Developmental language disorder is characterized by difficulties in auditory processing and prosody perception. Estonian word prosody features a unique three-way quantity distinction, characterized by changes in syllable duration and pitch contour, which differentiate word meaning and grammatical cases. We investigated auditory discrimination in 50 children (25 with developmental language disorder), aged 4-7 years, using the event-related potential Mismatch Response and behavioral tasks longitudinally at two assessment points. Here, we specifically focus on the results of the second assessment and compared these results with those reported previously (Themas et al., 2025a) In the duration change condition, we observed a shift from a positive at mean age of 5;8 years to a negative Mismatch Response at mean age of 6;8 years, which was less pronounced in the developmental language disorder group compared to their typically developing peers. Interestingly, we found a significant negative association between the change of the Mismatch Response amplitude and behavioral discrimination, suggesting a stronger change from positive to a more negative Mismatch Response to be associated with better behavioral discrimination performance for both groups. In the duration and pitch change condition, no Mismatch Response was observed in either group at the first or second assessment. This study sheds light on the maturation of auditory change detection processes and deepens our understanding of the interplay between neurophysiological and behavioral indicators in children with and without language impairments.

Increasing research efforts in recent years and new approaches in clinical studies provided significant insights into the pathophysiology of freezing of gait (FOG). However, the study of causative mechanisms for complex gait disorders typically needs refined in-vivo models, which are still lacking for FOG. The characteristics of FOG pose major difficulties not only for reproduction in animals with different types of gaits, but also for assessment of such episodic behavior in the animal environment. In this review, we examine the currently available animal models of FOG and FOG-like phenomena for their validity and applicability and present a prospective view of modeling based on novel technologies to manipulate integrated mechanisms.

Freezing of gait (FOG) is a disabling motor symptom in Parkinson’s disease (PD) with substantial impact on mobility and quality of life. Anxiety is frequently implicated in triggering or worsening FOG, yet the lived experience of this interaction remains poorly understood. This study explored the experience of anxiety related to FOG in people with PD, aiming to better understand how and why anxiety surrounding FOG develops and how it impacts the lives of individuals with PD. A thematic analysis was conducted using semi-structured interviews with 12 individuals with PD who reported daily FOG episodes influenced by anxiety or stress. Interviews were transcribed verbatim and analyzed iteratively to identify patterns of meaning. Five overarching themes emerged. First, participants described how anxiety was linked to a gradual loss of confidence in their walking abilities, driven by perceived loss of control, unpredictability of FOG, and feelings of vulnerability. Second, promoting confidence was mentioned to reduce anxiety, either through having a compensatory strategy available in case of a freezing episode, or through contextual factors (e.g. being in the dopaminergic ON-state). Third, anxiety typically developed gradually alongside the progression of FOG and the concomitant decline in confidence during walking, but could also intensify following negative events, such as falls. Fourth, anxiety was reported to divert attentional resources toward potential threats and make it more difficult to focus on strategies for managing FOG. Finally, many participants engaged in avoidance behaviors, causing negative downstream effects such as limiting social participation and physical activity. These findings highlight the importance of early recognition, as well as the potential for interventions that enhance confidence to help reduce anxiety surrounding FOG.

Since the early 1990s, mismatch negativity (MMN) has been widely used to investigate sensory memory traces and predictive processing of musically relevant acoustic features, including timbre, relational pitch, and rhythm. Evidence consistently demonstrates that the human brain possesses innate musical abilities, which can be further refined through training. The interplay between innate predispositions and experience is supported by robust associations between MMN parameters and behavioral listening skills in both musically trained and untrained children and adults. These findings align with the interpretation of MMN as a prediction-error signal reflecting the precision of internal predictive models: MMN amplitudes decrease with increasing contextual complexity and show more frontal scalp distributions in musicians. As stimulation paradigms have become increasingly ecologically valid, distinguishing low-level sensory prediction errors indexed by MMN from higher-level frontal prediction errors has grown more challenging, supporting an integrative perspective in which generative models dynamically merge bottom-up sensory input with top-down priors across hierarchical levels of the central nervous system. In this review, we summarize evidence for a “musical intelligence” of the automatic MMN mechanism, highlighting its role within widespread cortical predictive coding processes.

