Rett syndrome is a neurodevelopmental disorder caused by an X-linked mutation of the MeCP2 gene. Individuals with Rett syndrome, as well as rodent models of this disorder, demonstrate abnormal cortical responses to sound, which impair auditory discrimination ability. Vagus nerve stimulation (VNS) paired with tones has been shown to drive robust changes in the auditory cortex physiology of Mecp2+/- rats and has the potential to improve the communication abilities of individuals with Rett syndrome. The aim of this study was to describe the proteomic differences present in the auditory cortex of the Mecp2+/- rat model of Rett syndrome, as well as the molecular effect of VNS paired with tones. This study used global proteomic analysis of auditory cortex tissue taken from Mecp2+/- rats exposed to VNS paired with tones compared to untreated Mecp2+/- rats and wild-type (WT) littermate controls with no VNS exposure. Our results demonstrate dysregulation of mitochondrial and synaptic proteins in the Mecp2+/- rat auditory cortex. In addition, we show that VNS-tone pairing induces significant alterations to the auditory cortex proteome of Mecp2+/- rats by changing the expression of proteins involved in regulating synaptic vesicles and synaptic transmission. This work provides evidence of key mechanisms that may drive auditory processing dysfunction in Rett syndrome and demonstrates that VNS-tone pairing is sufficient to alter protein expression in the auditory cortex.

Atypical neural synchronization in the temporal gyrus during face processing in children with autism spectrum disorder.

Distinct cross-modal coupling between the written and auditory language networks during reading and spoken word processing.

How (not) to study deviance sensitivity and predictive coding in auditory cortex.

Dynamics of intra- and inter-regional activities of the auditory 'Where' pathway during sound localization: An fMRI study.

Congenital unilateral conductive hearing impairment alters auditory white matter tract connections of the brain. Unilateral conductive hearing loss has negative effects on speech perception in noise and sound localization ability. This study examines auditory white matter tracts in a rat model with surgically induced unilateral ear canal atresia, compared with controls. Twelve-month euthanized rats, 7 with left-sided surgically created ear canal atresia (UCA) and 4 controls, were scanned in a 9.4 T MRI scanner for animal research purposes. Diffusion-weighted images were acquired. Two different methods for probabilistic fiber tracking were used. Fractional anisotropy (FA) was calculated from whole brains and from tracts between defined auditory regions of interest. Both methods of fiber tracking show significantly higher global FA in rats with UCA. Within-group comparisons in UCA show higher FA on the hearing side between the cochlear nucleus and inferior colliculus, compared with the side of hearing loss, while in controls, there was no asymmetry. Lower FA was also found between the medial geniculate complex and the auditory cortex on the left side than on the right in UCA, in contrast to controls, where there was no difference between the hemispheres. The asymmetry found in UCA indicates alterations of auditory white matter tracts as a response to asymmetric hearing, partly confirming previous findings in experiments on ferrets.

Rapid sequential activation from A1 to V1 in congenitally blind and sighted subjects.

A glimpse into the expert lexicon: Behavioural evidence from Aviation English.

Cortical reorganization and listening effort in sound localization with left- vs. right-sided deafness.

Auditory brainstem response abnormalities in autism spectrum disorder: A deep learning approach to characterize time-frequency signatures.

Though schizophrenia is associated with disturbances in processing auditory and visual stimuli, it is unclear whether these anomalies reflect a shared abnormality in neural functions or modality-specific sensory impairments. It is also unclear to what degree these anomalies are associated with psychotic symptomatology or genetic risk for schizophrenia. We examined electrophysiological responses during auditory and visual target-detection tasks in probands with schizophrenia (SCZ, n = 107) and bipolar disorder (n = 62), first-degree biological relatives of SCZ (n = 62), and controls (n = 85). Principal components analyses of event-related potentials (ERPs) were used to evaluate (a) the covariation of ERPs across sensory modalities, (b) relationships with clinical and cognitive symptoms, and (c) associations with polygenic risk for schizophrenia. The covariance structure among ERPs for auditory and visual stimuli in controls revealed early, midlatency, and late components that were associated across sensory modalities. In SCZ, this covariation was disrupted with only midlatency components consistently covarying across modalities. SCZ also showed reduced ERP amplitudes across stages of visual processing and in late auditory processing. Reduced early and midlatency visual ERP components were associated with psychotic symptoms and polygenic risk, whereas reduced late auditory components were associated with lower cognitive performance. Neural responses reflecting separable stages of processing sensory stimuli covary across visual and auditory modalities. In schizophrenia, early sensory and late neural responses are independently disrupted within auditory and visual modalities, whereas reductions in midlatency neural responses are shared across modalities. Targeting midlatency neural responses may be advantageous in generalizing beneficial treatment effects across sensory modalities. (PsycInfo Database Record (c) 2026 APA, all rights reserved).

