In recent years, CryoEM has enabled scientists to decipher the structures of the fibrils that form various deposits in neurodegenerative disease. They have not only solved disease-specific folding ...

“Bruce had a brilliant career in both academia and industry and left an indelible mark on the Alzheimer’s disease drug development landscape,” noted Robert Vassar, Northwestern University, Chicago ...

The microglia, in turn, seem to benefit, revving up metabolism and phagocytosis. The liver protein ApoA-I was particularly good at bolstering the latter. Overall, the findings suggest that the brain’s ...

These observations open the door to more in-depth investigations looking into a potential mechanistic link between TMEM106b aggregation and pathological processes in neurodegeneration,” Rothstein ...

Scientists broadly agree that both apolipoprotein E and microglia are necessary ingredients for amyloidosis. In mice devoid of ApoE, or of their microglia, scant plaques form. Now, a sweeping study ...

These tau knockout rats were created through transcription activator-like effector nuclease (TALEN)-mediated targeting of exon 2 of the rat Mapt gene (Ayers, Lopez et al., 2024). Tau protein was ...

Tg12099 rats overexpress the 0N4R isoform of human tau with the P301S mutation linked to frontotemporal dementia. The MAPT transgene is driven by the rat Prnp promoter. Overexpress the 0N4R isoform of ...

This transgenic mouse model expresses a floxed ATPase type 13A2 (Atp13a2) gene, with loxP sites flanking exons 2 to 3 (The Jackson Laboratory). The ATP13A2 protein is a transmembrane lysosomal ATPase ...

SORL1 knockout, knockin, and transgenic mice are now in the Research Models database. The database will be updated as more models become available.