1527 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 specific growth trajectories of hippocampal subregions, particularly the right hippocampal head, and total sleep duration during early childhood are significant predictors of episodic memory performance in early school age.
This paper demonstrates that distinct dopamine-modulated spike-timing-dependent plasticity rules are differentially suited to specific computational tasks like value estimation and action selection, suggesting that the precise form of STDP may vary across brain regions to support their unique functional roles.
This study utilizes isotopic labeling and mass spectrometry to determine that brain PrP has a half-life of 5–6 days, a rate-limiting factor for therapeutic efficacy that varies slightly by tissue and mutation, thereby informing the design of future prion disease clinical trials.
This study employs simulation-based inference on a spiking neuronal network model to quantify how distinct compensatory mechanisms interact to restore healthy activity against specific causes of hyperexcitability, thereby providing a quantitative foundation for designing precise therapeutic interventions.
This study reveals that in *Drosophila*, chronic light stress triggers Toll-1 activation in photoreceptor neurons, which upregulates the glial phagocytic receptor Draper to drive the engulfment and degeneration of stressed axons, establishing a neuron-glia signaling axis that converts sustained stress into structural neural loss.
This study demonstrates that while both lamotrigine and levetiracetam modulate periodic EEG activity, only lamotrigine significantly alters aperiodic EEG parameters (specifically reducing offset and flattening the slope) in healthy volunteers during eyes-open conditions, suggesting aperiodic measures can differentiate the neurophysiological impacts of distinct antiseizure medications.
This paper systematically benchmarks assumption-lean community detection methods and model selection criteria on human connectome data, demonstrating that a likelihood-based criterion effectively identifies biologically plausible community structures that align with established sensory systems in adults and reveal distinct developmental mesoscale architectures in infants.
This study demonstrates that conscious access to sensory stimuli across multiple modalities is gated by transient bursts of prefrontal alpha activity that are temporally synchronized with specific phases of the cardiac and respiratory cycles, revealing that brain-body synchrony acts as a critical mechanism for determining awareness.
This study demonstrates that deleting the immune receptor LAG3 in a familial Alzheimer's disease mouse model rescues neurodegeneration by suppressing aberrant disease-associated microglia activation and reducing CD8+ T cell infiltration, thereby highlighting LAG3 as a promising therapeutic target for Alzheimer's disease.
This study demonstrates that the Alzheimer's disease risk allele APOE4 increases human microglial vulnerability to arsenic exposure by altering transcriptional stress responses and mitochondrial function, thereby establishing a gene-environment interaction framework for understanding environmental contributions to AD pathology.