The hippocampus supports episodic memory by binding sensory, spatial, and temporal information into event representations^[22,23]. Pattern separation and pattern completion are complementary computations within this system. Pattern separation reduces interference between similar inputs, whereas pattern completion permits an incomplete cue to reactivate a stored representation^[24-26]. Although these computations are not equivalent to memory generalization, they help explain how memories of similar people, settings, or repeated events may remain distinct or become confused.

Evidence for these computations initially came from computational models and animal studies. Sparse coding in the dentate gyrus (DG) reduces overlap between representations of similar inputs, whereas recurrent connections in Cornu Ammonis 3 (CA3) support retrieval from incomplete cues^[25,27]. CA3 may contribute to either separation or completion depending on input similarity and network state^[26,28]. CA1 is proposed to compare retrieved representations from CA3 with incoming information from the entorhinal cortex^[26]. Disruption of DG N-methyl-D-aspartic acid (NMDA) receptor signaling impairs rapid contextual discrimination, while changes in granule cell recruitment or inhibitory control can alter contextual generalization^[29-31].

Functional magnetic resonance imaging (fMRI) subsequently provided evidence consistent with analogous computations in humans. Bakker et al. showed that DG/CA3 responses to perceptually similar lure items more closely resembled responses to novel items than to repeated items, consistent with pattern separation^[32]. Subsequent mnemonic-similarity studies further demonstrated that DG/CA3 and CA1 responses vary with input similarity^[33,34]. Using an overlapping-event learning task, Molitor et al. found that reactivation of prior memories during new learning was associated with differentiation of related representations in DG/CA2,3 and integration in CA1^[35]. Together, these findings link hippocampal computations to the differentiation and integration of related memories and inform discussions of false recognition and eyewitness memory^[1].

The hippocampus operates within a broader network linking episodic context to emotional and behavioral responses. Anatomical studies in rodents have demonstrated direct projections from CA1 and the subiculum to the medial prefrontal cortex (mPFC)^[36,37]. Hippocampal-prefrontal communication is also coordinated through the nucleus reuniens (Re), which is reciprocally connected with the mPFC and hippocampal formation^[38]. Manipulation of the mPFC-Re pathway alters memory generalization, while Re function is required for precise hippocampus-dependent contextual memory^[39-41]. Other prefrontal projections, including pathways to the periaqueductal gray, regulate contextual fear discrimination and the expression of fear responses^[42]. Together, these findings support a role for hippocampal-prefrontal communication in contextual memory generalization.

The mPFC also interacts with the amygdala and extended amygdala to regulate fear expression^[43]. In rodent and primate conditioning paradigms, basolateral amygdala (BLA) responses to a conditioned stimulus can generalize to similar cues, with response strength varying according to cue similarity. Negative valence may broaden this generalization gradient by enhancing amygdala responses to stimuli that partially resemble the conditioned stimuli^[44,45]. Prefrontal circuits can regulate this process by integrating environmental information with safety signals and current behavioral demands^[43,46]. The bed nucleus of the stria terminalis (BNST), a component of the extended amygdala, is particularly involved in sustained responses to uncertain or diffuse threats^[47,48]. In a repeated-trauma mouse model, activity in the mPFC-to-BNST projection promoted fear memory generalization and subsequent distress-related behavior^[49].

These observations suggest two complementary dimensions of generalization. Hippocampal-prefrontal networks regulate the differentiation of contextual representations, whereas prefrontal interactions with the amygdala and BNST influence the range of cues and contexts that elicit fear responses. These findings suggest a possible basis for the coexistence of persistent emotional salience and reduced contextual precision in trauma-related recall.

At the cellular level, memory generalization can be examined through neuronal ensemble organization. A memory engram involves neurons recruited during encoding and can be reactivated during retrieval^[50,51]. Related experiences may engage partially overlapping ensembles, allowing new information to be linked with prior knowledge^[51-56]. Excessive overlap, however, may increase the likelihood that a cue associated with one event will coactivate elements of another representation^[57-59].

