Neuroscience Research
Neuroscience Research
Stereo-seq empowers researchers to explore the spatial organization of complex brain regions with unprecedented resolution. By capturing unbiased whole-transcriptome gene expression while preserving spatial context, it enables detailed mapping of neuronal subtypes and circuits.
Stereo-seq technology supports studies on brain development, neural connectivity, and functional heterogeneity. Researchers can investigate how distinct cell populations interact within specific anatomical regions.
In addition, Stereo-seq facilitates the study of neurological disorders by revealing spatial alterations in gene expression, providing valuable insights into disease mechanisms and potential therapeutic targets.
11
Peer-Reviewed Studies
5+
Species & Model Systems
Overview
The nervous system is organized across multiple biological scales—from molecular programs and cellular niches to neural circuits and complete brain regions. Dissociated sequencing can identify cell states, but it removes the anatomical relationships that connect those states to brain function and disease.
Stereo-seq preserves intact neural architecture while capturing whole-transcriptome information across large tissue sections. Researchers can resolve disease-associated cell states, map injury responses, compare brain organization across species, and construct foundational single-cell spatial atlases.
Profile intact brain regions and whole-brain architectures in a continuous spatial coordinate system.
Resolve neuronal, glial, vascular and immune-cell populations in their native tissue context.
Map disease niches, lesion evolution, molecular gradients and cell–cell interactions.
Integrate spatial transcriptomics with single-cell, epigenomic and connectivity datasets.
Research Themes Covered
Neurological Disease, Injury & Aging
Comparative & Evolutionary Neuroscience
Foundational Brain Atlases & Reference Maps
Research Themes
Published studies demonstrate how Stereo-seq advances neuroscience from disease mechanisms and therapeutic validation to comparative biology and foundational brain mapping.
01 — Disease & Injury
Neurological Disease, Injury & Aging
Resolve disease-driving cell states, pathological niches and therapeutic responses across neurodegeneration, sensory loss, stroke and neurovascular disorders.
02 — Comparative
Comparative & Evolutionary Neuroscience
Compare conserved and species-specific brain organization across model systems to improve biological interpretation and translational relevance.
03 — Brain Atlases
Foundational Brain Atlases & Reference Maps
Build comprehensive spatial references that connect cell identity, tissue architecture and neural circuits across whole brains and human cortical regions.
Featured Publications
11 peer-reviewed studies show how Stereo-seq resolves neural biology across human tissue, animal models, brain regions and complete nervous-system structures.
Resolve molecular and cellular alterations across human hippocampal subregions in Alzheimer's disease.
Conventional approaches lack single-cell spatial context across the entire human hippocampus.
Reveal region-specific pathology, cellular interactions, and plaque microenvironments within intact hippocampal architecture.
Mapped the entire human hippocampus with single-cell spatial transcriptomics.
Resolved cell-type organization within intact hippocampal subregions.
Reconstructed amyloid plaque microenvironments at cellular resolution.
Localized reactive microglia–astrocyte interactions across disease niches.
Captured spatial molecular gradients from plaques into surrounding tissue.
Identified vulnerable and resilient hippocampal subregions in Alzheimer's disease.
Revealed spatially restricted reactive microglia and astrocyte niches.
Reconstructed sequential glial organization surrounding amyloid plaques.
Mapped plaque-dependent molecular gradients at single-cell resolution.
Uncovered region-specific neuronal resilience mechanisms in human Alzheimer's.
Enabled clinically relevant plasma biomarkers from spatial transcriptomic discoveries.
TakeawayStereo-seq connected spatial Alzheimer's pathology to clinically actionable biomarkers, accelerating precision neuroscience.
Resolve the molecular and cellular architecture of the cochlear nucleus (CN) and identify the cell type driving auditory dysfunction after hearing loss.
CN subregions and cell types were historically defined by histology alone; how they shift in gene expression with hearing loss was unresolved.
Spatial context preserves the CN's fine subregional layers (AVCN, PVCN, DCN), needed to link cell identity, location, and auditory-input-dependent expression.
Resolved 13 molecularly defined CN subregions across sagittal and coronal sections, refining classical histology.
Segmented 219,457 cells to distinguish Spp1+ and Sst+ bushy cell subtypes within intact tissue.
Quantified how hearing loss altered bushy cell–microglia proximity and intra-type spatial clustering.
Anchored spatial subregions to snRNA-seq- and snATAC-seq-defined transcriptomic and chromatin states.
Mapped spatial reorganization of cell types across P1–P45 development and multiple hearing-loss genotypes.
Built the first single-cell-resolution atlas of the mouse CN, defining 13 molecular subregions and 20 cell types.
