Frances K. Wiseman

The paper develops an automated pipeline using machine learning to analyze mouse olfactory habituation-dishabituation behavior, achieving high accuracy comparable to manual methods.

The paper compares proteome and transcriptome changes in DSAD brains to AD and healthy controls, finding elevated APOE in specific cell types.

The paper investigates the effect of reducing Cystatin B on Cathepsin B activity in trisomy 21 models, finding increased activity in disomic controls but not in trisomy 21 conditions.

SynPull combines single-molecule pulldown, super-resolution microscopy, and computational analysis to study protein aggregates in synaptosomes from human and mouse samples, revealing AT8-positive tau as the predominant aggregate in Alzheimer's disease.

The paper uses long-read RNA-seq to study splicing changes in an Alzheimer's mouse model, identifying novel transcript isoforms and alternative splicing events in response to amyloid-beta.

The paper investigates the impact of elevated cystatin B on cathepsin B activity and microglial localization in Alzheimer's disease in Down syndrome and early-onset Alzheimer's disease.

This study identifies chromosome 21 genes other than APP that modulate amyloid-β accumulation in Down syndrome mouse models.

The paper investigates endosomal structure and APP biology in Down syndrome mouse models and finds no alterations in endosome number, size, or APP processing.

This study investigates the effect of Cstb duplication on amyloid-β pathology and cathepsin activity in a mouse model of Alzheimer's disease, finding no significant impact on Aβ levels or cathepsin activity.

This study identifies non-APP chromosome 21 genes that influence amyloid-β biology in Down syndrome mouse models, independent of APP copy number.

The paper shows that trisomy 21 cerebral organoids exhibit AD-like pathology, which can be suppressed by BACE2 trisomy and inhibited by BACE1 inhibitors, suggesting BACE2 as an AD-suppressor gene.

The paper identifies distinct hippocampal and prefrontal cortex circuit dysfunctions in DS mouse models linked to specific regions of human chromosome 21.