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<title>bioRxiv Subject Collection: Neuroscience</title>
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This feed contains articles for bioRxiv Subject Collection "Neuroscience"
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<link>https://www.biorxiv.org</link>
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<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.07.12.738112v1?rss=1">
<title>
<![CDATA[
Task-specific neural mechanisms underlie biases in human orientation perception 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.07.12.738112v1?rss=1
</link>
<description><![CDATA[
Prior experience shapes both visual perception and its underlying neural circuits. This is exemplified by the oblique effect - a strong perceptual advantage for cardinal (horizontal/vertical) over oblique orientations - which reflects how the brain adapts to statistical regularities in the natural environment. It remains unclear whether such adaptations are generalised across visual cortex or are specific to circuits supporting different perceptual judgements. To investigate, we examined human performance in contrast detection and orientation discrimination, using identical stimuli for a range of spatial frequencies, paired with a biologically-inspired model of visual orientation processing. Behaviourally, a robust oblique effect emerged for orientation discrimination but was found only at higher frequencies for contrast detection. The model explained detection changes via an increased pooled response from cardinal-tuned neurons alongside spatial frequency-dependent narrowing of orientation bandwidths, consistent with known properties of cortical V1 neurons. However, the discrimination oblique effect required a different constraint, narrower orientation tuning for cardinal versus oblique neurons. No single model captured both effects simultaneously, suggesting that the oblique effect results from task-specific mechanisms. More broadly, these findings demonstrate how, rather than relying on a fixed strategy, the brain employs flexible computational strategies to optimise sensory encoding for specific tasks.
]]></description>
<dc:creator><![CDATA[ Leadbeater, R., Ledgeway, T., McGraw, P. ]]></dc:creator>
<dc:date>2026-07-17</dc:date>
<dc:identifier>doi:10.64898/2026.07.12.738112</dc:identifier>
<dc:title><![CDATA[Task-specific neural mechanisms underlie biases in human orientation perception]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-07-17</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.07.12.738085v1?rss=1">
<title>
<![CDATA[
An Integrated EEG, TMS-EEG and Behavioural Dataset for Investigating the Neural Correlates of Working Memory 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.07.12.738085v1?rss=1
</link>
<description><![CDATA[
Working memory is a fundamental process that underlies cognition. Accordingly, the neural mechanisms that support working memory performance are of great interest in cognitive neuroscience. We present a publicly accessible dataset comprising 123 healthy adults (mean age = 28.58 years, SD = 7.56; age range = 18-46 years; 75 females) to facilitate investigation of the neural mechanisms underlying working memory performance in humans. Across two days of assessment, participants underwent a battery of cognitive tasks assessing working memory and other cognitive domains (day 1), followed by 62-channel EEG recordings (day 2). EEG data were acquired at rest, during a visual working memory task, and following single-pulse transcranial magnetic stimulation (TMS-EEG) targeting key brain regions involved in working memory. This article provides a detailed overview of the study design, methodology, and data characteristics.
]]></description>
<dc:creator><![CDATA[ Biabani, M., Fornito, A., Thompson, S., Hawi, Z., Yucel, M., Bellgrove, M. A., Rogasch, N. C. ]]></dc:creator>
<dc:date>2026-07-17</dc:date>
<dc:identifier>doi:10.64898/2026.07.12.738085</dc:identifier>
<dc:title><![CDATA[An Integrated EEG, TMS-EEG and Behavioural Dataset for Investigating the Neural Correlates of Working Memory]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-07-17</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.07.12.738100v1?rss=1">
<title>
<![CDATA[
Large-scale dimensional behavioral profiling dissociates fear memory from locomotor confounds in mice: The necessity of baseline-normalized metrics 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.07.12.738100v1?rss=1
</link>
<description><![CDATA[
Fear conditioning is widely used to assess associative memory in mice, yet percent freezing conflates memory with baseline locomotor and anxiety-related traits. A systematic survey of recent studies (2020-2025) found that fewer than 1% statistically integrate locomotor activity into freezing analyses. Here, we address this gap using a large-scale dataset of >10,000 mice across >160 comparisons, including genetic mutations, pharmacological interventions and aging, tested in 15 standardized behavioral paradigms. Conventional freezing scores covaried strongly with general locomotor activity, obscuring memory-related phenotypes. Multiple factor analysis identified two principal behavioral dimensions, locomotor activity and learning/memory: conventional freezing aligned with the locomotor dimension, whereas freezing subtraction and the activity suppression ratio mapped onto the memory dimension and improved detection of synaptic plasticity phenotypes. These analyses show that baseline locomotor normalization is essential for interpreting fear conditioning as a memory assay and provide an open framework for selecting and reporting locomotor-normalized metrics.
]]></description>
<dc:creator><![CDATA[ Sato, D. X., Chatzigiannis, M. M., Shoji, H., Sala, G., Hattori, S., Takao, K., Kinashi, T., Kishino, T., Morita, S., Hatada, I., Shinoda, Y., Hattori, K., Yagi, T., Matsumoto, A., Egawa, H., Nishihara, S., Shimizu, K., Ikegami, K., Yamada, M. K., Ageta, H., Setou, M., Tao, H., Ueno, N., Bhandari, P., Shigemoto, R., Wakatsuki, S., Araki, T., Yamanaka, A., Mukai, H., Nagaoka, T., Kishi, M., Furuya, S., Yamamoto, T., Kubo, Y., Iida, Y., Kazuki, Y., Enomoto, H., Fukasawa, M., Usuda, N., Inoue, S., Inokuchi, K., Hattori, T., Taniguchi-Ikeda, M., Toda, T., Kubo, A., Kawaai, K., Mikoshiba, K., van d ]]></dc:creator>
<dc:date>2026-07-17</dc:date>
<dc:identifier>doi:10.64898/2026.07.12.738100</dc:identifier>
<dc:title><![CDATA[Large-scale dimensional behavioral profiling dissociates fear memory from locomotor confounds in mice: The necessity of baseline-normalized metrics]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-07-17</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.07.13.732468v1?rss=1">
<title>
<![CDATA[
Aquaporin-4 mislocalization from astrocyte endfeet prolongs survival in a prion-cerebral amyloid angiopathy model 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.07.13.732468v1?rss=1
</link>
<description><![CDATA[
Aquaporin 4 (AQP4) water channels are polarized to astrocytic endfeet at blood vessel interfaces, and lose polarity in vascular diseases, including stroke, chronic traumatic encephalopathy, and Alzheimer's disease. AQP4 modulates water influx and efflux in the interstitial fluid, yet how AQP4 localization impacts cerebral amyloid angiopathy (CAA) remains poorly understood. Here, we show that astrocytic end feet and AQP4 are displaced from amyloid-bearing vessels in a prion-CAA mouse model that expresses GPI-anchorless PrPC. Displacing AQP4 genetically through deleting alpha-syntrophin (Snta1-/-) led to a marked prolongation in survival, together with reduced microglial inflammation and C1q, in prion-CAA-affected mice. Additionally, synaptic structural proteins were better maintained. Finally, the level and distribution of prion aggregates were similar among the mice, indicating that prion conversion and spread were not affected. These results suggest that reducing AQP4 water channel function slows the decline in a vascular amyloid disease by reducing neuroinflammation.