Animal studies show that both stress and the temporal proximity of experiences can alter ensemble overlap. Contextual memories formed within a limited time window can recruit overlapping hippocampal ensembles and become behaviorally linked^[52]. Loss of ensemble segregation in the DG accompanies the transition from context-specific to generalized fear^[53]. Recent work further shows that time-dependent reorganization of hippocampal engram circuits allows previously recruited neurons to support responding in related contexts, contributing to the emergence of generalized memories^[60]. Glucocorticoid exposure also enlarges the DG engram population and promotes fear in contexts not originally associated with threat^[57]. In the lateral amygdala, stress-induced endocannabinoid signaling disrupts parvalbumin-positive (PV⁺) interneuron-mediated inhibition, leading to denser threat-memory ensembles and generalized responding^[61]. Together, these findings indicate that changes in ensemble recruitment, overlap, and reactivation can contribute to generalized responding.

The ensemble boundaries can be shaped, at least in part, by the balance between excitation and inhibition. Feedforward and feedback inhibition limit the number of neurons incorporated into an engram and suppress competing representations during retrieval^[58,62,63]. Strengthening hippocampal feedforward inhibition improves memory precision, whereas reduced γ-aminobutyric acid (GABA)-mediated inhibition (GABAergic) control in hippocampal and amygdala circuits promotes the generalization of conditioned fear^{[30,31,64-66]}. The effects of inhibition nevertheless depend on cell type, circuit location, and phase of memory processing^[67,68]. Ensemble overlap and inhibitory regulation therefore provide complementary cellular mechanisms through which related experiences may influence subsequent memory retrieval and generalized responding.

Memory ensembles are stabilized and modified through synaptic plasticity^[69,70]. NMDA receptor activation, calcium-dependent signaling, α-amino-3-hydroxy-5-methyl-4-isoxazole-propionicacid (AMPA) receptor trafficking, de novo gene transcription and translation contribute to the strengthening of synaptic connections among coactivated neurons during encoding^[71-73]. Retrieval can render a memory trace transiently labile, allowing it to be updated before restabilization^[74-76]. Reactivation during new learning may promote the integration of semantic features across related memories^[12,77].

Molecular regulation of inhibition represents one route through which memory generalization may arise. GABA synthesis, presynaptic inhibition, and GABA receptor signaling constrain activity across hippocampal, prefrontal, and amygdala networks^[64,78]. Disruption of these processes can promote the generalization of conditioned fear, whereas molecular changes that enhance inhibitory interneuron recruitment can improve memory precision^[30,64,78]. Plexin-A1 has also been proposed to regulate fear memory generalization through its effects on excitatory-inhibitory balance in the mPFC^[79]. Collectively, these findings identify inhibitory regulation as an important molecular mechanism regulating memory generalization.

Actin remodeling provides an additional mechanism. Actin polymerization and depolymerization regulate dendritic-spine morphology, receptor anchoring, and synaptic stabilization^[80]. In the repeated-trauma mouse model, fear memory generalization was associated with actin depolymerization in mPFC neurons projecting to the BNST. Projection-specific manipulation of gelsolin and chromophore-assisted light inactivation provided causal evidence linking cytoskeletal remodeling to memory generalization and later distress-related behaviors^[49]. Actin remodeling may therefore enable structural reorganization of memory ensembles, thereby altering memory generalization.

In summary, current evidence supports a testable, multilevel hypothesis: hippocampal computations influence whether related experiences remain differentiated; prefrontal-limbic circuits regulate how broadly their emotional significance is expressed; and ensemble allocation, inhibitory control, and synaptic remodeling provide cellular and molecular substrates for these processes. Stress and repeated experience may increase overlap between memory representations and broaden threat responses. These changes could contribute to the persistence of emotional or schematic information alongside reduced event-specific precision. However, much of the causal evidence comes from experimental animal studies, whereas human evidence relies primarily on behavioral paradigms and neuroimaging. Proposed links between these mechanisms and the features of trauma-related accounts remain hypotheses, particularly at the cellular and molecular levels. This framework provides a basis for examining how memory generalization may shape trauma-related accounts and for defining the limits of its interpretation in forensic psychiatric assessment.

