Jane Tulloch

This study examines amyloid-beta pathology in feline cognitive dysfunction syndrome, finding increased synaptic engulfment by glia in aged and affected cats, mirroring Alzheimer's disease mechanisms.

This study uses live human brain slice cultures to show that physiological and pathological amyloid-beta have opposing effects on synapses, with physiological levels enhancing synaptic transcripts and pathological levels causing synaptic loss.

This study shows microglia promote beta-amyloid plaque formation but are not required for subsequent pathological changes in Alzheimer's disease.

The paper identifies transmembrane protein 97 as a synaptic receptor for amyloid beta in human Alzheimer's disease using advanced microscopy and drug intervention studies.

The paper shows human astrocytes and microglia ingest more synapses in Alzheimer's disease via MFG-E8, and inhibiting MFG-E8 reduces this ingestion in cultured cells.

This study shows reducing Kv3.4 levels in a mouse model of Alzheimer's disease reduces synapse loss and changes in spine morphology.

The paper identifies over 5,500 synaptic proteins in Alzheimer’s disease and controls, revealing APOE4-associated changes in synaptic and mitochondrial function and neuroimmune signaling.

This study shows that reducing tau improves behavioural and transcriptional issues in a mouse model of Alzheimer’s disease, suggesting synaptic tau reduction could be a therapeutic strategy.