]]></description>
<dc:creator><![CDATA[ Flores, S., Wilpitz, A., Ojeda-Juarez, D., Wang, J., Danque, G., Sumowski, P., Funk, G., Malik, A., Pizzo, D. P., Richards, E., Iliff, J. J., Sigurdson, C. J. ]]></dc:creator>
<dc:date>2026-07-17</dc:date>
<dc:identifier>doi:10.64898/2026.07.13.732468</dc:identifier>
<dc:title><![CDATA[Aquaporin-4 mislocalization from astrocyte endfeet prolongs survival in a prion-cerebral amyloid angiopathy model]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-07-17</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.07.12.738103v1?rss=1">
<title>
<![CDATA[
Turning an object into a scene: buildings activate scene-selective visual cortex independently of visual features 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.07.12.738103v1?rss=1
</link>
<description><![CDATA[
Human visual cortex contains regions that selectively respond to both scenes and large objects, particularly buildings. The cortical overlap between buildings and scenes has been attributed to shared visual features (e.g., cardinal orientations, rectilinearity). Alternative accounts propose that buildings may also activate scene representations indirectly, independently of specific visual features, for example because buildings evoke a sense of space. Here, we tested for such feature-independent activation by comparing EEG and fMRI responses in human participants (both sexes) to buildings and visually-matched boxes, and relating these responses to scene-selective responses. Buildings and boxes were matched, across exemplars, using image-based metrics, deep neural networks, and a perceptual similarity task. Time-resolved EEG decoding showed that buildings and boxes evoked discriminable responses from 360ms post-stimulus onset, incompatible with feedforward visual feature processing. Importantly, the building-box classifier generalized to discriminate scenes from chairs, providing EEG evidence for a representational overlap between buildings and scenes. Temporal generalization analyses further showed that the late building-selective response corresponded to an earlier scene-selective response, with a temporal offset of ~130ms. Finally, ultra-fast fMRI (TR=140ms) revealed that these findings were mirrored in the response of the scene-selective parahippocampal place area (PPA), which similarly showed a feature-independent building-selective response that was delayed and prolonged relative to the scene-selective response. These results clarify the nature of building selectivity in visual cortex by showing that this selectivity can arise independently of visual features, putatively reflecting associative processes between buildings and scenes (or space).
]]></description>
<dc:creator><![CDATA[ Zhao, Y., Hagen, S., Peelen, M. V. ]]></dc:creator>
<dc:date>2026-07-17</dc:date>
<dc:identifier>doi:10.64898/2026.07.12.738103</dc:identifier>
<dc:title><![CDATA[Turning an object into a scene: buildings activate scene-selective visual cortex independently of visual features]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-07-17</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.07.12.738094v1?rss=1">
<title>
<![CDATA[
Neural correlates of the subjective experience of free-will during value-based risky decisions: a pilot study 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.07.12.738094v1?rss=1
</link>
<description><![CDATA[
Underlying the very notion of choice is the fundamental idea of free-will, which is challenged by decision-neuroscience aiming to explain and predict choices using interactions of neurons. The question of whether any choice is truly a free-choice and born out of free-will has long been a subject of philosophical debate. In this work, we do not take a position on this debate, rather investigating the subjective experience of free-will, whose existence is more universally accepted. We had healthy participants report the level of their experienced free-will while performing value-based risky decision-making task to find the neural and behavioral correlates of this experience. We identified regions in mid-cingulum and middle frontal gyrus showing positive association with self-reported free-will as well as a region in hippocampus and parahippocampal gyrus showing a negative association. The requirement to report the experience of free-will was associated with a higher BOLD signal in striatum during decision-making. Behaviorally, we found a positive trend between RT and free-will. While our sample size is small, these results help forming hypotheses for further studies with larger cohorts and provide a proof-of-concept for the investigations of neural and behavioral mechanisms of the subjective experience of free-will in decision research.
]]></description>
<dc:creator><![CDATA[ Modak, P., Brown, J. W. ]]></dc:creator>
<dc:date>2026-07-17</dc:date>
<dc:identifier>doi:10.64898/2026.07.12.738094</dc:identifier>
<dc:title><![CDATA[Neural correlates of the subjective experience of free-will during value-based risky decisions: a pilot study]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-07-17</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.07.12.738026v1?rss=1">
<title>
<![CDATA[
Computational Counterfactuals Reveal Non-Additive Audiovisual Semantics in Natural Movie Responses 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.07.12.738026v1?rss=1
</link>
<description><![CDATA[
Natural audiovisual perception may not be fully captured by decomposing movies into auditory and visual streams. I introduce a computational-counterfactual framework that keeps movie viewing intact while varying only AI-derived descriptions of the same clips. Using 7 Tesla movie fMRI imaging data from 176 participants, I tested whether cortical responses were better predicted by native audiovisual semantics than by a dimension-matched additive reconstruction from audio-only and video-only descriptions. The native model outperformed the matched additive baseline under content-aware purged cross-validation, with strongest gains in auditory, visual, and dorsal attention systems. Representational-similarity, feature-replacement, and content-gating analyses showed that the advantage reflected feature- and network-specific routing linked to coherent audiovisual semantic emergence rather than raw auditory-visual discrepancy. The effect survived stronger temporal purging and repeat-content exclusion, suggesting that intact movie viewing evokes cortical structure aligned with native audiovisual meaning beyond additive unimodal semantics.
]]></description>
<dc:creator><![CDATA[ Li, M. ]]></dc:creator>
<dc:date>2026-07-17</dc:date>
<dc:identifier>doi:10.64898/2026.07.12.738026</dc:identifier>
<dc:title><![CDATA[Computational Counterfactuals Reveal Non-Additive Audiovisual Semantics in Natural Movie Responses]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-07-17</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.07.12.737168v1?rss=1">
<title>
<![CDATA[
Glial subcellular specialisation resolved with high resolution spatial transcriptomics 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.07.12.737168v1?rss=1
</link>
<description><![CDATA[
Cells in the brain have complex structures with extended processes. This complex morphology supports diverse specialized functions in health and disease, and specifically, cell processes appear to be critical for cellular integration and signalling. Here, we developed a new spatial averaging framework to recover and interrogate molecular phenotypes of glial processes in spatial transcriptomics (ST) data. We characterised cell type specific signatures associated with processes of astrocytes and microglia in both mouse and human brain tissue. Astrocytic processes were enriched for transcripts related to neuronal support relative to their soma, while microglial processes preferentially expressed genes liked to specific microglial states. When investigated in tissue from brains with Alzheimer's Disease (AD) pathology, we found that local amyloid-beta pathology was associated with subcellular differences in transcriptomes in both an amyloid-beta mouse model and human AD patient tissue. Specifically, astrocytic and microglial processes oriented towards amyloid-beta plaques exhibited distinct molecular changes in comparison to processes extending away into plaque free areas, suggesting polarized glial responses to pathology. Our work thus outlines a general method for the selective characterisation of transcriptomics of glial processes in mouse and human ST data and provides evidence for differential transcriptomic responses between the soma and processes of glia in health and disease.