One recurring forensic question is whether reported psychiatric symptoms and functional impairment are clinically consistent with the alleged traumatic exposure. In this context, posttraumatic stress disorder (PTSD) and anxiety disorders have been associated with broader threat generalization^[81,82]. Experimental studies in PTSD have reported altered generalization of the conditioned threat response to related stimuli^[82,83]. Such threat generalization may help explain why symptoms extend beyond the original context and affect social or occupational functioning.

Memory generalization may also influence the specificity with which traumatic experiences are reported. One clinically relevant pattern is overgeneralized autobiographical memory, in which an individual retrieves a category of repeated experiences rather than an event confined to a particular time and place^[84]. For example, “I was often threatened at home” may accurately convey a recurring experience while providing limited information about a specific occasion. Reduced autobiographical memory specificity has been documented in trauma-exposed populations and in individuals with depression, anxiety disorders, or PTSD, although the strength of these associations varies across studies^[85,86].

In forensic assessment, a generalized account should therefore be examined to identify which details are provided, which are missing, and under what conditions recall was elicited^[1,84,87]. Examining how the pattern of recall relates to psychiatric symptoms and functional impairment may inform the overall clinical formulation^[87-89]. However, reduced autobiographical specificity and generalized threat responding should be assessed separately; their co-occurrence and relationship within individuals should not be assumed.

Generalization may be especially relevant when trauma is recurrent, as in prolonged abuse, repeated interpersonal violence, or persecution^[12,90]. Research on repeated-event memory indicates that recurring episodes can be organized into a common event representation, or “script”. This representation supports recall of shared features but may be accompanied by difficulty remembering details specific to individual episodes. Details may consequently be remembered without reliable attribution to the episode in which they occurred^[12,15]. Studies of children questioned about repeated events similarly show relatively preserved memory for the recurring pattern alongside greater difficulty identifying the source of episode-specific details^[91,92].

Reduced differentiation may also increase false familiarity. An unfamiliar person or setting that resembles one encountered previously may evoke a sense of familiarity, while details shared across events may be attributed to the wrong episode^[15,24]. Information encountered after an event can add to this difficulty if it is subsequently attributed to the original experience^[14,93]. These processes may contribute to an account that remains stable in its central content but is less precise about the sequence, context, or episode to which particular details belong. This distinction matters because the recurring pattern and the circumstances of a particular incident may carry different clinical or legal significance^[12,90]. Uncertainty about episode-specific details should therefore not be treated, by itself, as either evidence of fabrication or confirmation that the repeated events occurred.

Research on investigative interviewing suggests that open-ended prompts generally yield more accurate information than suggestive or forced-choice questions. It also supports exploring the recurring pattern separately from details attributed to individual episodes^[94,95]. Documented or independently verified events may provide temporal anchors, but their use should be documented because exposing an interviewee to external information can itself influence later recall^[14,96,97]. In forensic psychiatric evaluation, these findings underscore the importance of reviewing how earlier accounts were elicited and minimizing further influence on recall.

Accounts used in forensic assessments are often obtained after substantial delay and revisited in multiple interviews. Experimental studies indicate that memory can become less specific over time and that stress can increase the generalization of established threat memories^[20,98-100]. As the interval between an event and its recall increases, an individual may become less certain about when the event occurred or which episode a remembered detail belongs to. Requests for exact dates, sequences, or wording therefore need to be considered in relation to the retention interval and the nature of the information requested.

Repeated retrieval has mixed effects. Additional questioning can recover previously inaccessible information^[101]. However, information introduced through questioning and discussions may later be misattributed to personal experience and influence subsequent accounts^[15,93,96]. In experimental eyewitness paradigms, recalling an event before exposure to misleading post-event information increased the later reporting of misinformation, a phenomenon termed retrieval-enhanced suggestibility^[102,103]. The magnitude of this effect varied with the number of prior retrieval attempts, the retention interval, and the testing procedure^[102]. Repeated questioning does not necessarily distort memory; however, subsequent exposure to misleading information can increase the risk of distortion.