Astrocytic ensembles as key cellular mediators of memory stabilizationJiahui Chen1,*1 College of Pharmaceutical Sciences, Zhejiang University, 310058, Hangzhou, Zhejiang, China.*Correspondence to: Jiahui Chen: tankahui@zju.edu.cn.For long, memory research has centered on the view that neuronal engrams store and retrieve memories 1,2. Extensive evidence demonstrates how perturbation of engram influences mnemonic processes, such as encoding, storage, retrieval and extinction3,4. Once recalled, memories become malleable and susceptible to distortion. This inherent fragility necessitates memory stabilization. Earlier evidence demonstrates neuron-astrocyte convergence in long-term memory consolidation 5, implying that engrams represent only part of the multicellular landscape. A recent study led by Prof. Nagai et al . underpinned that astrocytic ensembles are indispensable contributors for memory stabilization during recall 6.To identify behaviorally relevant astrocyte ensembles (BAEs), the authors employed a contextual fear conditioning (FC) paradigm and developed a sophisticated genetic imaging strategy for whole-brain BAEs tagging. This method revealed a systemically substantial increase in BAEs after fear recall (FR), particularly in the lateral and basolateral part of amygdala (LA/B), a canonical structure in fear memory. Notably, the activity of these epoch-specific BAEs aligns with neuronal Fos expression. To dissect the molecular architecture behind, researchers first uncovered that FR induced noradrenaline(NA)-driven cAMP signaling in astrocytes. Then, pharmacological perturbation of the NA-expressing area—locus coeruleus (LC)-LA/B circuit would trivially impede the phenomenon. In-vivo recordings gave evidence of fear-induced NA signals, which in turn elicited prolonged astrocytic cAMP signals through β-receptors during recall. Hitherto, FR induces a sustained increase in NA signals and recruits specific astrocytic ensembles, which left a central unresolved issue: Why are astrocytes specifically engaged during FR, not FC? They identified two critical adrenoreceptor genes, namelyAdra1a (α1-receptor) and Adrb1 (β1-receptor), with the latter gene remained elevated from 1.5 h to 3 days post-FC. In addition, upregulation of Adrb1 promoted Igfbp2 gene expression, which encodes a secreted protein essential for synaptic plasticity. Lastly, Adrb1 -OE did not affect FR-engram density, but significantly facilitated their reactivation, implying that BAEs play an important role in neuron-induced memory retrieval process.In summary, Prof. Nagai provides compelling evidence that astrocytes operate on behaviorally relevant delayed timescale than neurons in across-day memory stabilization process (Figure-1 ). Following FC, astrocytes shift from rapid cAMP responses to a delayed activation pattern through distinct transcriptional states marked by Adrb1 upregulation. This prime state heightens astrocytic responsiveness during subsequent recall, driving Fos and Igfbp2 expressions to stabilize memory. Importantly, perturbing astrocytic ensembles selectively interfere with subsequent but not initial FR, distinguishing astrocytes from typical neuronal engrams. Rather than being a passive support role, astrocytes provide a slow, permissive modulatory trace that may complement fast neuronal activity and preserve memory integrity over extended timescales. Alternatively, this study also holds significant promises for the advancement of artificial intelligence, particularly in neuromorphic computing, which mimics artificial neural networks 7. Current computational architectures may neglect the indispensable role of astrocytes in valence selection and neuronal dynamics modulation. A deeper understanding of neuron-astrocyte circuity model may unlock the potential in designing efficient biologically grounded logic algorithms and eliminating neural redundancy in artificial networks.Methodologically, this work advances an effective brain-wide Fos-based tagging strategy that leverages experience-dependent astrocytic transcriptional states, which directly overcomes long-standing challenges posed by astrocyte heterogeneity and bulk perturbation strategies, enabling functional mapping of astrocyte-relevant circuits. Beyond these immediate applications, the study carries profound broader implications. It challenges the conventional neuron-centric engram concept by positioning astrocytes as active mediators in memory stabilization. Furthermore, it provides a mechanistic template for how salient experiences are prioritized through cellular priming followed by NA-driven neuron-astrocyte convergence. Looking forward, several key avenues merge. First, earlier spatial transcriptomic work indicates thatIgfbp2 is likely one of several astrocytic genes involved in long‑term memory5. Future studies should define a broader molecular repertoire. Second, extending these analyses to other mnemonic stages, such as extinction or retrieval of memory at longer intervals (e.g.,7, 14, or 28 days), will clarify whether astrocytic ensembles or other cellular substrates contribute to long-term memory maintenance and fully elucidate neuron-astrocyte synergy. Third, this field has primarily focused on negative valence, leaving the astrocytic mechanisms underlying positive events, such as reward, comparatively less explored. Fourth, applying these methodologies to animal models of other neuropsychiatric disorders, including depression, stroke or epilepsy could yield novel astrocytic-centric pathophysiological insights. Lastly, while current findings are established under laboratory settings, extending this work into pathological conditions will be crucial for translating mechanistic insights into therapeutic relevance.Collectively, these findings provide strong evidence that deciphering the biochemical profiles of astrocyte-BAEs induced by salient experiences to include a glial modulatory aspect that extends timescales and shapes circuit stability. Thus, this could open new avenues targeting NA-astrocyte system for the treatment of neuropsychiatric disorders such as Alzheimer’s disease and post-traumatic stress disorder.

