Biology subjects

Maynard, K. R.

Publications and source records attributed to Maynard, K. R..

At least 19 recordsLinked to original sources

bioRxiv2026

Overlapping yet distinct spatiomolecular profiles across mood disorders and biological sex in the human prefrontal cortex

Major depressive disorder (MDD) and bipolar disorder (BD) exhibit both overlapping and distinct clinical features, including sex differences in prevalence and symptomatology, but how these similarities and differences are reflected at the molecular and cellular level in the human brain remains poorly understood. Here, we applied spatial transcriptomics to the human dorsolateral prefrontal cortex from individuals with MDD, BD, and neurotypical controls to resolve molecular programs associated with diagnosis and biological sex. Our analysis revealed sex- and diagnosis-specific differences across white matter, the neurovascular unit (NVU), and neuronal compartments. Within white matter, we identified female-specific survival-response programs shared in both MDD and BD, and divergent myelin-related gene expression patterns across disorders (CLDN11, CNDP1). Within the NVU, transcriptional evidence of impaired vascular integrity was accompanied by astrocytic response profiles in females with MDD and males with BD, with inflammatory responses further evident in females with MDD (IFITM3, CEBPD, IL1R1). In donors with BD of both sexes and in females with MDD, inhibitory neurons exhibited impaired neuropeptide expression (SST, CORT, CRH). Integration with donor genotype information highlighted that genetic risk for mood disorders influences MAPK3 expression, implicating altered ERK signaling, which was further supported by disorder-associated changes in Ras/MEK/ERK pathway components in neurons (MAPK3, DUSP6, RASD1, ELK1). Together, these findings reveal coordinated, cell type- and spatial domain-specific molecular programs that distinguish shared and disorder-specific transcriptomic changes across mood disorders in a sex-dependent manner.

neuroscience↗

bioRxiv2026

Multi-omic spatial mapping of the human habenula defines the molecular and anatomical organization of medial and lateral subregions

The habenula (Hb) is a small epithalamic midline structure critical for reward processing and mood regulation that is implicated in many complex brain disorders, including depression and addiction. The molecular anatomy of the Hb has been well-characterized in model organisms, but little is known about its organization in the human brain, including the transcriptomic and epigenetic signatures of spatially-organized lateral (LHb) and medial (MHb) cell types. Here, we generated a high resolution spatiomolecular map of the human Hb using both multiomic single nucleus sequencing (snMultiome) and spatially-resolved transcriptomics. We measured gene expression and chromatin accessibility across 4 MHb and 5 LHb neuronal cell types as defined by transcriptomic conservation with rodents and zebrafish. We identified cell type-specific molecular specializations related to GABAergic and glutamatergic signaling as well as regulatory relationships between open chromatin regions, transcription factors, and target genes associated with depression and addiction. High resolution spatial transcriptomics identified the anatomical location of heterogeneous LHb subpopulations, including two putative inhibitory populations in the LHb. We further characterized cell-type relationships between Hb neurons and glial subtypes and predicted ligand-receptor interactions between LHb and MHb neurons. Finally, we delineated Hb cell types and spatial domains enriched in genes associated with genetic risk for psychiatric disorders, identifying the strongest enrichment in the MHb. Collectively, the generated data and analyses resolve the spatiomolecular organization of the human Hb and identify molecular-genetic associations with neuropsychiatric disease.

neuroscience↗

bioRxiv2026

Three dimensional reconstruction of the human nucleus accumbens reveals topographic organization and molecular heterogeneity of D1-islands across the anterior posterior axis

Spatial transcriptomics has transformed molecular characterization of the human brain, but most studies profile individual two-dimensional tissue sections and therefore cannot capture molecular organization across 3D neuroanatomical axes. Here, we developed a spatial genomics framework to reconstruct the 3D cellular architecture of the human nucleus accumbens (NAc) by densely sampling and aligning serial sections across its anterior-posterior (AP) extent. Combining single-cell Xenium profiling with near-transcriptome-wide VisiumHD, we mapped cell type composition and topography across AP, mediolateral and dorsoventral axes. Neuronal populations varied in relative abundance across the AP axis while maintaining characteristic spatial topographies. These differences were particularly pronounced among D1-islands, a topographically organized structure within the NAc in which transcriptionally distinct subpopulations of DRD1-expressing medium spiny neurons (MSNs) aggregate into discrete cellular formations. D1-islands comprised two molecularly distinct spatial domains with conserved counterparts across species. Both domains varied in relative abundance across the AP axis, but demonstrated distinct 3D distribution; one was present throughout the NAc, whereas the other, corresponding to islands of Calleja (ICj), was more restricted to intermediate-to-posterior levels. Local spatial analyses revealed region- and AP-dependent cellular relationships, including segregation of the two island populations despite their anatomical proximity. Together, these findings establish a framework for three dimensional spatial genomics of human brain tissue and reveal molecular and cellular organization not captured by individual tissue sections.