Temporal dynamics of contextual processing in the inferior colliculus of a rat model of autism: Sex- and age-dependent trajectories.

Clinical care for patients who report substantial hearing difficulties despite having little or no hearing loss is a topic of great debate within and beyond audiology. Building on our previous retrospective review of veterans evaluated for auditory processing disorders across the Veterans Health Administration (VHA), the current work presents five such case studies. The goal is to work toward improved patient care by providing a more in-depth view highlighting both strengths and weaknesses of approaches to care for veterans whose hearing difficulties are not explained by hearing loss. Five case studies were selected for review with the goal of identifying individuals with a wide range of etiologies and experiences receiving care for auditory complaints across the VHA. All information provided is taken directly from chart notes available from VHA and Defense Health Agency sources. Etiologies included traumatic brain injury, jet fuel exposure, and nonspecific origins. Some patients experienced well-coordinated care across medical departments, while others experienced repeated barriers and high burdens of self-advocacy while trying to navigate the health care system. Furthermore, differences in the approach of audiologists and speech-language pathologists are highlighted, including differing emphasis on diagnostic tests versus self-report measures and use of top-down versus bottom-up rehabilitation tools. This work highlights several options likely to improve care for veterans with auditory processing deficits, including greater emphasis on addressing patient-specific needs and goals, improved communication and collaboration between audiology and other medical disciplines, and the potential role for auditory device-based rehabilitation options, even among patients with minimal hearing loss.

The parsing of sensory information into discrete topographic domains is a fundamental principle of sensory processing. In the auditory cortex, these domains evolve during a stimulus, with the onset and offset of tones evoking distinct spatial patterns of neural activity. However, it is not known where in the auditory system this spatial segregation occurs or how these dynamics are affected by hearing loss. Using widefield single photon neuronal Ca2+ imaging in the inferior colliculus (IC) of awake mice, we found that pure tone stimuli elicited both spatially constrained neural activity within isofrequency bands and simultaneous sideband suppression. At cessation of the stimulus, offset responses emerged within the region of sideband suppression, demonstrating that simple stimuli elicit spatiotemporally distinct neural activity patterns to represent the presence of sound and sound termination. Because sound frequency is spatially encoded in the IC, this spatial shift creates a tonotopically distinct offset (tdOFF) response relative to sound onset. High-resolution two-photon Ca2+ imaging confirmed that tdOFF neuron activity in the sideband region was suppressed during sound and elevated above baseline after stimulus termination, raising the possibility that rebound excitation could contribute to this post-stimulus activation. Loud noise exposure - a common model of hearing loss - abolished both sideband suppression and tdOFF responses. These results show that hearing loss profoundly reshapes the spatiotemporal pattern of sound processing by altering sideband activity. This preferential loss of sideband suppression and tdOFF activation after sound-induced injury in the auditory midbrain may contribute to hyperacusis and tinnitus by promoting neuronal hyperactivity. KEY POINTS: Sensory systems encode different features of stimuli by activating distinct neural networks. Sound onsets and offsets elicit distinct neural patterns in the auditory cortex, although it is unclear where this separation originates or how it may change with hearing loss. Using in vivo widefield Ca2+ imaging in awake mice, we find that pure tone stimuli evoke spatiotemporally distinct on and off patterns of neural activity in the auditory midbrain. Neurons active during stimulus offset were suppressed by sound in sideband regions, raising the possibility that rebound excitation may contribute to this post-stimulus activation. Both sideband suppression and off responses were preferentially abolished following noise-induced hearing loss, raising the possibility that these changes may contribute to hearing loss-related syndromes such as tinnitus and hyperacusis.

Hypnosis Reduces Decoding Accuracy of Visual and Auditory Representations.