]]></description>
<dc:creator><![CDATA[ Boulger, S. L., Melgosa-Ecenarro, L., Zielonka, M., Pilch, K. S., Wijesinghe, S. S., Radulescu, C. I., Matthews, P. M., Barnes, S. J., Mallach, A. ]]></dc:creator>
<dc:date>2026-07-17</dc:date>
<dc:identifier>doi:10.64898/2026.07.12.737168</dc:identifier>
<dc:title><![CDATA[Glial subcellular specialisation resolved with high resolution spatial transcriptomics]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-07-17</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.07.12.737445v1?rss=1">
<title>
<![CDATA[
Abdominal-B neurons selectively drive vibrations in Drosophila 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.07.12.737445v1?rss=1
</link>
<description><![CDATA[
Male Drosophila courtship includes two communication signals: airborne song and substrate-borne vibrations. While the neural control of song has been extensively characterized, little is known about the circuits underlying vibration production. Here, we identify neurons expressing the Hox gene abdominal-B (abdB) as a driver of vibration production. Optogenetic activation of abdB neurons selectively elicited vibrations in both males and females without inducing courtship song, whereas silencing these neurons did not impair vibration production during natural courtship. The vibration-driving abdB neurons are neither doublesex- nor fruitless-positive, defining a previously unrecognized component of the courtship circuit. Although abdB activation produced only stimulus-locked vibrations, co-activation of the persistence-promoting neuron cluster pCd converted this transient signal output into sustained vibration trains. Together, our results identify a dedicated pathway for vibration production and show that signal identity and persistence can be independently specified by distinct circuit components.
]]></description>
<dc:creator><![CDATA[ Steinfath, E., Alizadeh, K., Clemens, J. ]]></dc:creator>
<dc:date>2026-07-17</dc:date>
<dc:identifier>doi:10.64898/2026.07.12.737445</dc:identifier>
<dc:title><![CDATA[Abdominal-B neurons selectively drive vibrations in Drosophila]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-07-17</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.07.11.737965v1?rss=1">
<title>
<![CDATA[
Resolving early cochlear inflammation prevents lasting damage from noise exposure 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.07.11.737965v1?rss=1
</link>
<description><![CDATA[
Noise-induced hearing loss (NIHL) is a leading cause of permanent hearing impairment worldwide, yet no pharmacological therapies are currently available to prevent or treat this disorder. Although inflammation is increasingly recognized as a key contributor to cochlear degeneration, the therapeutic potential of targeting early inflammatory signaling remains poorly understood. Here, we combined phenotypic screening in zebrafish with mechanistic and functional validation in complementary mouse models to identify quinoxaline derivatives with otoprotective activity following acoustic trauma. Lead compounds preserved cochlear synapses and auditory function after moderate noise exposure, while one derivative also protected sensory hair cells in a model of permanent hearing loss. Mechanistic analyses demonstrated that this protection was associated with attenuation of early NF-{kappa}B signaling and modulation of the cochlear inflammatory response toward a reparative state, consistent with suppression of pathogenic innate immune activation before irreversible tissue damage occurred. Together, these findings identify early NF-{kappa}B-dependent inflammatory signaling as a therapeutically actionable mechanism in NIHL and establish quinoxaline derivatives as promising candidates for pharmacological intervention. More broadly, this work demonstrates the utility of a cross-species discovery platform for identifying therapies that preserve sensory function by targeting early inflammatory pathways.
]]></description>
<dc:creator><![CDATA[ Barbush, L., Fedorchuk, K., Ezzat, I., Manickam, V., Gawande, D., Chavez, A., Zallocchi, M. ]]></dc:creator>
<dc:date>2026-07-17</dc:date>
<dc:identifier>doi:10.64898/2026.07.11.737965</dc:identifier>
<dc:title><![CDATA[Resolving early cochlear inflammation prevents lasting damage from noise exposure]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-07-17</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.07.12.738020v1?rss=1">
<title>
<![CDATA[
Autonomic challenge uncovers hidden link between diastolic blood pressure and mental imagery vividness 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.07.12.738020v1?rss=1
</link>
<description><![CDATA[
Mental imagery is viewed as a fundamental component of human cognition, supporting memory, emotional processing, future simulation, and conscious experience. Although mental imagery vividness has traditionally been attributed to differences in sensory processing, emerging evidence suggests that internally generated images are also shaped by ongoing bodily and interoceptive signals. Here, we investigated whether cardiovascular physiology contributes to individual differences in mental imagery vividness using a virtual reality paradigm in which participants encoded and reconstructed emotional and neutral scenes during a tilt-table-induced autonomic challenge. Acute autonomic changes induced by a tilt table did not alter imagery vividness. However, elevated diastolic blood pressure during the tilt-up condition predicted reduced mental imagery vividness, with the strongest effects observed for disgust and neutral imagery. Our findings provide direct evidence that the vividness of the mind eye is linked to cardiovascular physiology and support interoceptive accounts of consciousness in which mental imagery emerges from dynamic interactions between neural and bodily systems. More broadly, these results identify cardiovascular function as a potential physiological contributor to altered imagery experiences, including those observed in aphantasia and related clinical conditions.
]]></description>
<dc:creator><![CDATA[ Nagai, Y. ]]></dc:creator>
<dc:date>2026-07-17</dc:date>
<dc:identifier>doi:10.64898/2026.07.12.738020</dc:identifier>
<dc:title><![CDATA[Autonomic challenge uncovers hidden link between diastolic blood pressure and mental imagery vividness]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-07-17</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.07.12.738010v1?rss=1">
<title>
<![CDATA[
A validated neuronal SH-SY5Y platform reveals critical experimental variables for reproducible Aβ 1-42 self-assembly neurotoxicity assessment 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.07.12.738010v1?rss=1
</link>
<description><![CDATA[
Reliable in vitro evaluation of amyloid-{beta} (A{beta}) toxicity is essential for the development of anti-amyloid therapeutics, yet experimental workflows often lack standardization. In our previous work, we established a reproducible protocol for the synthesis, characterization and controlled aggregation of highly pure A{beta}1-42. Here, we address the biological component of this variability by evaluating the impact of neuronal differentiation and toxicity assays on A{beta}-induced neurotoxicity. SH-SY5Y cells were differentiated using retinoic acid and brain-derived neurotrophic factor, generating a neuron-like phenotype validated by immunofluorescence, gene expression profiling and resistance to H2O2-induced oxidative stress. Using this characterized model, we investigated the effects of non-aggregated and pre-aggregated A{beta}1-42 species on cell viability and transcriptional responses. Strikingly, A{beta} toxicity was highly dependent on the aggregation state of the peptide, the differentiation status of the target cells and the viability assay employed. Our results suggest that the lack of standardization in peptide quality, aggregation procedures, neuronal maturation and toxicity assessment represents a major source of variability in the amyloid field. Together, these findings provide a methodological framework to improve the reproducibility and translational relevance of in vitro screening strategies for anti-amyloid therapeutics.