Resolved Spp1+ and Sst+ bushy cell subtypes, corresponding to globular and spherical bushy cell identity.
Showed Spp1+ bushy cells were the primary cell type with transcriptomic and spatial changes after hearing loss.
Spp1 deletion delayed auditory brainstem response wave latencies and altered bushy cell synaptic physiology.
Found Spp1+ bushy cells cluster in the pAVCN, nominating it as a preferred site for brainstem implant stimulation.
Identified Nfe2l1 and Zbtb7a as candidate transcription factors regulating activity-dependent Spp1 expression via snATAC-seq.
TakeawayStereo-seq pinpointed Spp1+ bushy cells as the auditory-input-dependent cell type and therapeutic/implant target in the cochlear nucleus.
Characterize cellular and molecular changes in the canine brain during healthy ageing and canine cognitive dysfunction (CCD), a spontaneous large-animal model of Alzheimer's disease.
Ageing-related and AD-associated microglial states have largely been studied in isolation, with no single-cell spatial atlas of the ageing or CCD dog brain.
Spatial context localizes microglia–neuron interactions, such as complement-mediated synaptic pruning, within intact hippocampal and cortical architecture.
Profiled 620,344 spatial spots across prefrontal cortex, temporal cortex, hippocampus, and striatum.
Localized microglia to grey matter and oligodendrocytes to white matter within intact brain architecture.
Showed C1q-expressing microglia spatially adjacent to CRT-positive dentate gyrus granule cells.
Mapped a reduced proportion of SYN1-positive spatial spots in CCD hippocampus, confirming synapse loss in situ.
Enabled direct comparison of canine and human AD-risk gene expression across matched brain cell types.
Built a multiregional snRNA-seq atlas across newborn, adult, and aged dog brain, plus a CCD vs nonCCD comparison.
Identified ageing-related Micro MBP+ and Astro MBP+ subtypes that contribute to myelin synthesis.
Validated ZEB1 as a transcription factor driving oligodendrocyte differentiation, with expression declining with age.
Discovered microglial C1QA–CRT binding drives synaptic loss in canine CCD, confirmed via microglia–neuron co-culture.
Found microglial APP-metabolism activity was reduced in CCD versus elevated during normal ageing.
Showed broadly conserved cell type-specific and AD-risk gene expression between canine CCD and human Alzheimer's disease.
TakeawayStereo-seq localized microglia-driven synaptic pruning in a spontaneous large-animal Alzheimer's model, bridging mouse studies and human translation.
Develop a noninvasive, low-intensity focused ultrasound protocol to clear neurotoxic hemorrhagic debris from the CSF and brain interstitium after stroke.
Pharmacologic clearance therapies require invasive administration or carry systemic toxicity risks, and no approved therapy directly enhances intracranial fluid clearance.
Spatial context localizes neuroinflammatory and microglial-state changes to the perihematomal region, distinguishing on-target injury responses from off-target effects.
Localized inflammation and microglial gene scores specifically to the striatum–thalamus perihematomal region.
Distinguished UDC-driven, injury-specific gene expression changes from limited off-target effects in healthy control tissue.
Mapped glymphatic (Aqp4), microglial (Aif1, P2ry12), and inflammatory (Cd68, Lgals3) markers across intact brain sections.
Quantified UDC-driven gene downregulation specifically within the perihematoma versus unaffected brain regions.
Compared spatial transcriptomes across control, control+UDC, ICH, and ICH+UDC to confirm injury-specific correction of gene networks.
UDC reduced CSF/interstitial red blood cells and increased their clearance to deep cervical lymph nodes in SAH and ICH stroke models.
Reduced microglial and astrocytic activation and neuronal degeneration in both hemorrhage models.
Improved behavioral outcomes and survival (83% vs 50%) after ICH, outperforming a pharmacologic benchmark therapy.
UDC restored ICH perihematomal gene expression toward baseline, with minimal off-target changes in healthy brain tissue.
Met FDA mechanical-index safety guidelines, supporting a path to clinical translation.
Mechanosensitive ion channel blockade eliminated ultrasound's clearance effect, identifying channel activation as the primary mechanism.
TakeawayStereo-seq spatially confirmed that noninvasive ultrasound corrects injury-specific neuroinflammatory gene networks, supporting a nonpharmacologic therapeutic strategy for stroke.
Build a single-cell-resolution spatiotemporal transcriptomic atlas of the mouse brain following intracerebral hemorrhage (ICH) to map local and global cellular responses.
Prior ICH studies focused on individual molecules and could not capture the full complexity of cellular interactions in the perihematomal region over time.