Interactional context is increasingly recognized as a key modulator of neural activity, yet its influence on sensorimotor dynamics is often examined using static or categorical contrasts. Here, we investigated whether and how interactional context systematically shapes the temporal organization of sensorimotor neural activity when the overt motor act is held constant. Using a scalable experimental design based on a rock–paper–scissors task, we examined mu (8–13 Hz), beta (13–30 Hz), and a composite mu+beta (8–30 Hz) event-related desynchronization/synchronization (ERD/ERS) signals across four interactional contexts, ranging from no interaction to real-time hyperscanning. Time-resolved generalized additive models (GAMs) were applied at the single-trial level to characterize non-linear, non-stationary context effects aligned to a shared motor event (button press).Across all frequency bands, sensorimotor ERD/ERS trajectories diverged across contexts in structured and temporally specific ways. Context-related modulation was most robust in the post-action interval, unfolding across early, mid, and late phases of the response rather than as static amplitude differences. Mu- and beta-band dynamics exhibited complementary temporal sensitivities, while the composite signal emphasized post-action patterns shared across rhythms and preserved a graded ordering of contexts. Importantly, contrasts involving hyperscanning did not reveal qualitatively distinct dynamics, but rather amplified and extended patterns already present in simpler interactional contexts.Together, these findings support a continuity-based view in which hyperscanning constitutes the upper bound of a scalable interactional continuum rather than a methodological exception. Methodologically, the results highlight the value of time-resolved modeling approaches for bridging traditional single-brain paradigms and real-world social interaction, and theoretically, they reinforce accounts of sensorimotor cognition as dynamically organized by interactional context over time.

Anhedonia is a debilitating facet of major depressive disorder (MDD) linked to worse treatment outcomes. To investigate anhedonia-related alteration, an adaptation of the widely used gPPI toolbox was developed, which allows modelling of whole-brain functional connectivity between an unlimited number of regions. Using this network-gppi toolbox, connectivities between all 246 regions of the Brainnetome atlas were estimated for the fMRI data of 99 patients with MDD and 28 healthy controls acquired during a monetary incentive delay task. Resulting components, i.e., interlinked structures of thresholded connections ( p < .001), were statistically evaluated using network-based statistic (NBS). For reward consumption, both groups did not differ significantly ( pNBS = .082). However, the comparison with a subset of 54 anhedonic patients was significant ( pNBS = .017). Interestingly, anhedonic patients were found to have increased connectivities between the left lateral orbitofrontal cortex and multiple regions of the dorsal striatum, potentially indicating a more negative evaluation of the gained rewards. A trend was observed for the correlation between reward consumption connectivities and an anhedonic subscale of the Beck Depression Inventory-II (p NBS = .068). Most noteworthy, symptoms correlated positively with stronger connectivities between the caudate and dorsomedial prefrontal cortex. Given the role of the latter in rumination, this could possibly reflect an increased impact of negative self-related cognitions. Similar analyses for reward anticipation connectivities were not significant. Overall, the results could indicate that anhedonic patients might devaluate winning trials, so they are not too incongruent with existing negative self-related beliefs.