]]></description>
<dc:creator><![CDATA[ Van Baelen, A. C., Poteaux, C., Robin, P., Iturrioz, X., Panek, S., Sewald, N., Servent, D., Tonali, N. ]]></dc:creator>
<dc:date>2026-07-17</dc:date>
<dc:identifier>doi:10.64898/2026.07.12.738010</dc:identifier>
<dc:title><![CDATA[A validated neuronal SH-SY5Y platform reveals critical experimental variables for reproducible Aβ 1-42 self-assembly neurotoxicity assessment]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-07-17</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.07.11.737986v1?rss=1">
<title>
<![CDATA[
Edge controllability is associated with treatment response to repetitive transcranial magnetic stimulation in depression. 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.07.11.737986v1?rss=1
</link>
<description><![CDATA[
Repetitive transcranial magnetic stimulation (rTMS) is an established treatment for major depressive disorder (MDD), yet variability in treatment response remains a significant challenge. Network control theory provides a framework to quantify how brain networks facilitate state transitions, but prior work has focused primarily on node level metrics. Here, we investigate whether edge based controllability of the structural connectome is associated with rTMS outcomes. Twenty five patients with treatment-resistant depression underwent diffusion MRI prior to a 5 week course of high frequency rTMS targeting the dorsolateral prefrontal cortex. Structural connectomes were constructed using MRtrix3 and the Destrieux atlas, and edge based controllability metrics were computed at baseline. Controllability of specific middle frontal gyrus centered edges showed significant associations with changes in HAMD-24 scores, including connections to the superior frontal gyrus, hippocampus, angular gyrus, and orbital gyrus (r = 0.470 - 0.597, p < 0.05). These findings suggest that edge based controllability captures circuit level properties relevant to treatment response and may inform personalized neuromodulation strategies.
]]></description>
<dc:creator><![CDATA[ Dey, S. ]]></dc:creator>
<dc:date>2026-07-17</dc:date>
<dc:identifier>doi:10.64898/2026.07.11.737986</dc:identifier>
<dc:title><![CDATA[Edge controllability is associated with treatment response to repetitive transcranial magnetic stimulation in depression.]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-07-17</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.07.11.737109v1?rss=1">
<title>
<![CDATA[
Amplitude-Modulated Kilohertz Stimulation Targeting Beta-Band Activity Disrupts Motor Learning 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.07.11.737109v1?rss=1
</link>
<description><![CDATA[
Sensorimotor learning is associated with the modulation of neural rhythms in the primary motor cortex (M1). Beta-band activity ("beta"; 15-30 Hz) is suppressed during learning, while delta oscillations (1-4 Hz) become increasingly correlated with movement kinematics as skill improves. These observations have been complemented by experimental manipulations designed to perturb oscillatory activity with externally applied electric fields (E-fields). In non-human primates, invasive beta stimulation has been shown to disrupt motor learning whereas delta stimulation enhanced motor recovery in a stroke model. Causal evidence in humans remains limited, partly because established non-invasive methods cannot achieve continuous, narrowband E-fields at sufficient amplitude in the brain. To address this gap, we employed kilohertz transcranial magnetic perturbation (kTMP), a non-invasive magnetic induction technique that delivers continuous narrowband kilohertz E-fields which can be amplitude-modulated (AM) to target cortical rhythms. We applied AM-kTMP to test the functional relevance of beta and delta activity in human motor learning. In a double-blind mixed design, 40 participants performed a force-control task while receiving AM-kTMP at E-field amplitudes of 8 V/m in M1. We targeted either beta or delta, each paired with a sham condition. AM-kTMP influenced motor performance in a frequency-dependent manner: Beta-kTMP suppressed performance gains relative to both delta-kTMP and sham, whereas delta-kTMP showed no effect. These results suggest that increased beta activity in human M1 can interfere with motor learning. More broadly, kTMP offers a novel approach to probe frequency-specific cortical dynamics.
]]></description>
<dc:creator><![CDATA[ Reber, P., Merrick, C. M., Avraham, G., Killebrew, I., Thayer-Pham, K., Ahmad-Ali, H., Peterchev, A. V., Ganguly, K., Luu, C., Sheltraw, D., Labruna, L., Ivry, R. B. ]]></dc:creator>
<dc:date>2026-07-17</dc:date>
<dc:identifier>doi:10.64898/2026.07.11.737109</dc:identifier>
<dc:title><![CDATA[Amplitude-Modulated Kilohertz Stimulation Targeting Beta-Band Activity Disrupts Motor Learning]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-07-17</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.07.11.737958v1?rss=1">
<title>
<![CDATA[
Can the heartbeat-evoked potential (HEP) be separated from Cardiac Artefact (CA) using beamforming? 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.07.11.737958v1?rss=1
</link>
<description><![CDATA[
The heartbeat-evoked potential (HEP), a cortical response to heartbeats and a neural marker of interoception, is increasingly considered clinically relevant, but is heavily contaminated by cardiac artefact (CA) on the scalp, making reliable distinction of HEP from CA challenging. Because the HEP and cardiac potentials are anatomically distinct, they may be separable via beamforming, a source localisation method that isolates brain activity at specific locations while suppressing external noise and interference. Here, the first known ground-truth validation of EEG beamforming for HEP source reconstruction was attempted, aiming to quantify source waveform recovery and spatial localisation accuracy using simulated EEG data. Using linearly constrained minimal variance (LCMV) beamforming, the following was investigated. (A) To test whether beamforming can recover a known signal, 128-channel EEG datasets were simulated for 3 models with a known HEP waveform: a single right insula (R-Ins) HEP (1), two temporally distinct HEPs in the R-Ins and right anterior cingulate cortex (R-ACC) (2), and two temporally overlapping HEPs in the same regions (3). Recovery was investigated by correlating the virtual electrode waveforms at the true location with the known true input waveform. (B) To test CA suppression, CA extracted from isoelectric EEG of brain-dead individuals providing CA with limited cortical activity, was integrated into the simulated EEG data. Source (-10 to -50dB) and sensor (0 to -30dB) signal-to-noise ratios (SNR) were systematically varied for each model with and without CA. (C) LCMV beamforming was then applied to retrospective empirical EEG data from hypertensive and anxiety individuals (n=106). Across simulations and empirical data, T-tests compared power in a HEP-dominated window to an earlier CA-dominated window. Null-space projection, using subject-specific QRS waveform and its temporal derivative, was applied to remove residual CA in reconstructed source waveforms. In model 1, beamforming achieved near-perfect recovery without CA (r>0.99, 0mm error) at source SNR of -30dB, remaining robust in the presence of CA (r=0.72-0.94, 0-5.7mm error). Recovery degraded at low SNR (<-20 dB; r<0.3, up to 27mm error). Models 2 and 3 showed similar patterns but introduced R-ACC to R-Ins leakage. Applied to empirical data, beamforming revealed significant HEP activity in the R-Ins and R-ACC across all pooled data in source space (p < 0.001). LCMV beamforming also revealed a significant HEP difference in the late R-ACC window (250-500 ms post R-peak) in hypertension versus controls (p = 0.040, d = 0.92) when poor SNR subjects were excluded. This effect strengthened after QRS cleaning (p = 0.035, d = 0.96). LCMV beamforming can reliably recover the simulated HEP while suppressing CA, provided source SNR is sufficiently high. Applied to empirical data, LCMV beamforming recovered HEP activity from interoceptive regions (R-Ins and R-ACC) and was sufficiently sensitive to detect clinically meaningful group differences. This study offers a source level approach to separate HEP activity from CA, a distinction that sensor-level analysis can struggle to make. Together, LCMV beamforming and scalp-based methods can provide converging evidence for genuine HEP activity.