neuroscience↗

bioRxiv2026

Multiscale spatial transcriptomics resolves the cellular and molecular architecture of the human amygdala

The amygdala is a central hub for emotional learning that is dysregulated across numerous psychiatric disorders, yet its molecular architecture in humans remains poorly defined. We here present a spatial transcriptomic atlas of the human amygdala from nine neurotypical donors. Integrating Visium, Xenium, and VisiumHD technologies, we profiled over 1.1 million cells across 13 spatial domains spanning the basolateral complex, central, medial, and cortical nuclei, as well as the intercalated islands, each defined by distinct marker genes and gene co-expression networks. By integrating snRNA-seq reference atlases, we found that each subdivision of the basolateral subnucleus contains distinct excitatory neuron classes. We additionally found three transcriptionally distinct populations of intercalated neuron types, two of which form spatially distinct islands neighboring the basolateral complex, and were able to refine cell type diversity across the central nucleus and related amygdalostriatal transition areas. Finally, we localized psychiatric genetic risk across the amygdala, revealing both broad neuronal enrichment and subnuclear specificity. Together, this atlas provides a foundational resource and framework for accelerating cross-species comparisons and human disease-focused investigations.

neuroscience↗

bioRxiv2026

Perturbation of genes linked to common schizophrenia risk variants identifies cilia programs

Schizophrenia (SCZ) is a common psychiatric disorder characterized by psychosis, emotional withdrawal, and cognitive deficits. Most SCZ risk variants reside in non-coding regions of the genome and are thought to influence disease risk by modulating gene regulation. However, the target genes, biological pathways, and cell types through which these variants exert their effects remain poorly understood. To address this gap, we employed in vivo CRISPR droplet sequencing (CROP-seq) in the postnatal mouse neocortex. We perturbed 12 SCZ risk genes previously linked to functionally validated risk variants, followed by single-cell RNA sequencing. We identified 3,031 differentially expressed genes (DEGs) that recapitulate transcriptional alterations observed in postmortem SCZ brains. Integrative analysis using DEG clustering, factor analysis, and gene regulatory network inference uncovered convergent gene programs with distinct biological functions and cell type specificity. Notably, ciliary transcriptional programs consistently emerged across analytical frameworks. The primary cilium is a neurocircuit modulating signaling organelle in neurons and glia that remains understudied in SCZ. Perturbation of key contributors to the ciliary transcriptional programs led to significant alterations in ciliary structure, suggesting that SCZ genetic risk factors may influence how brain cells sense and transduce extracellular signals through synapse-independent mechanisms. Together, this study provides the first in vivo characterization of the functional consequence of common variant architecture in SCZ and implicates ciliary dysfunction as a convergent downstream mechanism.

neuroscience↗

bioRxiv2026

Mapping spatially organized molecular and genetic signatures of schizophrenia across multiple scales in human prefrontal cortex

The dorsolateral prefrontal cortex (dlPFC) is central to cognitive dysfunction in schizophrenia (SCZ), yet how molecular changes are organized across cortex remains unclear. Here, we applied complementary spatial transcriptomic approaches spanning laminar domains, microenvironments, and cell types in postmortem human dlPFC. At the laminar level, SCZ-associated transcriptional changes were strongest in glia-enriched domains (layer 1/meninges and white matter), including down-regulation of microglia-associated genes, whereas genetic risk localized to neuronal-rich gray matter. We next analyzed SCZ-linked microenvironments including neuropil, neuronal, perineuronal net, and vascular compartments. Within these, neuronal and synaptic transcriptional changes were most prominent in neuropil, showing down-regulation of activity-dependent synaptic genes and inhibitory neuron markers. At the cellular level, these signals reflected intrinsic alterations localized to cell types. Across analyses, patterns converged on altered BDNF-TrkB signaling and inhibitory circuit dysfunction. Together, our findings highlight spatial scale as a key determinant in resolving neuronal and non-neuronal aspects of SCZ-associated biology.

