates that a domain-general executive control supports semantic memory retrieval, yet the nature of this interaction remains elusive. To shed light on such control mechanisms, we conducted two dual-task experiments loading distinct executive capacities (working memory maintenance, monitoring, and switching), while participants carried out automatic (free-associative) and controlled (dissociative) word retrieval tasks. We found that these forms of executive load interfered with retrieval fluency in both tasks, but these negative effects were more pronounced for the dissociative performance. Together, these findings indicate that the domain-general executive control supports accessing contextually relevant knowledge as well as the inhibition of automatically activated but task-inappropriate retrieval candidates, putatively via an adaptive gating of semantic activation and interference control. Moreover, the processing costs related to retrieval inhibition and switching were negatively correlated, suggesting a trade-off between the ability to constrain semantic activation (i.e., inhibition) and the ability to initiate flexible transitions between semantic sets (i.e., switching), which may thus represent two complementary control functions governing semantic memory retrieval.

BackgroundFear of negative evaluation (FNE), referring to negative expectation and feelings toward other people’s social evaluation, is closely associated with social anxiety that plays an important role in our social life. Exploring the neural markers of FNE may be of theoretical and practical significance to psychiatry research ( e.g., studies on social anxiety).MethodsTo search for potentially relevant biomarkers of FNE in human brain, the current study applied multivariate relevance vector regression, a machine‐learning and data‐driven approach, on brain morphological features ( e.g., cortical thickness) derived from structural imaging data; further, we used these features as indexes to predict self‐reported FNE score in each participant.ResultsOur results confirm the predictive power of multiple brain regions, including those engaged in negative emotional experience ( e.g., amygdala, insula), regulation and inhibition of emotional feeling ( e.g., frontal gyrus, anterior cingulate gyrus), and encoding and retrieval of emotional memory ( e.g., posterior cingulate cortex, parahippocampal gyrus).ConclusionsThe current findings suggest that anxiety represents a complicated construct that engages multiple brain systems, from primitive subcortical mechanisms to sophisticated cortical processes.

As rates of mental health disorders increase throughout the years, more and more studies have emerged to investigate their effects, such as the effects of Obsessive-Compulsive disorder on memory. Obsessive-Compulsive Disorder was first described in the Diagnostic and Statistical Manual of Mental Disorders in the 1980s.1 It is organized into 5 main categories: checking, contamination, symmetry/ordering, intrusive thoughts, and hoarding and can be measured using the Y-BOCS. OCD is caused by genetic, neurobiological, behavioral, and environmental factors. Neuroimaging studies reveal overactivation of the orbitofrontal cortex and the basal ganglia. Scientists have discovered the effects of OCD on episodic and procedural memory. In 2004, Robert M Roth conducted a Pursuit Rotor Task with 46 participants. The results reveal that the OCD group has enhanced procedural memory, likely due to the overactivation of some parts of the brain. Furthermore, in 2011, Mika Konishi used the “directed forgetting paradigm” method on 45 participants. The results reveal reduced retrieval inhibition and difficulties in selective encoding in OCD brains, which lead to decreased memory recall performance.

ABSTRACT It is important for mental health to be able to control unwanted intrusive memories. Previous studies suggest that middle frontal gyrus (MFG) down regulates pathways underlie the suppression of retrieval of general memories. However, the neural basis of motivated forgetting of autobiographical memories is unclear. Therefore, this study used two samples to explore the neural mechanisms of motivated forgetting of self-referential memories. Every participant provided 40 life events (20 negative and 20 neutral) from their past personal experience, and then completed the Think/No-Think task while undergoing functional magnetic resonance imaging (fMRI). The first sample showed a significant reduction in recall in the No-Think condition relative to the Think condition. Attempting to exclude negative autobiographical memories from awareness was associated with increased activity in the right MFG, superior frontal gyrus (SFG), and inferior frontal gyrus (IFG), while reduced activity was observed in the bilateral Brodmann areas BA18 and BA19, bilateral medial prefrontal cortex (mPFC), bilateral precuneus, bilateral post cingulate cortex (PCC), the left parahippocampus, and the left hippocampus. Functional connectivity analyses showed that the right MFG projected into the bilateral mPFC, bilateral precuneus, and bilateral middle occipital gyrus (MOG) for negative autobiographical memories. The second sample replicated the results of the first sample at both the behavioral and brain levels. These results suggest that retrieval suppression of autobiographical memories involve the pathway between the MFG and the mPFC and precuneus to exclude self-referential memories. These results reveal how people engage in motivated forgetting of negative events in their daily lives.

TRPV1 modulation of contextual fear memory depends on stimulus intensity and endocannabinoid signalling in the dorsal hippocampus