]]></description>
<dc:creator><![CDATA[ Virjee, R.-I., Kandasamy, R., Garfinkel, S. N., Yogarajah, M., Litvak, V., Carmichael, D. ]]></dc:creator>
<dc:date>2026-07-17</dc:date>
<dc:identifier>doi:10.64898/2026.07.11.737958</dc:identifier>
<dc:title><![CDATA[Can the heartbeat-evoked potential (HEP) be separated from Cardiac Artefact (CA) using beamforming?]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-07-17</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.07.12.737635v1?rss=1">
<title>
<![CDATA[
Task-Based Value Generalization Correlates With Positive Overgeneralization and Bipolar Symptoms 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.07.12.737635v1?rss=1
</link>
<description><![CDATA[
Positive overgeneralization -- the tendency to generalize from specific successes to broad expectations of future reward -- has been linked to vulnerability to mania. Because positive overgeneralization has primarily been assessed using self-report measures, we have limited insight into the underlying cognitive process. Here, we introduce a behavioral paradigm designed to quantify how learned value generalizes to novel stimuli. We quantify individual generalization profiles by fitting psychometric functions to choice data. In an online transdiagnostic study (N=163), we show that task-based breadth of reward generalization is associated with both higher self-reported positive overgeneralization and subclinical bipolar symptoms. To provide a computational account of positive overgeneralization, we implement a reinforcement-learning model in which self-efficacy modulates the influence of anticipated future value during learning. We show that increasing this modulation reproduces the broader value propagation observed empirically. Together, these findings provide a behavioral and computational framework for studying positive overgeneralization, and suggest a mechanistic pathway by which success-related shifts in value representations may bias learning in ways relevant to bipolar risk.
]]></description>
<dc:creator><![CDATA[ Li, J., Malaviya, M., Bennett, D., Radulescu, A. ]]></dc:creator>
<dc:date>2026-07-17</dc:date>
<dc:identifier>doi:10.64898/2026.07.12.737635</dc:identifier>
<dc:title><![CDATA[Task-Based Value Generalization Correlates With Positive Overgeneralization and Bipolar Symptoms]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-07-17</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.07.12.738011v1?rss=1">
<title>
<![CDATA[
Decoding the oxytocinergic and behavioral signatures of milk ejection 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.07.12.738011v1?rss=1
</link>
<description><![CDATA[
Oxytocin-mediated milk ejection (ME) is pivotal to effective breastfeeding and productive health, yet behaviorally decoding and revealing neural mechanisms of ME remains challenging. Here, we combined in vivo calcium imaging and intramammary pressure recording to uncover the temporal connections between episodic activity of oxytocin neurons and ME in conscious lactating rats. Leveraging the association and behavioral responses in dam and pup, we developed a supervised machine learning framework (ME Decoder) to enable automated analyses of ME. Inspired by its interpretable features, we defined the activity-coupled dam-pup interactions (ADPI), manifested by high kyphosis of the dam followed by pup treading and stretch, as the behavioral signatures of ME. By ME Decoder and ADPI analyses, we detected reduced ME but unaffected activity of oxytocinergic neurons after systemic blockade of oxytocin receptor. Our study uncovers the oxytocinergic and behavioral signatures of ME and provides a generalizable approach for further investigation.
]]></description>
<dc:creator><![CDATA[ Xiao, W., Zheng, Q., Wang, Y., Yuan, Y., Chen, Y., Zheng, T., Chen, Y., Gao, Y., Song, B., Zhang, B., Qiu, L., Zeng, L., Huan, M., Brown, C. H., Duan, S., Pan, G., Gao, Z. ]]></dc:creator>
<dc:date>2026-07-17</dc:date>
<dc:identifier>doi:10.64898/2026.07.12.738011</dc:identifier>
<dc:title><![CDATA[Decoding the oxytocinergic and behavioral signatures of milk ejection]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-07-17</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.07.16.738569v1?rss=1">
<title>
<![CDATA[
Age-Related Increases in 40Hz Neural Synchrony Are Specific to Typical Development: A Cross-Sectional Study of Autism Spectrum Disorder 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.07.16.738569v1?rss=1
</link>
<description><![CDATA[
Background: The 40Hz auditory steady-state response (ASSR) is a measure of gamma-band neural synchrony sensitive to excitation-inhibition (E/I) balance. Disruptions to E/I balance have been implicated in autism spectrum disorder (ASD), making ASSR an efficient tool for investigating neural synchrony development in this population. Whether age-related differences in 40Hz ASSR are detectable across development in ASD remains understudied. Phelan-McDermid syndrome (PMS), a rare genetic disorder with a phenotype overlapping with autism, caused by SHANK3 disruption, provides a genetically defined model for further investigating E/I-related neural synchrony disruptions. Methods: We examined 40Hz inter-trial phase coherence (ITPC) as an index of neural synchrony across a wide age range (2-37 years) in 127 participants from four groups: TD (n=43), ASD without intellectual disability (w/o ID; n=37), ASD with intellectual disability (w/ID; n=24), and PMS (n=23). Given the distinct age and cognitive profiles of ASD subgroups in this sample, analyses were conducted in separate models: TD vs. ASD w/o ID across all ages, and TD vs. ASD w/ID vs. PMS restricted to participants under 18. Results: For the first time in a cross-sectional sample spanning a large age range, we show that 40Hz ITPC increases significantly with age in TD individuals, while this developmental trajectory is absent in ASD without intellectual disability. Among children and adolescents under 18, 40Hz ITPC did not differ across TD, ASD w/ID, and PMS, and IQ did not predict ITPC in clinical groups. A post-hoc analysis revealed higher ITPC in TD males than females, with no sex differences in ASD or PMS. Conclusions: We demonstrate that gamma-band ITPC trajectories diverge between TD and ASD, specifically in adulthood, with no such difference detectable in childhood. No significant group differences were found among TD, ASD w/ID, and PMS individuals under 18. These findings highlight the importance of age as a critical variable when measuring ASSR, and underscore the need for lifespan studies, particularly in genetically defined conditions such as PMS, to determine whether similar divergence emerges in adulthood.