Age influences the ability to maintain distinct representations of similar experiences. Human studies indicate that memory distinctiveness continues to develop from childhood through adolescence, in parallel with hippocampal maturation^[104]. At the other end of the lifespan, healthy older adults show poorer discrimination between previously encountered items and similar lures than younger adults, accompanied by altered DG/CA3 activity^[24,105]. Animal studies likewise identify developmental and aging-related differences in contextual discrimination and fear generalization^[31,106,107].

Sex may also modify fear generalization, but the evidence is less consistent. Rodent studies have reported sex-dependent differences in remote contextual fear generalization and in the cues used to discriminate threat from safety^[108,109]. Human studies have reported sex differences in some aspects of fear generalization, although differences in the width of the generalization gradient have not been consistent^[110,111]. Sex should therefore be considered as a potential moderator in research, but current evidence does not support sex-based conclusions about memory generalization in an individual forensic case.

Emotional factors are also relevant to the interpretation of trauma-related accounts. Emotional arousal can strengthen memory for the central or threatening features of an experience without equivalent preservation of contextual detail^[112]. Experimental studies further suggest that materials with negative valence may elicit broader mnemonic generalization than neutral materials, while conditioned threat responses can extend to perceptually or conceptually related cues^[18,113]. Strong memory for threatening features may therefore coexist with difficulty distinguishing related events, contexts, or cues.

Taken together, the evidence suggests that trauma-related psychopathology, repeated or similar experiences, delays in recall, retrieval conditions, post-event information, and individual characteristics may influence different aspects of remembering. In forensic evaluations, these findings may help evaluators consider how observed recall patterns relate to documented clinical features and the conditions under which accounts were elicited. However, the evidence derives largely from group-level studies, and its application to individual trauma-related accounts requires further validation. Accordingly, these findings may inform hypotheses about patterns of recall and the factors influencing them, but should not be used alone to establish the factual accuracy of a specific allegation or to infer fabrication, malingering, or deception. The next section examines candidate behavioral and neurobiological measures for studying these processes.

The Autobiographical Memory Test assesses retrieval specificity by asking participants to recall personal experiences in response to emotional cue words. Responses are classified as event-specific, categoric or extended memories. This approach has been widely applied in research on depression, trauma exposure, and PTSD, in which reduced specificity is commonly expressed as the retrieval of recurring experiences rather than individual episodes^[114-116]. However, this measure does not establish the factual accuracy of recalled events, and performance can be influenced by executive function, language ability, current mood, avoidance, and task instructions.

Mnemonic similarity tasks assess the capacity to discriminate previously encountered stimuli from similar but novel alternatives. Participants first view objects or scenes and are subsequently presented with repeated items, perceptually similar “lures”, and new items. Correctly identifying a lure as similar rather than previously seen provides an index of mnemonic discrimination. These paradigms were developed from experimental studies of hippocampal pattern separation and have been combined with fMRI to relate discrimination performance to DG/CA3 activity^[32,117,118]. Reduced discrimination has been demonstrated in aging, mild cognitive impairment, and neuropsychiatric conditions^[119,120]. Contextual variants similarly examine whether environments sharing multiple features remain distinguishable^[121]. Forensic studies could test whether mnemonic discrimination performance predicts difficulty distinguishing similar or repeated episodes.

Similar to animal studies, fear generalization paradigms in humans first associate a cue or context with an aversive outcome and then measure responses to stimuli that vary systematically in their similarity to that cue or context. Threat-expectancy ratings, skin conductance, startle, or other physiological responses can be used to derive a generalization gradient^[122,123]. A broader gradient indicates that learned threat value extends to less similar cues. Such paradigms have demonstrated altered generalization in anxiety-related conditions and provide an experimental basis for examining why trauma-related reactions may be triggered outside the original context^[124,125]. However, these paradigms measure the spread of threat responding rather than the specificity or accuracy of recall.

