Taking Out OGA. The rationale behind small-molecule OGA inhibition is that these drugs will decrease tau hyperphosphorylation and aggregation into neurofibrillary tangles (right). [Courtesy of Eli ...

In Japan, clinical use is climbing faster, with about 4,500 people now on the drug. ARIA rates in Japan are half those in the U.S., which was also the case in the Phase 3 Clarity trial. Meanwhile, use ...

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Seeking ways to improve the safety of anti-amyloid antibodies, John Sims of Eli Lilly & Company presented a simple option to do so for donanemab at this year’s Clinical Trials on Alzheimer’s Disease ...

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 ...

TMEM106b’s rap sheet is growing. Some of its genetic variants are linked to both Alzheimer’s disease and frontotemporal dementia, and fibrils of this lysosomal protein accumulate in several ...

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.