neuroscience↗

bioRxiv2025

spaTransfer: transfer learning for single-cell and spatialtranscriptomics data using non-negative matrix factorization

Recent advances in spatially-resolved transcriptomics have enabled profiling of gene expression in a spatial context, which has led to the generation of large-scale single-cell and spatial atlases with computationally-derived cell type or spatial domain labels. An increasingly important task with these data has become the transfer of cell type or spatial domain annotations from a given reference (or source) atlas into a new target tissue or sample. The reference and target datasets could be at different resolutions or measured on different experimental platforms. Here, we present a method to perform cross-platform transfer learning that takes as input single-cell or spatial domain labels from a reference atlas or dataset and transfers the labels to a target dataset at a similar or different resolution. Specifically, we use non-negative matrix factorization (NMF) on the reference data to identify factors associated with labels of interest and project these factors into the target dataset to label each new observation. We use a multinomial model with the factors as covariates and labels as the response to predict labels in the target dataset. In contrast to existing approaches, the advantage of our approach is interpretability, without compromising on accuracy. We demonstrate the performance of the method in two human brain tissues and show that our model identifies spatially coherent domains in the target datasets with concordance of marker gene expression. We implement spaTransfer in open-source software as an R package (github.com/cindyfang70/spaTransfer).

bioinformatics↗

bioRxiv2025

Transcriptional response to chronic long-access fentanyl self-administration in rat habenula and amygdala

Fentanyl is a potent synthetic opioid associated with overdose. However, little is known about fentanyl-induced molecular adaptations in the habenula and amygdala, two brain regions implicated in opioid use and withdrawal. We performed bulk RNA-sequencing in the rat habenula and amygdala to identify transcriptomic changes associated with fentanyl intake. Rats self-administered intravenous saline or fentanyl over 22-24 days. Ninety minutes following the final session, brains were collected for transcriptomic profiling. In Hb, we identified 453 differentially expressed genes (DEGs) between saline and fentanyl rats, with upregulated genes associated with synaptic transmission and ionic conductance. In amygdala, we identified 3,041 fentanyl-associated DEGs with upregulated genes implicated in metabolic and vesicular functions. Downregulated genes in both regions were enriched for extracellular matrix functions. Integration of DEGs with single-cell RNA-sequencing data from rodents and humans revealed that fentanyl DEGs were enriched in specific habenula and amygdala cell type markers. Furthermore, fentanyl downregulated DEGs in amygdala were enriched in genes associated with risk for substance use disorders. Together, we define how fentanyl intake alters transcriptional programs in the rat habenula and amygdala, and we link these changes to specific human cell types and risk genes for neuropsychiatric disorders and addiction.

neuroscience↗

bioRxiv2025

Orchestrating Spatial Transcriptomics Analysis with Bioconductor

Spatial transcriptomics technologies provide spatially-resolved measurements of gene expression through assays that can either target selected genes or capture transcriptome-wide expression profiles. The complexity and variability of these technologies and their associated data necessitate multi-step workflows integrating diverse computational methods and software packages. We provide a freely accessible, open-source, continuously updated and tested online book containing reproducible code examples, datasets, and discussion about data analysis workflows for spatial omics data using Bioconductor in R, including interoperability with Python.

bioinformatics↗

bioRxiv2025

APOE E4 Alzheimer's Risk Converges on an Oligodendrocyte Subtype in the Human Entorhinal Cortex