]]></description>
<dc:creator><![CDATA[ Thinakaran, A., Foss-Feig, J., Cai, S., Savino, J., Suh, M., Lavi, A., Siper, P., Levy, T., Buxbaum, J., Kolevzon, A., Beker, S. ]]></dc:creator>
<dc:date>2026-07-17</dc:date>
<dc:identifier>doi:10.64898/2026.07.16.738569</dc:identifier>
<dc:title><![CDATA[Age-Related Increases in 40Hz Neural Synchrony Are Specific to Typical Development: A Cross-Sectional Study of Autism Spectrum Disorder]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-07-17</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.07.16.738961v1?rss=1">
<title>
<![CDATA[
When meaning becomes decodable: Linking the N400 evoked response to semantic representations 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.07.16.738961v1?rss=1
</link>
<description><![CDATA[
In non-invasive studies of the human brain, semantic processing during language comprehension has been extensively studied using the N400, a component of the electrophysiological evoked response that is strongly modulated by semantic context. More recently, a complementary approach has emerged that uses multivariate pattern analysis to perform neural decoding of semantic vectors from brain activity, operating on the basis that semantic vectors that more closely align with representations in the brain can be more accurately decoded. To consolidate these two approaches, we investigated the relationship between N400 modulation and semantic decoding performance using magnetoencephalography (MEG) in a controlled priming experiment. Twenty-five native speakers of Finnish read word triplets, for which the semantic relatedness between the two primes and the target word was manipulated based on distance in a word2vec embedding space (highly related, moderately related, or unrelated). We found that words presented after unrelated primes elicited higher N400 responses and provided the best examples for training a decoder to map distributed MEG responses to semantic vectors. Semantic information was decodable from approximately 100 to 500 ms after stimulus onset, at all three levels of contextual support. Soon after the N400 peak, neural responses no longer seemed to encode information that could be mapped to context-invariant semantic vectors. This suggests that the end of the N400 window may correspond to a turning point where the representation shifts from being word-specific to encoding the greater semantic context.
]]></description>
<dc:creator><![CDATA[ Ghazaryan, G., Saranpää, A., Lindh-Knuutila, T., van Vliet, M., Salmelin, R. ]]></dc:creator>
<dc:date>2026-07-17</dc:date>
<dc:identifier>doi:10.64898/2026.07.16.738961</dc:identifier>
<dc:title><![CDATA[When meaning becomes decodable: Linking the N400 evoked response to semantic representations]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-07-17</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.07.16.738989v1?rss=1">
<title>
<![CDATA[
When Music Loses Its Pleasure: Hippocampal Cingulum White Matter as a Structural Mediator of Musical Reward Decline in Aging 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.07.16.738989v1?rss=1
</link>
<description><![CDATA[
Individuals' ability to obtain pleasure from music, referred to as musical reward sensitivity, declines with age, yet the neural mechanisms underlying this decline remain unclear. In this study, we investigated musical reward sensitivity measured in 58 older adults and 131 young adults. Consistent with prior findings, young adults reported higher musical reward sensitivity than older adults (p < 0.05). To identify neuroanatomical predictors of musical reward sensitivity, we employed the elastic-net model to predict musical reward sensitivity using white matter microstructural properties and gray matter morphometric properties from the whole brain. In older adults, fractional anisotropy (FA) in the bilateral hippocampal cingulum (CGH) and external capsule (EC) reliably predicted individual differences in musical reward sensitivity. Moreover, FA in the right CGH significantly mediated the relationship between age and musical reward sensitivity in older adults. Notably, these associations were specific to musical reward sensitivity in older adults, that is, they did not replicate in young adults, and did not extend to general reward sensitivity. Together, these findings highlight the critical role of white matter integrity, particularly within the hippocampal-limbic pathways, in age-related changes in musical reward processing, and suggest a potential neurobiological target for interventions aimed at enhancing well-being in older adulthood.
]]></description>
<dc:creator><![CDATA[ Wang, J., Kathios, N., Kubit, B., Lopez, K., Kim, J. C., Large, E., Noble, S., Loui, P. ]]></dc:creator>
<dc:date>2026-07-17</dc:date>
<dc:identifier>doi:10.64898/2026.07.16.738989</dc:identifier>
<dc:title><![CDATA[When Music Loses Its Pleasure: Hippocampal Cingulum White Matter as a Structural Mediator of Musical Reward Decline in Aging]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-07-17</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.07.14.737938v1?rss=1">
<title>
<![CDATA[
Investigating fNIRS Test-Retest Reliability During Lexical Decision 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.07.14.737938v1?rss=1
</link>
<description><![CDATA[
Significance. fNIRS is highly suitable for the study of reading development, however, the reliability of its signals is not well understood during reading tasks. Aim. Therefore, this study assessed the test-retest reliability of the fNIRS signal during a common event-related reading paradigm. Approach. English-speaking adults (n = 30) completed a lexical decision task during fNIRS recording twice, one week apart. Results. Our results demonstrated contrast effects partially consistent with prior neuroimaging literature, insofar as for each contrast, at least one predicted region of interest was activated. However, we did not identify significant activation in all predicted brain areas. Regarding group level test-retest reliability, we observed poor reliability across predicted brain regions for most conditions, with the exception of fair test-retest reliability in the left posterior temporal lobe for coarse lexical tuning. At the single-subject level, test-retest reliability ranged from poor to excellent across subjects, but was poor for most subjects. Conclusion. These results suggest fNIRS can detect changes in brain activation during a fast event-related reading task at the group level. However, reliability does not appear sufficient to interpret individual-level data. Further research should explore reliability across a wider range of designs to assess the generalizability of these findings.
]]></description>
<dc:creator><![CDATA[ Elliott, L. M., Rankaduwa, S. S., Hamon-Hill, C., Bode, D. A., Hulls, M. V. M., Lavoie, P. J. A., Newman, A. J. ]]></dc:creator>
<dc:date>2026-07-17</dc:date>
<dc:identifier>doi:10.64898/2026.07.14.737938</dc:identifier>
<dc:title><![CDATA[Investigating fNIRS Test-Retest Reliability During Lexical Decision]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-07-17</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.07.17.739117v1?rss=1">
<title>
<![CDATA[
The role of the Angular Gyrus in the Elaboration of Specific and Categoric Memories 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.07.17.739117v1?rss=1
</link>
<description><![CDATA[
This study investigated the role of the angular gyrus (AG) and its subregions in the elaboration of specific and categoric autobiographical memories (AMs). Using a cue-word fMRI paradigm, thirty-nice participants retrieved and elaborated on episodic (specific) and semantic (categoric) memories, rating the amount of detail of each recollection. Parametric analyses revealed that AG activity, particularly in posterior AG, was positively associated with the amount of detail retrieved, regardless of memory type. Specific memories elicited greater activation in right AG subregions compared to categoric memories. These findings support the AG's involvement in both episodic and semantic memory retrieval and suggest functional differentiation between its subregions.
]]></description>
<dc:creator><![CDATA[ Bush, A., Lancelotte, F., Johnen, A.-K., Melega, G., Guo, D., Lopez Saquisili, C. E., Jefferies, E., Brooks, J., Renoult, L. ]]></dc:creator>
<dc:date>2026-07-17</dc:date>
<dc:identifier>doi:10.64898/2026.07.17.739117</dc:identifier>
<dc:title><![CDATA[The role of the Angular Gyrus in the Elaboration of Specific and Categoric Memories]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-07-17</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.07.15.737608v1?rss=1">
<title>
<![CDATA[
A Role for Astrocyte Metabolism in Species-Specific Neuronal Development 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.07.15.737608v1?rss=1
</link>
<description><![CDATA[
Human neurons develop more slowly than non-human primate neurons. This phenomenon, termed neoteny, is thought to contribute to several human-specific features of the brain, including humans' expanded cortices. However, much of the research on this difference in neuronal development rate has focused on neuron-intrinsic drivers of developmental timing. Because astrocytes serve as critical support cells of neurons and are increasingly implicated in neuronal maturation during development, we hoped to further elucidate any species-specific divergence in function and the astrocytes' role in influencing species-specific development rate. In this study, we began with a transcriptomic characterization of human and non-human primate astrocytes in vitro. We then measured how the metabolic role of astrocytes differs between humans and non-human primates. We then performed a multi-electrode array assay and observed an increase in electrophysiological maturation in human neurons cultured with rhesus macaque astrocyte conditioned media as opposed to human astrocyte conditioned media and a change in the trajectory of neuronal development, as measured by transcriptomics. Curiously, we observed an increase in synaptogenic and axon growth-related proteins in the secretome of human astrocytes, suggesting that human astrocytes play a different, more synaptogenic and dendritic arborization-focused role in neurodevelopment than non-human primate astrocytes. Finally, we demonstrated that these changes in neuronal differentiation are in part mediated by the different metabolic roles that astrocytes play in humans versus non-human primates through chemical inhibition of a key metabolic pathway. Our results collectively suggest a cell-extrinsic role for astrocyte metabolism in shaping the differences in neurodevelopment rate and trajectory in humans versus non-human primates.