Fibromyalgia involves widespread musculoskeletal pain and hypersensitivity, often accompanied by neurological, cognitive, and affective disturbances. Resting-state electroencephalography studies have revealed abnormal brain activity in chronic pain conditions, with anxiety and symptom duration potentially exacerbating these alterations. This study applied multivariate pattern analysis to differentiate resting-state electroencephalography signals between fibromyalgia patients and healthy controls across frequency bands associated with pain processing, incorporating state and trait anxiety scores. It also examined differences between patients with short and long duration symptoms and identified the most relevant scalp regions contributing to the models. Fifty-one female participants (25 fibromyalgia patients, 26 controls; aged 35-65) were included. Patients were classified into short-term (12) and long-term (13) groups. Normalized power spectral density values were extracted from electroencephalography data and used to train machine learning classifiers, with Haufe-transformed weights computed to determine key scalp contributions. The models distinguished patients from controls with accuracies exceeding 0.70 across all frequency bands, reaching 0.99 in beta and gamma bands when anxiety was included. Symptom duration was also a relevant factor, as the model differentiated short- from long-term fibromyalgia patients with accuracies up to 0.96 in beta and gamma bands. Alterations in theta power within frontal and parietal regions, along with frequency-specific contributions, highlight disrupted pain processing in fibromyalgia and suggest cumulative effects of prolonged symptom duration. Resting-state combined with multivariate pattern analysis may support the development of biomarkers to improve diagnosis and guide treatment strategies in clinical settings.

Freezing of gait (FOG) is a common and disabling symptom in people with Parkinson’s Disease (PD), characterized by paroxysmal episodes where there is an inability to step effectively, despite attempting to do so. Anxiety and stress exacerbate FOG, particularly in situations where people with FOG anticipate not being in control of their movements. Some people with PD use compensatory strategies that target anxiety and stress to improve FOG. However, tailored strategies to ameliorate anxiety- and stress-related FOG have never been evaluated in a systematic manner. TACKLING-FOG aims to evaluate the effectiveness of a novel 4-week Managing-the-Mental-State-intervention in reducing FOG-related anxiety and stress, in order to improve FOG. We also aim to identify the key determinants influencing the response to the intervention. This study is a randomized controlled trial (RCT) with a waitlist control group. Forty participants with PD who experience anxiety- or stress-related FOG will be included. All participants receive a baseline measurement and are subsequently randomized to the intervention or control group in a 1:1 ratio. The intervention group immediately receives 4 weekly sessions of the Managing-the-Mental-State-intervention, whereas the control group enters a waitlist period. Afterwards, both groups are reassessed. Next, the intervention group enters a 10-week follow-up period, while the control group receives the intervention, is re-assessed, and enters the follow-up period. Both groups receive a final measurement at the end of the follow-up. The primary outcome is the percentage of time frozen during a home-based walking course that includes self-selected FOG ‘hotspots’. Secondary outcomes involve the percentage of time frozen during the same trajectory under elevated-stress conditions and during a standardized FOG-provoking protocol. Additionally, heart rate is collected as a physiological marker of stress and anxiety, and questionnaires are administered to assess domains that may improve in response to the intervention, including anxiety, quality of life, and self-esteem. TACKLING-FOG will be the first RCT to examine the use of tailor-made behavioral strategies to tackle anxiety- and stress-related FOG in people with PD.

