Rachel E. Bennett

The paper uses subcellular spatial transcriptomics to identify why some neurons in Alzheimer's disease accumulate tau while others resist it, finding differences in molecular programs and neuron-glia interactions.

This study examines depth-dependent changes in cerebral oxygenation in Alzheimer's disease models, finding that tau disrupts oxygen levels and that neuronal loss is not due to local hypoxia.

This study develops a method to isolate and profile membrane lipids of vulnerable and resilient neurons to investigate their differential responses to oxidative stress.

The paper uses single-nucleus RNA-seq to analyze cerebrovascular transcriptomic changes in Alzheimer's Disease and primary tauopathies, identifying shared heat-shock responses and disease-specific vascular remodeling.

This study shows that tau accumulation leads to neuronal silencing and network dysfunction in the hippocampal formation without neuron loss, contributing to progressive network disruption.

This study identifies molecular changes in white matter hyperintensities in Alzheimer's disease using transcriptomic analysis of brain regions and blood vessels.

The paper identifies an AAV capsid, MC5, that efficiently and specifically transduces microglia via direct and intracerebroventricular injection in mice.

The paper shows tau accumulates around blood vessels in Alzheimer's disease brains and is linked to tau tangle pathology.

The paper analyzes endothelial cell heterogeneity across brain regions in Alzheimer's disease using single nucleus RNAseq, revealing region-specific gene expression changes and disease-related transcriptomic alterations.

This study uses single-nucleus RNA-sequencing to analyze astrocyte transcriptomic changes across the spatiotemporal progression of Alzheimer's disease, revealing gene expression trajectories and heterogeneity.