Beth Stevens

The paper compares microglia-targeted AAVs, finding that capsid choice affects in vitro efficiency but not in vivo transduction when using specific promoters.

This study develops a behavioral platform to study decision making in marmosets and finds that reward predictability influences behavioral states and error correction during task performance.

The paper develops a method to generate functional induced astrocytes (iAstrocytes) from human pluripotent stem cells and shows their role in promoting synchronized neuronal network activity.

This study identifies brain macrophages in the African turquoise killifish that engulf brain extracellular material, showing age-related decline in engulfment capacity.

The paper introduces Synapse-seq, a method to link transcriptomes to synaptic architecture by using protein-guided RNA barcoding, revealing new insights into neural connectivity and cell type-specific dendritic structures.

This study generates and characterizes human brain border-associated macrophages (BAMs) using iPSC-derived models, showing a conserved hyper-endocytic phenotype across species.

This study identifies brain border-associated macrophages (BAMs) as rhythmic cells regulated by the circadian clock, showing that their endocytic activity and amyloid-beta uptake are disrupted with age and in a mouse model of Alzheimer's disease.

This study investigates Akap11 mutant mice to explore the neurobiological effects of AKAP11 loss, finding increased PKA activity and transcriptomic changes linked to schizophrenia and bipolar disorder.

This study identifies the murine dura mater as a transient niche for early-postnatal B lymphopoiesis, highlighting the role of CXCL12-expressing fibroblasts in supporting B cell development.

This study shows that GPR34 maintains microglial homeostasis and limits disease-associated microglial responses in Alzheimer's disease models.

This study uses heterochronic myeloid cell replacement to show that the local brain environment, not intrinsic factors, drives microglia aging.

The paper identifies CD72 as a regulator of microglial tiling through proteomic profiling and functional assays.

This study uses spatial transcriptomics and single-nucleus RNA-seq to analyze remyelination dynamics, identifying an interferon-responsive glial state that coordinates immune infiltration and oligodendrocyte differentiation.

This study shows that SORL1 deficiency in human microglia leads to lysosomal dysfunction, including impaired degradation and enzyme activity, contributing to Alzheimer's disease pathogenesis.

CSF YWHAG:NPTX2 synapse protein ratio, from proteomics of 3,416 individuals across six cohorts, explains cognitive impairment beyond amyloid and tau and predicts decline (hazard ratio 15.4).

The paper identifies a unique population of regulatory T cells in the murine meninges that maintain brain homeostasis by suppressing interferon-gamma-producing lymphocytes and preventing hippocampal damage.

This study examines how early Alzheimer's disease-related pathology affects synaptic transmission and morphology in human cortical neurons using biopsies from patients with idiopathic normal pressure hydrocephalus.

This study investigates how lysosomal dysfunction in microglia drives epigenetic and transcriptional changes in a mouse model of Sanfilippo syndrome, revealing shared mechanisms with Alzheimer's disease.

This paper develops an iPSC platform to rapidly generate alpha-synuclein inclusions and investigates their formation, subtypes, and molecular interactions.

The paper identifies cell type-specific molecular changes in ALS patients, showing enrichment of genetic risk factors in extratelencephalic neurons and altered responses in oligodendrocytes and microglia.

This study shows that frontal cortical circuits in mice continue to mature beyond sexual maturity, affecting decision-making behaviors with age.

The paper investigates the role of CSMD1 in opposing the complement cascade in neural tissues and links its dysfunction to schizophrenia risk.

This paper develops a platform to model and manipulate human microglial states in vitro using single-cell RNA sequencing and genetic tools, identifying disease-associated transcriptional signatures.

The paper identifies a transient hyperactive neuronal state in early Alzheimer's disease using single-nucleus transcriptomics from living patients.

Microglia selectively engulf synapses in Alzheimer-like mouse brains via PtdSer-TREM2 signaling.

The paper shows enzymatic dissociation causes gene expression changes in microglia and proposes a protocol to reduce these artifacts in scRNA-seq.

This study shows that microglia and complement proteins drive early synapse loss and cognitive deficits in Huntington's disease by eliminating corticostriatal synapses, and that targeting this pathway can prevent these effects.

The paper profiles gene expression in human microglia from 141 patients, identifies population shifts in acute brain injury, maps eQTLs, and fine-maps Alzheimer's risk variants using hIPSC-derived macrophages.

This study shows that deleting Presenilin 1 in microglia during development enhances memory and neuronal activity in mice, with effects dependent on GluN2B and mitigating Alzheimer's symptoms.

This study identifies phosphatidylserine (PS) as a neuronal signal that marks synapses for elimination by microglia during development.