Source memory paradigms present information from distinguishable sources and later ask participants to identify both the remembered content and its origin. Designs incorporating post-event information can test whether details introduced later are misattributed to the original event^[93]. Experimental manipulation of post-event information can therefore model how later information influences accounts elicited across multiple interviews. Source memory performance remains distinct from memory for the content itself: a person may remember a detail but be uncertain or mistaken about where it was acquired^[21,96].

Collectively, these behavioral paradigms assess related but distinct aspects of memory generalization. Table 1 summarizes their measurement targets, potential relevance to forensic research, and key interpretive limits.

Behavioral measures provide limited information about the underlying neural process. Neurobiological measures can be added to relate task performance to alterations in memory- and threat-related neural circuits.

Hippocampal subfield imaging has been applied to relate mnemonic discrimination performance to activity within specific hippocampal regions. Studies combining fMRI acquisition with specialized segmentation and analytical procedures have identified separation-like responses in the human hippocampal DG/CA3 during mnemonic-similarity tasks^[32,117]. Related studies have further linked impaired lure discrimination to altered hippocampal function in aging, mild cognitive impairment, and psychiatric disorders^[126-128]. Because conventional fMRI protocols generally cannot reliably distinguish the DG from CA3, these subfields are commonly analyzed together. These measures provide a useful link between task performance and hippocampal activity, but remain sensitive to motion, image quality, and analytical methods^[129,130].

Threat generalization paradigms combined with fMRI extend measurement from hippocampal discrimination to distributed networks. Studies using stimuli that vary in similarity to a conditioned threat stimulus have related generalization in behavioral and autonomic responses to altered activity in the hippocampus, amygdala, insula, and prefrontal and cingulate cortices^[131,132]. Dunsmoor et al., for example, showed that generalized skin-conductance responses covaried with amygdala activity, whereas amygdala-extrastriate visual cortex connectivity correlated with trait anxiety^[17]. Other studies suggest that neural responses during threat generalization tasks reflect both the assignment of threat value to similar cues and uncertainty about whether those cues predict danger^[133]. These designs allow researchers to examine how stimulus similarity and threat expectancy relate to neural activity and physiological responses within the same experiment.

Electroencephalography (EEG) can characterize the timing of neural processes during threat generalization. Event-related potential (ERP) studies suggest that fear generalization involves multiple stages of information processing, from the initial discrimination of similar cues to their subsequent emotional and cognitive evaluation. Differences have been reported in components including P2, N400, P600, and the late positive potential, with some effects varying with conceptual similarity or intolerance of uncertainty^[134-137]. However, these electrophysiological findings do not consistently parallel behavioral generalization gradients and vary across tasks and study populations^[138]. Standardized paradigms and replication in trauma-exposed and clinical populations are therefore needed to establish reliable EEG indicators of threat generalization.

Molecular approaches are more exploratory. Magnetic resonance spectroscopy (MRS) can estimate regional glutamate and GABA concentrations, providing indirect information relevant to excitatory and inhibitory neurochemistry^[139,140]. However, direct evidence linking these measures to individual memory generalization phenotypes remains limited. Altered circulating levels of inflammatory mediators and neurotrophic factors have been reported in PTSD, depression, and anxiety, but their associations with memory generalization and their specificity for these processes remain unclear^[141,142]. No molecular measure presently constitutes a validated biomarker for individual forensic classification.

Taken together, behavioral and neurobiological measures provide complementary information about processes relevant to memory generalization [Figure 1]. However, behavioral performance is influenced by task demands, mood, and cognitive abilities, while biological signals can be indirect or nonspecific. Combining behavioral tasks may reveal convergence and dissociation across cognitive and emotional processes, while integrating behavioral and neurobiological measures can help identify the neural correlates of these patterns. Future research should test whether these measures covary or dissociate within individuals and whether their neural correlates remain stable across repeated assessments. At present, these measures remain research tools. Their use in individual forensic evaluations, however, requires further validation, as discussed below.