Jörg Hanrieder

The paper identifies gene expression changes in microglia around Aβ plaques in human Alzheimer's disease tissue and finds cross-species concordance with mouse data.

This paper introduces a new mouse model, NLFTaum/h, that shows ageing and amyloid-β can initiate tau pathology without MAPT mutations, revealing interactions between age, Aβ, and human tau.

The paper discovers that levetiracetam prevents Aβ42 production by modulating synaptic vesicle cycling, altering APP localization, and favoring non-amyloidogenic processing in Alzheimer's disease models.

This paper uses isotope-encoded mass spectrometry imaging and single plaque transcriptomics to track Aβ plaque maturation and its impact on synaptic function and toxicity in Alzheimer's disease.

This study uses chemical imaging and deep learning to identify distinct amyloid plaque subtypes in Alzheimer's disease, revealing differences in Aβ composition and associations with disease progression.

The paper shows that Trem2 gene expression in microglia is upregulated only when they contact plaques, and this effect is reduced by the Trem2R47H mutation.

The paper uses iSILK to track Aβ plaque aggregation dynamics in AD mouse models, identifying cortical deposition and structural heterogeneity in plaque composition.