]]></description>
<dc:creator><![CDATA[ Steiner, S. C., Foster, K., Chinn, R. R., Pratt, J., Fernandes, S., Sharma, A., Santos, R., Metallo, C. C., Marchetto, M. C., Gage, F. H. ]]></dc:creator>
<dc:date>2026-07-17</dc:date>
<dc:identifier>doi:10.64898/2026.07.15.737608</dc:identifier>
<dc:title><![CDATA[A Role for Astrocyte Metabolism in Species-Specific Neuronal Development]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-07-17</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.07.16.738788v1?rss=1">
<title>
<![CDATA[
A consensus atlas of human brain development defines cell type-specific maturation trajectories across the lifespan 
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</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.07.16.738788v1?rss=1
</link>
<description><![CDATA[
Human neurodevelopment is a continuous process that begins prenatally and extends into postnatal life. Current transcriptomic datasets are limited, fragmented across analytical frameworks, precluding comprehensive reconstruction of cellular trajectories linking developmental states to mature cell types. Here we present a consolidated cellular-resolution transcriptomic atlas of human brain development from the onset of neurogenesis to adulthood, covering ~2.2 million cells from 156 donors across nine studies. All data were reprocessed from raw sequencing reads and annotated within a unified cell-type taxonomy, enabling reliable mapping across the lifespan. Cell types were highly replicable across heterogeneous datasets, enabling us to chart their maturation and cortical layer localization over time. We identify dynamic gene programs predictive of cell-type maturation, validate gene modules tracking known fate transitions, and leverage our atlas' scale to characterize rare populations, including microglia. This resource establishes a standardized reference of human brain development and maturation gene modules for future comparisons across model systems, species, and disease states.
]]></description>
<dc:creator><![CDATA[ Venkatesan, S., Nano, P., Werner, J., Malaiya, S., Herb, B., Gao, Y., Wang, L., Bhaduri, A., Nowakowski, T. J., Colantuoni, C., Ament, S. A., Gillis, J. ]]></dc:creator>
<dc:date>2026-07-17</dc:date>
<dc:identifier>doi:10.64898/2026.07.16.738788</dc:identifier>
<dc:title><![CDATA[A consensus atlas of human brain development defines cell type-specific maturation trajectories across the lifespan]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-07-17</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.07.16.738868v1?rss=1">
<title>
<![CDATA[
Hippocampal-midcingulate connectivity is associated with representational integration during cognitive map updating 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.07.16.738868v1?rss=1
</link>
<description><![CDATA[
Cognitive maps organize experience into structured internal models that support goal-directed behavior. Although map formation has been extensively studied in the human hippocampus, the neural mechanisms supporting flexible updating of established maps remain unclear. We used fMRI to track the formation and updating of a spatial cognitive map across three days. Participants learned object-location associations and later updated them by remapping objects among fixed locations. Representational similarity analysis revealed two concurrent signatures in the right hippocampus: prior relational structure remained differentiated, whereas updated associations became integrated. Map updating engaged a frontoparietal network and modulated hippocampal-cortical connectivity. Critically, hippocampal-midcingulate connectivity was associated with the integration of updated associations, but not with the differentiation of prior relational structure. These results suggest that cognitive map updating involves coordinated hippocampal-cortical interactions that incorporate new information while preserving prior relational structure, reflecting a balance of stability and plasticity in internal models.
]]></description>
<dc:creator><![CDATA[ Fu, J., Huang, C., Wang, R., Hasegawa, I., Jimura, K., Nakahara, K. ]]></dc:creator>
<dc:date>2026-07-17</dc:date>
<dc:identifier>doi:10.64898/2026.07.16.738868</dc:identifier>
<dc:title><![CDATA[Hippocampal-midcingulate connectivity is associated with representational integration during cognitive map updating]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-07-17</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.07.15.738539v1?rss=1">
<title>
<![CDATA[
Mapping Focal and Generalized Effects of Common Genetic Variants on Human Brain Structure 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.07.15.738539v1?rss=1
</link>
<description><![CDATA[
Genome-wide association studies (GWAS) have advanced the quest to understand how specific genetic variants influence human brain structure and function. Recent work has identified hundreds of common variants associated with subcortical brain volumes, sparking interest in how these genetic markers overlap across brain networks. While this can be estimated by hierarchical clustering of the genetic correlation matrix to identify modular patterns of shared architecture, no brain-wide maps of these effects are available. To address this, we computed polygenic scores (PGS) from loci associated with ten brain volume regions of interest (ROIs): nine major subcortical structures and intracranial volume, with each locus weighted by its association with regional volume. In an independent sample from the discovery GWAS, we performed large-scale segmentation of 3D volumetric T1-weighted MRI scans using voxel-based morphometry (VBM) to map 3D profile of regions where gray matter volume (GMV) was associated with each PGS. We found statistically significant, localized effects for PGS defined for the amygdala, thalamus, and basal ganglia, but PGS for brainstem volume was associated with widespread differences throughout the brain. These brain-wide maps reveal patterns consistent with both localized and distributed genetic influences, offering a novel approach to interpret the genomic architecture of brain structure.
]]></description>
<dc:creator><![CDATA[ Gleave, E. J., Garcia-Marin, L. M., Ceja, Z., Renteria, M. E., Chattopadhyay, T., Gaser, C., Rajagopalan, P., Thompson, P. M. ]]></dc:creator>
<dc:date>2026-07-17</dc:date>
<dc:identifier>doi:10.64898/2026.07.15.738539</dc:identifier>
<dc:title><![CDATA[Mapping Focal and Generalized Effects of Common Genetic Variants on Human Brain Structure]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-07-17</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.07.16.738654v1?rss=1">
<title>
<![CDATA[
Measuring excitation/inhibition balance through field potentials 
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</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.07.16.738654v1?rss=1
</link>
<description><![CDATA[
Several electroencephalography-based metrics have been proposed to index excitation/inhibition balance (E/I). We used single-unit and local field potential recordings from rat medial prefrontal and orbitofrontal cortex and mouse visual cortex and hippocampus to evaluate four candidate metrics against empirically-measured E/I. While 1/f slope and gamma oscillations showed region and context dependencies, broadband (6-80 Hz) and high gamma (80-150 Hz) power consistently correlated with E/I, supporting their use as proxy measures.