The entorhinal cortex (ERC) is implicated in early progression of Alzheimers disease (AD). Here we investigated the impact of established biological risk factors for AD, including APOE genotype (E2 versus E4 alleles), sex, and ancestry, on gene expression in the human ERC. We generated paired spatially-resolved transcriptomics (SRT) and single-nucleus RNA sequencing data (snRNA-seq) in postmortem human ERC tissue from middle aged brain donors with no history of AD. APOE-dependent changes in gene expression predominantly mapped to a transcriptionally-defined oligodendrocyte subtype, which varied substantially with ancestry, and suggested differences in oligodendrocyte differentiation and myelination. Integration of SRT and snRNA-seq data identified a common gene expression signature associated with APOE genotype, which we localized to the same oligodendrocyte subtype and a white matter spatial domain. This suggests that AD risk in ERC may be associated with disrupted oligodendrocyte function, potentially contributing to future neurodegeneration. Lay SummaryAlzheimers disease (AD) is a neurodegenerative disorder that accounts for 60-80% dementia cases. Apolipoprotein E (APOE) genotype is the strongest genetic risk factor for AD, and the entorhinal cortex (ERC) is a brain region implicated in its earliest progression. Our study investigated how APOE genotype impacts gene expression in the ERC. We identified genotype-dependent effects on oligodendrocytes with different transcriptional profiles related to maturation that may help explain how APOE genotype mediates its effects on AD risk.

neuroscience↗

bioRxiv2025

Impact of Alzheimer's disease risk factors and local neuromelanin content on the transcriptomic landscape of the human locus coeruleus

The locus coeruleus (LC) is a small noradrenergic nucleus in the dorsal pons that sends projections across the brain regulating sleep, arousal, attention, stress responses, and some forms of cognition. LC neurons show pathology in the earliest stages of Alzheimers disease (AD), including age-related accumulation of hyperphosphorylated tau (pTau) and accelerated loss of neuromelanin (NM) pigmentation. NM-sensitive neuroimaging of the LC predicts previous cognitive decline, clinical severity, and future AD progression. While these findings suggest that the LC plays an etiologic role in AD, the molecular landscape of the LC prior to clinical manifestation of sporadic AD remains largely uncharacterized. This information is critical for developing interventions that preserve LC integrity and function. We performed spatially-resolved transcriptomics on 85 sections of human postmortem LC from N=33 neurotypical middle-aged donors, balanced for epidemiologic AD risk factors including sex, African or European ancestry, and APOE genotype (carriers of the E4/risk or E2/protective alleles). Comparing across APOE genotypes, we find astrocytic gene expression differences proximal to LC neurons. Associating NM content with local gene expression, we show that higher overall APOE gene expression correlates with reduced NM content and an enrichment of NM-associated genes in aging pathways. Unexpectedly, we find enriched LC expression of cholesterol synthesis genes, alongside evidence for lipid synthesis gene regulatory network activity in NM-containing LC specifically, revealing a potential intersection between intrinsic lipid metabolism in LC neurons, NM, and the role of APOE-mediated lipid biology in AD. Together, these data illuminate the molecular features of the human LC at spatial resolution with unprecedented sampling depth, revealing how AD risk factors and NM content influence resilience and susceptibility of this critical brain nucleus to pathology accumulation and degeneration.

neuroscience↗

bioRxiv2025

Spatio-molecular gene expression reflects dorsal anterior cingulate cortex structure and function in the human brain

In the human brain, the dorsal anterior cingulate cortex (dACC) plays key roles in various components of cognitive control, and is particularly relevant for reward processing and conflict monitoring. The dACC regulates expression of fear and pain, and its dysfunction is implicated in a number of neuropsychiatric disorders. Compared to more recently specialized neocortical areas, such as the dorsolateral prefrontal cortex (dlPFC), the dACC is evolutionarily older. The regions agranular structure, and other evolutionary specializations, such as the presence of von Economo neurons (VENs), contribute to its specialized roles in cognitive and emotional processing. Here, we generated paired spatially-resolved transcriptomics (SRT) and single-nucleus RNA-sequencing (snRNA-seq) data from adjacent tissue sections of the dACC in ten adult neurotypical donors to define molecular profiles for dACC cell types and spatial domains. Using non-negative matrix factorization (NMF), we integrated these data by identifying gene expression patterns within the snRNA-seq data, which were projected onto the SRT data to infer the spatial localization. Combining these data with publicly available resources, we revealed insights about molecular profiles, spatial topography, enrichment of disease risk, and putative connectivity of spatially-localized dACC cell types, including VENs. Utilizing published dlPFC snRNA-seq and SRT data collected in the same neurotypical brain donors used here, we deployed cross-region comparison analyses between dACC and dlPFC to understand spatio-molecular specializations and laminar organization across human brain evolution. To make this comprehensive molecular resource accessible to the scientific community, we made both raw and processed data freely available, including through interactive web applications.

neuroscience↗

bioRxiv2024

Spatially-resolved molecular sex differences at single cell resolution in the adult human hypothalamus