Spatial context preserves cellular organization in and around the hematoma, revealing spatially graded gene-expression programs invisible to dissociated single-cell approaches.
Captured single-cell transcriptomes across 9 post-ICH time points, preserving native spatial organization of the lesion.
Used nuclear/perinuclear transcript segmentation to resolve individual cells within intact hematoma architecture.
Modeled gene expression as a function of distance from the lesion center, revealing distinct phagocytic, antioxidant, and repair zones.
Compared collagenase and autologous blood injection models and confirmed astrocyte markers in human postmortem ICH tissue.
Quantified ipsilateral vs. contralateral gene expression changes to map local and remote effects of ICH.
Mapped 3,342,277 single cells across 9 time points (3 h to 28 days), resolving 26 main cell types and 100 subclasses.
Identified 17 ICH-associated cell subclasses; by day 7 the lesion core was replaced by macrophages and glia within an astrocyte scar.
Discovered lipid-laden foam-cell-like macrophages and C3+ neurotoxic-like reactive astrocytes accumulating in perihematomal tissue.
Showed ICH activates a latent neurogenic program, converting some striatal astrocytes into Dcx+ neuroblasts.
Compared collagenase and autologous blood injection ICH models, finding largely shared but some model-specific gene programs.
Validated key reactive-astrocyte markers (PTX3, TGM1, C3) in human postmortem ICH brain tissue, confirming clinical relevance.
TakeawayStereo-seq built the first spatiotemporal single-cell atlas of ICH, revealing the lesion's cellular choreography and providing a resource for hemorrhagic stroke therapeutics.
Human blood-brain barrier (BBB) development during early corticogenesis.
BBB formation requires coordinated interactions among endothelial, mural, neural, and glial cells, but conventional approaches cannot resolve these developmental programs within intact tissue.
BBB maturation is governed by spatially organized cell-cell interactions and signaling niches that are lost after tissue dissociation.
Mapped BBB development across entire human cortex from GW6–GW21.
Resolved neurovascular-unit cell types within intact developing tissue architecture.
Reconstructed endothelial maturation directly within native spatial context.
Localized neural–vascular signaling niches driving BBB establishment.
Preserved spatial continuity across endothelial, mural, neural, and glial compartments.
Identified BBB transcriptional initiation at gestational week 8.
Revealed CDH2 signaling induces BBB transporter expression from neighboring neural cells.
Discovered neural progenitors spatially drive mural-cell proliferation through PDGFD.
Mapped progressive endothelial–mural communication during BBB maturation.
Demonstrated conserved BBB developmental programs between humans and mice.
Identified H2A.Z.1 as a master regulator of BBB maturation and transporter function.
TakeawayStereo-seq uncovered spatial mechanisms governing BBB maturation, enabling new therapeutic strategies for neurological diseases.
Define conserved and divergent hippocampal cytoarchitecture across rodents and primates.
Cross-species hippocampal organization cannot be resolved without spatial cellular context.
Preserve anatomical architecture to compare conserved circuits and species-specific cellular niches.
Mapped entire rodent and primate hippocampi within intact anatomical architecture.
Resolved hippocampal cell types while preserving native laminar organization.
Generated directly comparable spatial atlases across multiple mammalian species.
Localized species-specific neuronal and glial populations within discrete hippocampal niches.
Captured continuous molecular transitions across hippocampal subregions and cell lineages.
Revealed conserved hippocampal architecture across rodents and primates.
Identified primate-specific neuronal populations absent in rodents.
Discovered species-specific glial organization within hippocampal subregions.
Reconstructed evolutionary divergence of hippocampal cellular architecture.
Mapped conserved spatial gene programs across mammalian hippocampi.
Established a spatial reference atlas for translational neuroscience research.
TakeawayStereo-seq created the first cross-species spatial hippocampal atlas, accelerating translational neuroscience and brain disease research.
Primate cortical organization and the molecular principles governing regional specialization.
Brain-wide cortical architecture, developmental gradients, and connectivity cannot be resolved without preserving spatial context across the entire cortex.
Continuous molecular gradients, cortical boundaries, and long-range spatial relationships require intact whole-brain architecture rather than dissociated sequencing.
Captured continuous molecular landscapes across the entire primate cortex.
Resolved laminar organization while preserving native cortical anatomy.
Integrated serial sections into continuous three-dimensional cortical maps.
Identified subtle molecular transitions defining previously unrecognized cortical regions.
Reconstructed opposing molecular gradients across cortical development and connectivity.
Established the first multimodal whole-brain primate spatial transcriptomic atlas.