]]></description>
<dc:creator><![CDATA[ Rodriguez-Sanchez, J., Diehl, G. W., Cunningham, P. J., Pinotsis, D., Adams, R. A., Redish, A. D. ]]></dc:creator>
<dc:date>2026-07-17</dc:date>
<dc:identifier>doi:10.64898/2026.07.16.738654</dc:identifier>
<dc:title><![CDATA[Measuring excitation/inhibition balance through field potentials]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-07-17</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.07.17.738592v1?rss=1">
<title>
<![CDATA[
Expectation Shapes Neural Preparation for AI-generated and Real Image Processing: Evidence from EEG 
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</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.07.17.738592v1?rss=1
</link>
<description><![CDATA[
Abstract: AI-generated images, videos, and news have become an inseparable part of daily life, leading to increasing skepticism toward online information. Understanding how expectations about the presence of AI-generated content influence perception is crucial for elucidating the underlying neural mechanisms and facilitating the generation of naturalistic avatars. In this study, we analyzed an existing EEG dataset (N = 29) in which participants viewed emotional facial photographs of only real individuals while being informed that upcoming faces were either real ('REAL') or AI-generated ('FAKE'). We examined pre-stimulus oscillatory activities in the one-second EEG interval before stimulus onset and found significantly lower alpha power when participants expected 'FAKE' compared to 'REAL' faces. This effect was region-specific, particularly in right occipito-parietal and temporo-parietal regions, as identified by both sensor- and source-level analyses. In addition, the modulation effect between pre-stimulus alpha activity and post-stimulus event-related potentials (ERPs) was measured. A significant correlation between changes in late positive potential (LPP) amplitudes and pre-stimulus alpha power was observed exclusively for 'FAKE' smiling faces, consistent with our previous findings. These results suggest that AI-related expectations modulate neural preparatory states, with lower alpha activity presumably reflecting increased attentional demands for stimuli believed to be artificially generated. This study demonstrates that top-down beliefs systematically shape both pre- and post-stimulus neural dynamics, providing new insights into how cognitive expectations bias perceptual processing, with implications for understanding human-AI interaction and improving the design and evaluation of AI-generated content in real-world contexts.
]]></description>
<dc:creator><![CDATA[ Chen, Y., Eiserbeck, A., Maier, M., Klotzsche, F., Hofmann, S. M., Baum, J., Nierula, B., Hilsmann, A., Bosse, S., Villringer, A., Rahman, R. A., Gaebler, M., Nikulin, V. ]]></dc:creator>
<dc:date>2026-07-17</dc:date>
<dc:identifier>doi:10.64898/2026.07.17.738592</dc:identifier>
<dc:title><![CDATA[Expectation Shapes Neural Preparation for AI-generated and Real Image Processing: Evidence from EEG]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-07-17</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.07.11.737916v1?rss=1">
<title>
<![CDATA[
Anticipatory modulation of motor unit discharge rate before rapid isometric elbow flexion force production 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.07.11.737916v1?rss=1
</link>
<description><![CDATA[
Surface electromyography (EMG) studies have demonstrated anticipatory muscle activation prior to predictable voluntary actions. However, the mechanism through which this preparation is expressed, whether through motor-unit recruitment or discharge-rate modulation, remains to be elucidated. We employed surface decomposition EMG to quantify motor-unit behavior prior to self-paced rapid isometric elbow-flexion force pulses. Twelve healthy young men were instructed to generate elbow-flexion pulse force at 30%, 40%, and 50% of the maximal voluntary contraction (MVC) at a self-selected time. Motor-unit activity was decomposed from the biceps brachii and triceps brachii muscles, and the normalized active motor-unit number and mean discharge rate were analyzed prior to pulse onset. In the agonist, the pre-pulse increase mean discharge rate exhibited a higher value than the change in detected motor-unit count, particularly at the 40% and 50% MVC targets. The discharge-rate increase scaled with the target force, with a heightened response observed in high-threshold as compared to low-threshold motor units. Antagonist recordings with sufficient decomposition yield exhibited a similar discharge-rate-dominant pattern; however, these data were available from a smaller sample size. Present findings suggest that discharge-rate modulation is a primary motor-unit-level feature of anticipatory preparation for rapid isometric force production.
]]></description>
<dc:creator><![CDATA[ Park, J., Park, J.-W., Lee, S., Choi, Y.-S., Park, D., Hur, H., Park, J., Kim, H.-S. ]]></dc:creator>
<dc:date>2026-07-17</dc:date>
<dc:identifier>doi:10.64898/2026.07.11.737916</dc:identifier>
<dc:title><![CDATA[Anticipatory modulation of motor unit discharge rate before rapid isometric elbow flexion force production]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-07-17</prism:publicationDate>
<prism:section></prism:section>
</item>
<item rdf:about="https://www.biorxiv.org/content/10.64898/2026.07.13.737722v1?rss=1">
<title>
<![CDATA[
Functional relevance of mobile and clustered CaV2.1 channels in central synapses 
]]>
</title>
<link>
https://www.biorxiv.org/content/10.64898/2026.07.13.737722v1?rss=1
</link>
<description><![CDATA[
Reliable neurotransmitter release critically depends on the spatial relationship between voltage-gated calcium channels (VGCCs) and presynaptic release sites. Single particle tracking of endogenous CaV2.1 channels at glutamatergic synapses of hippocampal neurons revealed that apart from CaV2.1 channels aggregated in stable nanodomain clusters, a substantial fraction of Cav2.1 channels remained mobile, raising the question of whether these dispersed channels contribute to synaptic function. Mathematical modelling predicted that dispersed Cav2.1 channels cooperatively enhance release reliability. Upon repetitive stimulation, mobile CaV2.1 channels enable alternative use of release sites and thereby reduce the probability of failed presynaptic release. Both optogenetic immobilisation of CaV2.1 channels per se or activation of GABAB receptors (GABABRs) alone increase the failure rate and can lead to synaptic silencing. However, optogenetic clustering CaV2.1 channels prior to GABABR activation increases the fraction of synapses that remain active even in presence of GABABR agonist. The contribution of mobile channels to reliable neurotransmitter release is frequency-dependent and is minor at stimulation frequencies 1 Hz but becomes strong at frequencies over 10 Hz. These results demonstrate that mobile presynaptic CaV2.1 channels increase the frequency range of synaptic transmission but are particularly sensitive to metabotropic GABABR-mediated inhibition in glutamatergic hippocampal synapses.
]]></description>
<dc:creator><![CDATA[ El khallouqi, a., Amaral, C., Lassen, A. S., Weissbach, S., Werkmann, C., Bikbaev, A., Mark, M., Herlitze, S., Heck, J., Walter, A., Heine, M. ]]></dc:creator>
<dc:date>2026-07-17</dc:date>
<dc:identifier>doi:10.64898/2026.07.13.737722</dc:identifier>
<dc:title><![CDATA[Functional relevance of mobile and clustered CaV2.1 channels in central synapses]]></dc:title>
<dc:publisher>Cold Spring Harbor Laboratory</dc:publisher>
<prism:publicationDate>2026-07-17</prism:publicationDate>
<prism:section></prism:section>
</item>
</rdf:RDF>