The PET radiotracer [ 15O]H 2O is the reference standard for quantifying myocardial blood flow and cerebral blood flow. However, the requirement for an invasive arterial input function limits clinical applicability. An alternative, non-invasive image-derived input function from the left ventricle has been validated for the heart, and recent work has shown that the image-derived input function obtained in an additional scan of the heart can be applied for the brain at rest and during acetazolamide-induced vasodilation. To further establish its clinical and research utility, we investigated the intra-individual day-to-day variability. Eight healthy participants underwent [ 15O]H 2O PET to assess cerebral blood flow on 2 occasions within 14 days using an image-derived input function placed in the left ventricle of the heart at rest. Day-to-day variability was assessed with Bland-Altman Plots, correlation coefficients, and Coefficient of Variation across three larger and three smaller brain regions. Day 1 and Day 2 measurements showed strong linear associations at rest (r = 0.75–0.85), during stress (r = 0.78–0.86) and for perfusion capacity (r = 0.75–0.82). Limits of agreement ranged from -0.096 to 0.121 mL/(g·min) at rest, -0.164 to 0.164 mL/(g·min) during stress and -0.255 to 0.189 mL/(g·min) for perfusion capacity. Coefficient of variation ranged from 11.9% to 12.6% at rest, 12.3% to 12.9% during stress and 7.8% to 8.2% for perfusion capacity. This non-invasive method is reproducible on a group level with coefficients of variation below 13% and is thus suitable for detecting group-level changes in intervention studies, although individual variability is substantial.

Freezing of gait (FOG) is a burdensome Parkinson’s disease (PD) symptom. Gait control in people with PD relies on compensation from cognitive, sensory, and limbic networks. Their integration is influenced by the noradrenergic ascending arousal system, modulated by the locus coeruleus. In PD, locus coeruleus degeneration has been linked to increased FOG severity. Atomoxetine, a selective noradrenaline reuptake inhibitor, may provide a novel therapeutic approach for FOG. However, to date, studies on atomoxetine’s effect on FOG have been underpowered and inconsistent. This study will evaluate the effects of atomoxetine on FOG severity, both in the dopaminergic OFF- and ON-states. Moreover, we will assess its mode of action by examining its influence on brain network topology. Additionally, we will examine clinical and imaging markers to predict an individual’s treatment response. Sixty patients with frequent FOG will be recruited for a multi-centre, single-dose, double-blind, placebo-controlled, cross-over clinical trial. Assessments include clinimetrics, MDS-UPDRS III, gait assessments, pupillometry, and neuroimaging, conducted in the dopaminergic OFF- and ON-states. The primary outcome is FOG severity in the dopaminergic OFF-state, quantified based on the percentage of time spent frozen during gait assessments. Resting-state fMRI is conducted to assess network integration and segregation across brain regions and task-fMRI for revealing neural circuitry changes during FOG. Lastly, locus coeruleus and substantia nigra integrity will be assessed using structural MRI. This study will provide insights into the role of the noradrenergic ascending arousal system and potentially identify a novel pharmaceutical treatment pipeline for FOG in PD.

Autism spectrum disorder (ASD) is a highly heritable neurodevelopmental condition with a well-characterised genetic architecture, yet how ASD-associated genes map onto discrete brain regions remains poorly understood. This study applied a recently validated analysis pipeline (ATLANTE) to discover regions of the human brain enriched for high expression of 234 high-confidence ASD-associated genes. 11 discrete brain regions were identified, spanning cortical, limbic, and cerebellar systems including: the anterior orbitofrontal gyrus, cerebellar cortex, flocculonodular lobe, vermis, posterior cingulate cortex, temporo-occipital transitional zone, hippocampal subfields CA1 and CA3, postcentral gyrus, occipital cortex, and perirhinal gyrus. Notably, the anterior orbitofrontal gyrus exhibited significant enrichment for syndromic ASD genes, suggesting a core role in the neuropsychiatric features of syndromic presentations. Network and community clustering analyses revealed three major gene communities corresponding to distinct biological processes: synaptic dysfunction in limbic regions, histone modification in cerebellar regions, and axonal ion channel regulation in cortical regions. Nodal analysis identified 8 high-priority genes with broad relevance across multiple brain regions, including NR3C2, GABRB2, and NBEA. These findings provide a refined neuroanatomical framework for ASD pathophysiology, identify understudied brain regional targets, and imply that ASD-associated genes exert primary effects in specific brain regions.

