Sally Temple

This paper identifies APOE-ϵ4-induced fibronectin accumulation at the blood-brain barrier as a key mediator of astrocyte-endothelial dysfunction in Alzheimer's disease, highlighting it as a potential therapeutic target.

This study shows that pathogenic MAPT mutations impair microglial lysosomal and autophagic functions, affecting tau clearance and degradative capacity.

The paper characterizes 85 MAPT mutation-bearing iPSC lines using multiomic approaches, revealing cellular diversity and factors influencing organoid development.

The paper compares single-cell transcriptomic and surface protein profiles of RPESC-RPE and PSC-RPE, finding differences in gene expression and surface markers that suggest functional and immunomodulatory differences.

This study shows that inosine misincorporation into mRNA activates the integrated stress response and an innate immune gene expression signature, linking ITPase deficiency to cellular stress.

Discovery of SMCs that correct MAPT splicing, reduce 4R tau, and rescue pathology in patient-derived neuronal and in vivo models of 4R tauopathies.

This paper integrates 36 single-cell transcriptomics datasets from human neural organoids into a unified atlas to assess cell type coverage and compare organoid protocols with primary brain tissue.

The paper develops fully human bifunctional anti-tau intrabodies that reduce intracellular tau and improve neuronal survival in disease-associated mutations.

The paper analyzes regional and age-related differences in adult mouse leptomeninges using snucRNA-seq, revealing gene expression patterns linked to mental disorders.

The paper develops a scalable cortical organoid platform with quality control metrics and identifies early dysregulation of phosphatase and prefoldin genes in FTD-tau neurons.

The paper uses single-cell RNA sequencing to identify immune cell populations and interactions in mouse spinal cord injury, revealing microglial and B cell heterogeneity and crosstalk.

This study shows that caspase inhibition reduces tau cleavage and neurotoxicity in iPSC-derived neurons with the V337M MAPT mutation.

This study shows that glutamatergic dysfunction occurs before neuron loss in cerebral organoids with MAPT mutations, suggesting therapeutic targets for FTD.

The paper extends the RiboTag system for cell-type specific RNA depletion in vitro, showing variable efficiency across replicates.