Jamie L. Rose

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.

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.

This study identifies truncated Aβ fragments that form SDS-stable, low molecular weight oligomers impairing synaptic plasticity and evading conventional antibodies.

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 applies blood-derived epigenetic predictors of lifestyle traits to brain samples, finding variable correlations across brain regions and a strong link between smoking and the dorsolateral prefrontal cortex.

This study examines C9orf72 ALS/FTD patient-derived iPSC-microglia mono-cultures, finding they form RNA foci, have reduced C9orf72 protein, and show endosomal-lysosomal dysfunction, but no significant microglial-enriched gene expression differences.

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.