The ability to detect unexpected sounds within regular acoustic patterns is fundamental to adaptive behavior. This capacity is reflected in the mismatch negativity (MMN) event-related potential and has been extensively studied in humans and animal models. Surprisingly, single-unit recordings during auditory deviance detection in humans remain exceptionally rare. Here, we characterized single-unit responses to auditory deviants in frequency, space, intensity, and time dimensions, using the Optimum-1 multi-feature oddball paradigm during unattended listening. Microwire recordings from 13 patients with drug-resistant epilepsy yielded units from amygdala (n=40), hippocampus (n=52), Heschl’s gyrus (n=2), anterior insula (n=2), and posterior insula (n=2). Amygdala showed multi-phase responses, with timing deviants eliciting the strongest and earliest effects: suppression around 60 ms followed by enhancement around 200 ms. Intensity deviants produced suppression around 300 ms. Hippocampus showed sparse engagement (0–10% of units across contrasts and epochs) with no apparent feature specificity besides a weak late frequency effect at the population level (350–400 ms). Case-level Heschl’s gyrus recordings revealed functional heterogeneity, with responses ranging from early gap-specific to late multi-feature activity. Case-level anterior insula units showed intensity-selective responses and late spatial processing with contralateral enhancement for location deviants. Our results revealed that the amygdala provides rapid alerting signals that precede detailed cortical analysis. On the other hand, sparse hippocampal responses suggest limited engagement in deviance detection during passive listening. Overall, these findings provide the first human single-unit characterization of multi-feature auditory deviance processing, establishing a critical baseline for understanding cellular mechanisms of predictive auditory processing.

The minimum intervention principle (MIP) in motor control suggests that feedback corrections are made only for deviations that prevent achieving task goals. While most supporting evidence derives from studies on reaching movements, this study tested this hypothesis in the context of human steering behavior. Using a self-steerable motion platform, participants (n=22) steered a vehicle along roads of different widths (narrow, medium, wide) while experiencing time-varying physical perturbations. Steering control strategies were assessed in terms of the frequency dependent gain and phase of compensatory steering for the different road widths. Participants’ task performance depended on the order in which the road widths were encountered. After transitioning from wide to narrow roads, participants increased their corrective responses, consistent with MIP. In contrast, when moving from narrow to wide roads, they carried over their existing strategy, reflecting persistence in control. This persistence was reflected in the vehicle spending less time on the narrow road than on the wide ones. In terms of frequency-dependent control strategies, road order effects appeared primarily in reduced phase rather than gain, indicating that corresponding control policy adjustments were in the relative timing of the perturbation and response. Together, these findings provide partial evidence for the minimum intervention principle in steering but also suggest that control feedback gains are tuned for robustness and stability, at the expense of optimizing the steering demands imposed by road width.

Learning disorder (LD) and developmental language disorder (DLD) are traditionally diagnosed behaviorally but show significant overlap in their higher-level manifestations. Although auditory processing deficits have been reported in both disorders, prior findings have been inconsistent. Crucially, it remains unclear whether LD and DLD can be differentiated from each other based on their neurophysiological profiles. We conducted a systematic review and meta-analyses of mismatch negativity (MMN) studies comparing children with LD (primarily dyslexia) and DLD to each other and to typically developing controls. Analyses included 22 studies (34 latency effect sizes, 104 amplitude effect sizes) with moderator examination of stimulus type, age, cortical region, and analysis time windows. While no amplitude differences emerged between LD and DLD groups, we found a significant clinical group and stimulus type interaction for latency (p = 0.02). Post-hoc analysis revealed that children with DLD showed significantly prolonged latency for speech sounds (g = 0.47), with no significant difference for non-speech stimuli. Conversely, children with LD showed significantly prolonged latency for non-speech sounds (g = 0.85), with no significant difference for speech stimuli. Although we could not directly compare LD and DLD groups due to the limited number of studies that included both clinical groups and controls, our analyses revealed that their effects relative to controls differ from each other. Future research is warranted to evaluate the influence of participant characteristics and methodological features on the auditory response measured by MMN.