The hypothalamus contains multiple regions, including the ventromedial hypothalamus (VMH) and arcuate (ARC), which are responsible for sex-differentiated functions such as endocrine signaling, metabolism, and reproductive behaviors. While molecular, anatomic, and sex-differentiated features of rodent hypothalamus are well-established, much less is known about these regions in humans. Here we provide a spatially-resolved single cell atlas of sex-differentially expressed (sex-DE) genes in human VMH and ARC. We identify neuronal populations governing hypothalamus-specific functions, define their spatial distributions, and show increased retinoid pathway gene expression compared to rodents. Within VMH and ARC, we find correlated autosomal expression differences localized to ESR1/TAC3-expressing and CRHR2-expressing neurons, and extensive sex-DE of genes linked to sex-biased disorders including autism, depression, and schizophrenia. Our molecular mapping of disease associations to hypothalamic cell types with established roles in sex-divergent physiology and behavior provides insights into mechanistic bases of sex bias in neurodevelopmental and neuropsychiatric disorders.

genomics↗

bioRxiv2024

Molecular impact of nicotine and smoking exposure on the developing and adult mouse brain

Maternal smoking during pregnancy (MSDP) is associated with significant cognitive and behavioral effects on offspring. While neurodevelopmental outcomes have been studied for prenatal exposure to nicotine, the main psychoactive component of cigarette smoke, its contribution to MSDP effects has never been explored. Comparing the effects of these substances on molecular signaling in the prenatal and adult brain may provide insights into nicotinic and broader tobacco consequences that are developmental-stage specific or age-independent. Pregnant mice were administered nicotine or exposed to chronic cigarette smoke, and RNA-sequencing was performed on frontal cortices of postnatal day 0 pups born to these mice, as well as on frontal cortices and blood of the adult dams. We identified 1,010 and 4,165 differentially expressed genes (DEGs) in nicotine and smoking-exposed pup brains, respectively (FDR<0.05, Ns = 19 nicotine-exposed vs 23 vehicle-exposed; 46 smoking-exposed vs 49 controls). Prenatal nicotine exposure (PNE) alone was related to dopaminergic synapses and long-term synaptic depression, whereas MSDP was associated with the SNARE complex and vesicle transport. Both substances affected SMN-Sm protein complexes and postsynaptic endosomes. Analyses at the transcript, exon, and exon-exon junction levels supported gene level results and revealed additional smoking-affected processes. No DEGs at FDR<0.05 were found in adult mouse brain for any substance (12 nicotine-administered vs 11 vehicle-administered; 12 smoking-exposed vs 12 controls), nor in adult blood (12 smoking-exposed vs 12 controls), and only 3% and 6.41% of the DEGs in smoking-exposed pup brain replicated in smoking-exposed blood and human prenatal brain, respectively. Together, these results demonstrate variable but overlapping molecular effects of PNE and MSDP on the developing brain, and attenuated effects of both smoking and nicotine on adult versus fetal brain.

neuroscience↗

bioRxiv2024

Reelin marks cocaine-activated striatal ensembles, promotes neuronal excitability, and regulates cocaine reward

Drugs of abuse activate defined neuronal ensembles in brain reward structures such as the nucleus accumbens (NAc), which are thought to promote the enduring synaptic, circuit, and behavioral consequences of drug exposure. While the molecular and cellular effects arising from experience with drugs like cocaine are increasingly well understood, the mechanisms that sculpt NAc ensemble participation are largely unknown. Here, we leveraged unbiased single-nucleus transcriptional profiling to identify expression of the secreted glycoprotein Reelin (encoded by the Reln gene) as a marker of cocaine-activated neuronal ensembles within the rat NAc. Multiplexed in situ detection confirmed selective expression of the immediate early gene Fos in Reln+ neurons after cocaine experience, and also revealed enrichment of Reln mRNA in Drd1+ medium spiny neurons (MSNs) in both the rat and human brain. Using a novel CRISPR interference strategy enabling selective Reln knockdown in the adult NAc, we observed altered expression of genes linked to calcium signaling, emergence of a transcriptional trajectory consistent with loss of cocaine sensitivity, and a striking decrease in MSN intrinsic excitability. At the behavioral level, loss of Reln prevented cocaine locomotor sensitization, abolished cocaine place preference memory, and decreased cocaine self-administration behavior. Together, these results identify Reelin as a critical mechanistic link between ensemble participation and cocaine-induced behavioral adaptations.