Discovered opposing molecular gradients organizing the entire primate cortex.
Reconciled competing theories of cortical expansion into one unified model.
Association cortex emerged at intersections of opposing molecular gradients.
Spatial molecular boundaries revealed previously unrecognized cortical subdivisions.
Cortical molecular gradients aligned with thalamic connectivity and gene expression.
TakeawayStereo-seq revealed the molecular blueprint underlying primate cortical organization.
Cellular organization and whole-brain connectivity of the macaque claustrum.
Claustral cell types, spatial zonation, and circuit organization remained unresolved due to its thin, heterogeneous anatomy.
Defining claustral functional zones requires preserving spatial organization together with molecular identity and anatomical connectivity.
Mapped molecular cell types while preserving native anatomical architecture.
Resolved discrete claustral domains with precise spatial boundaries.
Detected spatially restricted neuronal subtypes within thin claustrum tissue.
Integrated claustral organization with large-scale anatomical connectivity.
Linked molecular identity, spatial location, and functional projection patterns.
Established the first single-cell spatial and connectivity atlas of macaque claustrum.
Identified four molecularly distinct claustral functional zones.
Mapped 48 spatially organized claustral cell types.
Revealed glutamatergic neurons resemble deep-layer insular cortical neurons.
Linked claustral zones to functionally matched cortical networks.
Demonstrated widespread subcortical inputs converge onto the claustrum.
TakeawayStereo-seq revealed the spatial organization and connectivity blueprint of the macaque claustrum, enabling functional circuit mapping.
Whole-brain molecular and cellular architecture underlying brain function and development.
Brain complexity requires genome-wide, single-cell spatial mapping across intact brain structures.
Brain organization depends on spatial cell relationships, regional gradients, and preserved tissue architecture.
Generated a continuous whole-brain atlas at single-cell resolution across 123 intact brain sections.
Captured 29,655 genes without targeted panels, enabling unbiased molecular brain characterization.
Resolved fine anatomical subregions through transcriptome-based spatial organization beyond conventional atlases.
Identified region-specific cell populations and molecular programs across the entire brain.
Mapped continuous developmental regulatory programs from embryonic to adult brain.
Generated the first genome-wide single-cell spatial atlas of the entire mouse brain.
Resolved 308 spatially organized cell clusters across over four million cells.
Discovered previously unrecognized molecular brain subregions through transcriptomic parcellation.
Mapped developmental transcription factor programs across space and time.
Identified hundreds of region-specific lncRNAs with developmental regulatory potential.
Created a comprehensive reference atlas for neuroscience and neurological disease research.
TakeawayStereo-seq redefined brain organization through whole-brain, single-cell, genome-wide spatial mapping.
Build a comprehensive single-cell spatial atlas of the human cerebral cortex across functional regions.
Neural cell diversity, laminar organization, and regional architecture cannot be simultaneously resolved across the entire cortex.
Cortical function depends on continuous spatial organization, laminar context, and cell-cell proximity that dissociated methods lose.
Mapped nearly 1.9 million cells across 14 human cortical regions while preserving intact architecture.
Resolved uninterrupted laminar organization and transcriptomic continuity across the entire cortex.
Captured region-specific neuronal populations and sparse cortical cell niches impossible to resolve with dissociated methods.
Mapped layer-specific cell-cell interactions and neuron-glia communication directly in situ.
Connected spatial cell organization with cortical functions across multiple human brain regions.
First comprehensive single-cell spatial atlas spanning 14 human cortical regions.
Continuous laminar organization defines molecular architecture across the human cortex.
Distinct superficial and deep SST neuronal families occupy separate spatial niches.
Regional neuronal gradients reveal functional specialization across neighboring cortical areas.
Spatial interaction networks uncover region-specific neuron-glia communication programs.
Brain-wide cellular architecture provides a reference for neurological disease research.
TakeawayStereo-seq revealed the spatial architecture governing human cortical organization and function.
Why neuroscience researchers choose Stereo-seq?
Four capabilities support discovery across neural cell biology, disease research, translational neuroscience and reference-atlas development.
Tissue-scale spatial biology
Profile intact brain regions and whole-brain architectures while preserving relationships among neurons, glia, vasculature and immune cells.
Single-cell resolution discovery
Resolve diverse neural populations, rare cell states, disease-associated niches and spatially organized gene-expression programs.
Translational neuroscience
Discover biomarkers, validate therapeutic mechanisms and compare preclinical models with human neurological disease.
Reference atlases & systems neuroscience
Build foundational brain maps that connect molecular identity, anatomical regions and neural connectivity across species.