Predictive coding is the theory that each level of the nervous system constructs a model of its inputs and then tests new inputs against the model. If the new inputs match the model, then no change in the model is required. If not, then extra brain processing is required to update the model. We tested the precision of such a model in the auditory system by using Shepard tones arranged into a discrete Shepard scale—a series of notes, each comprising sine tones of different amplitudes and one octave apart, and with each tone separated from the next by one semitone, yielding a scale that ascends or descends forever. We unpredictably and occasionally replaced an expected tone in the scale by one that was two thirds of a semitone less, one third of a semitone less, one third of a semitone more, or two thirds of a semitone more. We measured the electrical activity of 20 participants’ brains with 128 scalp electrodes (electroencephalography, EEG) while the tones were delivered to their ears. We found that event-related potentials (ERPs) from 180-220 ms to these unpredictable tones were more negative the farther they were from the predicted note and more negative for tones that were less than the expected note. We conclude that the predictive model for the kind of regularity in a discrete Shepard scale has a sensitivity to tones less than one third of a semitone and is more sensitive to undershoots than to overshoots.

Objective: This study examined how older and younger adults process silent gaps in auditory stimuli by recording cortical evoked potentials using a multi-deviant paradigm that is compared to a psychophysical gap-detection task. Design: Participants passively listened to pairs of noise markers separated by silent intervals. Markers were either spectrally identical (within-channel) or spectrally distinct (between-channel) narrowband noises. Seven gap durations served as deviants in a multi-deviant sequence. The deviance-related negativity (DRN) and the P2/P3a were recorded from fronto-central electrodes. Study Sample: Thirty-two subjects with normal hearing or minimal hearing loss participated in this study. They were separated into an older adult (mean age = 63 years) and younger adults (mean age = 24 years) group. Results: Gapped deviants significantly enhanced DRN amplitude in both within- and between-channel conditions. Age effects emerged in the peak-to-peak DRN-P2/P3a measure. Older adults showed a longer DRN latency compared to the younger group, but no condition effects. In contrast, the younger group had longer latencies in the between-channel condition only. P2/P3a responses did not show any condition or age-specific effects. Behavioral gap-detection thresholds did not differ across conditions in older adults. Conclusions: Overall, results demonstrate that electrophysiological indices provide a more sensitive marker of age-related auditory changes, revealing subtle neural alterations in temporal resolution that may precede behavioral decline.

Instrumental music performance is associated with enhanced perceptual processing as evidenced by auditory discrimination and speech-in-noise perception. However, little is known about the extent to which auditory perceptual processes support cognition in aging. We investigated whether music training enhances precision in perception in 26 older amateur and professional musicians (62–85 years, 13 females) and 25 older non-musicians (61–82 years, 16 females). Participants completed a novel paradigm of auditory mnemonic discrimination while electroencephalography (EEG) was recorded. The mismatch negativity (MMN), an event-related potential of change detection, was measured during a passive auditory oddball paradigm with standard and deviant pure-tone sequences differing in pitch contour. Participants subsequently completed an incidental memory test for oddball stimuli (i.e., targets) amongst similar lure sequences (matched for frequency but differing in contour) and dissimilar foil sequences (differing in frequency and contour), as well as a back-to-back perceptual discrimination task. Musicians showed enhanced amplitudes, left-lateralized source activity of the MMN, and increased memory discriminability for targets compared to lures and foils, which was not explained by perceptual discrimination ability or MMN amplitude. No group differences were found for neural or behavioural measures on a mnemonic discrimination task for visual everyday objects. Our results clarify the role of music training on precision in perception and auditory memory in older adult musicians compared to non-musicians. Our findings underscore the contribution of musical engagement to perception and memory to the development of cognitive reserve in aging.