neuroscience↗

bioRxiv2024

An integrated single-nucleus and spatial transcriptomics atlas reveals the molecular landscape of the human hippocampus

The hippocampus contains many unique cell types, which serve the structures specialized functions, including learning, memory and cognition. These cells have distinct spatial organization, morphology, physiology, and connectivity, highlighting the importance of transcriptome-wide profiling strategies that retain cytoarchitectural organization. Here, we generated spatially-resolved transcriptomics (SRT) and single-nucleus RNA-sequencing (snRNA-seq) data from adjacent tissue sections of the anterior human hippocampus in ten adult neurotypical donors to define molecular profiles for hippocampal cell types and spatial domains. Using non-negative matrix factorization (NMF) and label transfer, we integrated these data by defining gene expression patterns within the snRNA-seq data and inferring their expression in the SRT data. We identified NMF patterns that captured transcriptional variation across neuronal cell types and indicated that the response of excitatory and inhibitory postsynaptic specializations were prioritized in different SRT spatial domains. We used the NMF and label transfer approach to leverage existing rodent datasets, identifying patterns of activity-dependent transcription and subpopulations of dentate gyrus granule cells in our SRT dataset that may be predisposed to participate in learning and memory ensembles. Finally, we characterized the spatial organization of NMF patterns corresponding to non-cornu ammonis pyramidal neurons and identified snRNA-seq clusters mapping to distinct regions of the retrohippocampus, to three subiculum layers, and to a population of presubiculum neurons. To make this comprehensive molecular atlas accessible to the scientific community, both raw and processed data are freely available, including through interactive web applications.

neuroscience↗

bioRxiv2024

lute: estimating the cell composition of heterogeneous tissue with varying cell sizes using gene expression

Relative cell type fraction estimates in bulk RNA-sequencing data are important to control for cell composition differences across heterogenous tissue samples. Current computational tools estimate relative RNA abundances rather than cell type proportions in tissues with varying cell sizes, leading to biased estimates. We present lute, a computational tool to accurately deconvolute cell types with varying sizes. Our software wraps existing deconvolution algorithms in a standardized framework. Using simulated and real datasets, we demonstrate how lute adjusts for differences in cell sizes to improve the accuracy of cell composition. Software is available from https://bioconductor.org/packages/lute.

bioinformatics↗

bioRxiv2024

Transcriptomic analysis of the human habenula in schizophrenia

Pathophysiology of many neuropsychiatric disorders, including schizophrenia (SCZD), is linked to habenula (Hb) function. While pharmacotherapies and deep brain stimulation targeting the Hb are emerging as promising therapeutic treatments, little is known about the cell type-specific transcriptomic organization of the human Hb or how it is altered in SCZD. Here we define the molecular neuroanatomy of the human Hb and identify transcriptomic changes in individuals with SCZD compared to neurotypical controls. Utilizing Hb-enriched postmortem human brain tissue, we performed single nucleus RNA-sequencing (snRNA-seq; n=7 neurotypical donors) and identified 17 molecularly defined Hb cell types across 16,437 nuclei, including 3 medial and 7 lateral Hb populations, several of which were conserved between rodents and humans. Single molecule fluorescent in situ hybridization (smFISH; n=3 neurotypical donors) validated snRNA-seq Hb cell types and mapped their spatial locations. Bulk RNA-sequencing and cell type deconvolution in Hb-enriched tissue from 35 individuals with SCZD and 33 neurotypical controls yielded 45 SCZD-associated differentially expressed genes (DEGs, FDR < 0.05), with 32 (71%) unique to Hb-enriched tissue. eQTL analysis identified 717 independent SNP-gene pairs (FDR < 0.05), where either the SNP is a SCZD risk variant (16 pairs) or the gene is a SCZD DEG (7 pairs). eQTL and SCZD risk colocalization analysis identified 16 colocalized genes. These results identify topographically organized cell types with distinct molecular signatures in the human Hb and demonstrate unique genetic changes associated with SCZD, thereby providing novel molecular insights into the role of Hb in neuropsychiatric disorders. One Sentence SummaryTranscriptomic analysis of the human habenula and identification of molecular changes associated with schizophrenia risk and illness state.

neuroscience↗