During the first period of life, human infants rapidly and effortlessly acquire the languages they are exposed to. Although memory is central to this process, the nature of early verbal memory systems, and the factors that determine retention and forgetting, remain largely unknown. Behavioral and brain measures have demonstrated memory formation in newborns. However, word traces fade in the face of acoustic overlap, leading to interference and forgetting. Here, we investigate whether speakers' identity changes facilitate the separation into distinct acoustic episodes and the creation of non-overlapping verbal memories. Newborns (0-4 days-old) were tested in a familiarization-interference-test protocol, while neural cortical activity was recorded using functional Near-Infrared Spectroscopy (fNIRS). The results showed higher neural activation to novel words than to familiar ones during the test phase, indicating that the infants recognized the familiar words despite potentially interfering sounds. The recognition response was measured over the left inferior frontal gyrus (IFG) and superior temporal gyrus (STG) areas known to be crucial for encoding auditory information and language processing. The neural response also included the right IFG and STG, involved in interpreting vocal social cues and speaker recognition. The results indicate that speaker identity is a key feature in the formation of verbal memories from birth, facilitating separability, possibly through early source-content binding (i.e. what-who), a precursor to fully mature episodic memory.

Adaptation to stimulus duration causes a repulsive aftereffect on the perceived duration of subsequent stimuli. Most studies investigating duration adaptation have found that the effect is confined to the adapted modality, highlighting unimodal components of duration processing. Here, we use adaptation to test whether motor and auditory duration processing rely on partially shared neural mechanisms by looking for a transfer of the duration aftereffect between these modalities. We asked participants to estimate the perceived duration of auditory stimuli following auditory or motor adaptation. While we replicated the unimodal effects of auditory adaptation, we report that motor adaptation did not produce the typical repulsive aftereffect. We interpret this result as evidence that duration processing by the motor and auditory systems is based on independent mechanisms.

Inner speech and the neurobiology of psychosis.

The forward modeling of electroencephalogram (EEG) plays a crucial role in solving source localization and, consequently, in the detection of EEG connectivity networks in the rat brain. We investigated the impact of skull tissue properties-inhomogeneities, anisotropy, and thickness-on measured skull potentials. Five cuboid head phantoms with identical geometry, differing in skull material parameters, and a realistic head phantom with varying skull anisotropy ratios were tested. Simulations were verified by four electromagnetic solvers and an EEG measurement on a physical phantom. The cuboid phantom with sutures yields similar electric potentials as the isotropic one, but noticeable differences appear at electrodes near sutures, particularly in real brain sensing of somatosensory, motor, and visual cortices, as well as the retrosplenial dysgranular cortex, for a dipole located close to the surface. Skull thickness reduces potentials at the top electrodes but increases them at side electrodes, in real brain sensing somatosensory, auditory, association, and entorhinal cortices. Skull anisotropy alters electric potentials with differences up to 60% for dipoles near electrodes at the limiting anisotropy ratio of 10:1, and its effect decreases with increasing distance. Varying anisotropy ratios (10:1 to 1.3:1) show that nearby dipoles are the most affected, while the impact is reduced for lower, more realistic ratios (1.3:1 to 1.8:1) and for more distant sources. This trend was consistently observed in realistic head phantoms as well. Tangential dipoles are most strongly affected in the vicinity of the electrodes and gradually become radial at more distant positions near the inner skull surface.

Hearing impairment has emerged as a consistently associated and potentially modifiable risk factor for cognitive decline and dementia, including Alzheimer's disease (AD). Epidemiological studies demonstrate an increased dementia risk among individuals with hearing loss, with evidence of dose-response relationships across levels of auditory decline. Despite the robustness of this association, the mechanisms linking auditory dysfunction to cognitive deterioration remain multifactorial and incompletely understood. Current evidence points to several interacting pathways, including sensory deprivation and cortical reorganization, increased cognitive load during effortful listening, psychosocial consequences such as social isolation and depression, and potentially overlapping neurobiological processes. Emerging research further suggests that central auditory processing deficits may represent early functional markers of cortical vulnerability associated with neurodegeneration. Clinically, these insights emphasize the importance of routine hearing assessment in older adults and highlight observational evidence indicating that hearing rehabilitation, particularly hearing aid use, may be associated with more favorable cognitive outcomes, although causal effects have yet to be established. By integrating biological, cognitive, and psychosocial perspectives while explicitly addressing persistent uncertainties, this critical narrative review provides a balanced framework for interpreting the relationship between hearing impairment and AD and discusses its implications for prevention and clinical practice. Overall, hearing loss should be regarded as a robustly associated and potentially modifiable marker of dementia risk rather than a confirmed causal determinant. From a neurological standpoint, central auditory dysfunction may therefore reflect underlying brain vulnerability in aging rather than act as a direct causal driver of Alzheimer's disease.