1795 papers
Neuroscience explores the intricate machinery of the brain and nervous system, seeking to understand how we think, feel, and move. From the microscopic dance of individual neurons to the complex networks that shape our memories and behaviors, this field peels back the layers of our biological selves to reveal the origins of consciousness and disease.
At Gist.Science, we bring these discoveries directly from bioRxiv, the leading preprint server for biological sciences, to a broader audience. We process every new neuroscience preprint as it is uploaded, transforming dense academic manuscripts into clear, plain-language explanations alongside detailed technical summaries. This ensures that both curious readers and specialists can stay current with the latest breakthroughs before they are formally published.
Below are the latest neuroscience papers we have processed from bioRxiv, offering fresh insights into the workings of the mind.
This study reveals that RTEL1, a DNA helicase linked to autism risk, maintains social behavior and oxytocin output in mice by resolving G-quadruplex structures at the Oxt promoter to ensure proper oxytocin gene expression in hypothalamic neurons.
This study reveals that the epigenetic modifier DOT1L acts as a critical barrier regulating cortical astrogenesis by orchestrating transcription factor networks that control astrocyte state conversion, de-differentiation, and the emergence of diverse astrocyte populations originating from both dorsal and ventral telencephalic lineages.
This study demonstrates that normative modeling-derived brain deviation scores are more effective than conventional structural metrics in identifying a transdiagnostic emotion-dysregulation dimension in children and adolescents, revealing specific regional cortical abnormalities and sex differences.
This study reveals that while PSD-95 knockout mice appear to have subtle sensory deficits as adults, they exhibit profound impairments in ethologically relevant binocular vision and prey capture, demonstrating that PSD-95 is essential for binocular integration in the primary visual cortex during critical periods.
This study demonstrates that during esports, a distinct high-performance state characterized by superior objective outcomes and lower subjective workload can be identified through sustained pupil-heart synchrony, revealing that central-autonomic coordination serves as a biomarker for efficient cognitive-sensorimotor performance that often escapes players' subjective awareness.
This study identifies USP15 as a critical driver of neuroinflammation and synucleinopathy pathogenesis, demonstrating that its deletion protects against disease in mouse models while human genetic and expression data link elevated USP15 levels in myeloid cells to increased Parkinson's disease risk.
This study demonstrates that neural entrainment measures derived from EEG, specifically the correlation between attended and unattended speech stimuli, serve as significant predictors of individual speech-in-noise perception and narrative comprehension abilities in healthy listeners.
This study combines computational modeling with experimental imaging in dopaminergic cell models to demonstrate that oxidative stress enhances membrane excitability by shifting the voltage-dependence of L-type calcium channels, a mechanism that can be mitigated by the calcium channel blocker nicardipine.
While older adults do not exhibit greater overall balance variability than younger adults during repeated visual perturbations, they demonstrate earlier and larger deviations in specific conditions and a unique reversal in response direction, indicating an age-related deficit in accurately estimating self-motion through sensory integration, though they retain the capacity to adapt by downweighting visual information over time.
This study identifies a distinct, activated SPP1+ microglial population as the primary CNS reservoir for HIV in ART-suppressed individuals, where chronic interferon signaling and immune evasion drive complement-mediated synaptic pruning and glutamatergic neuronal injury, leading to persistent neurocognitive dysfunction.