Steven A. Sloan

This study develops human spinal cord organoids and assembloids to model oligodendrocyte development and disease states, showing they recapitulate developmental signatures and cytokine-induced dysfunction seen in multiple sclerosis.

This paper identifies a novel mechanism by which manganese disrupts mitochondrial transcriptome processing, leading to dsRNA accumulation and neuroinflammation through MDA5 activation.

This paper introduces SPARO, a method to simultaneously profile transcriptomes and proteomes of neural cell types, revealing mRNA-protein discordance patterns in astrocytes and neurons.

This study shows human astrocytes can present antigens via MHCII after chronic cytokine exposure, revealing their potential as antigen-presenting cells.

The paper investigates how neurodevelopmental disorder-associated variants affect mitochondrial proteins and finds convergent effects on mitochondrial translation in two high-risk CNVs.

This study shows that gut microbes influence the transcriptional states of brain cell types and affect neurodegenerative disease susceptibility, with E. coli specifically worsening Alzheimer's disease outcomes in mice.

This study investigates the effects of Zika virus infection on infant brain development using single-cell transcriptomics and other methods, identifying disrupted pathways and behavioral changes.

This study shows that Kv1.3 inhibitors reduce neuropathology in a mouse AD model by modulating neuroinflammation, resilience, and neurovascular pathways through distinct cellular mechanisms.

This study uses human brain organoids to show that glioblastoma cells adopt neuron-like states and interact with region-specific synaptic inputs to drive invasion.

This study shows that prenatal lead exposure biases neural cell fate in human brain development by increasing neurons and reducing astrocytes through epigenetic changes.

This study shows that AV flicker at specific frequencies can mitigate stress-induced changes in mice, with 10Hz effective in males and 40Hz in females.

This study uses cortical organoids to show that ALG13 loss-of-function causes glycosylation defects, neuronal maturation issues, and network hypoactivity in CDG.

This study shows that astrocyte cilia regulate Sonic Hedgehog signaling during astrocyte development, affecting proliferation and morphology.

The paper identifies Myocilin as a marker for glia limitans superficialis astrocytes in mouse and human, showing their specialized morphology and evolutionary conservation.

The paper introduces ScISOr-ATAC to measure splicing and chromatin accessibility in frozen brain tissues, finding convergent and divergent patterns in different cell types and conditions.

This study shows hypoxia disrupts astrocytic circadian rhythms, reducing synaptosome phagocytosis and linking this to ASD-related synapse defects.

This study uses cross-species scRNA-seq to show that the 3q29 deletion causes mitochondrial dysfunction in both human cortical organoids and mouse models, suggesting a conserved metabolic disruption in schizophrenia.

This study shows that tyrosinase-induced neuromelanin accumulation in mouse locus coeruleus neurons causes hyperactivity, transcriptional changes, and degeneration, mimicking early stages of Alzheimer's and Parkinson's disease.

This study uses DSP-4 to model early LC-NE system changes in AD and PD, showing axon damage, neuroinflammation, and behavioral changes without LC cell death.

This study shows Schwann cells promote sensory neuron excitability during development by secreting prostaglandin E2, which is essential for normal sodium channel expression and action potential firing.

The paper identifies and validates synergistic ligand-receptor pairs that drive astrocyte development in the human brain using computational methods and experimental testing.

This study investigates the molecular effects of the 3q29 deletion on the human neural transcriptome, identifying convergent and distributed impacts across gene clusters and pathways related to psychiatric disorders.

This study evaluates 32 individuals with 3q29 deletion syndrome to identify common medical and neurodevelopmental features and provides clinical care recommendations.

The paper identifies brain-region specific splicing patterns at single-cell and spatial resolution in postnatal mice, revealing cell-type specific and region-specific isoform expression.

The paper introduces a machine learning method to detect somatic L1 insertions in human brain tissue, revealing their widespread distribution in neurons and glia and potential role in neuropsychiatric diseases.

The paper introduces ScISOr-Seq, a method combining single-cell full-length cDNA amplification with short-read and long-read sequencing to identify isoforms in cerebellar cell types across thousands of cells.

This study uses single-cell RNAseq to analyze infiltrating neoplastic cells in human glioblastoma, identifying consistent gene signatures and distinct myeloid cell populations across patients.