Carlo Sala Frigerio

The paper identifies neuronal vulnerability to C9orf72 repeat expansion by analyzing transcriptional states in a Drosophila model, finding that Xbp1 expression correlates with resistance to toxicity.

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.

This study shows that oligodendrocytes produce amyloid beta in Alzheimer's Disease and that suppressing this production improves brain pathology and neuronal function.

This study identifies SPP1 as a key mediator of microglial synaptic engulfment in Alzheimer's disease models, showing its role in neuroimmune interactions.

The paper identifies a genetic variant in OAS1 linked to increased Alzheimer's disease risk and severe COVID-19 outcomes, showing its role in microglial inflammation.

The paper uses spatial transcriptomics and in situ sequencing to study gene networks in the amyloid-β plaque niche of AD, revealing microglia-astroglia interactions and myelination abnormalities.

The paper shows that single nucleus RNA-Seq fails to detect microglial activation genes in human brain samples compared to single cell RNA-Seq.

This study identifies miR-132 deficiency as a cause of impaired adult hippocampal neurogenesis in Alzheimer's disease and shows that restoring miR-132 levels can reverse these deficits and memory issues.

The paper demonstrates that human microglia derived from embryonic stem cells can engraft mouse brains and express Alzheimer's risk genes when exposed to Aβ, offering a new model to study genetic risk in AD.