In addition to neurotoxic Aβ42, the Aβ43 variant is also abundant in Aβ plaques in the brains of individuals with sporadic and familial Alzheimer's disease. As the functional difference between the two species of Aβ fragments are not known, Saido et al. used a presenilin-1 (PS1) mutation that increases Aβ43 production over other Aβ fragments and generated a knock-in mouse line mimicking the human PS1 mutation. They report that Aβ43 is highly amyloidogenic in this line of mice and leads to behavioral deficits.
- Takashi Saito
- Takahiro Suemoto
- Takaomi C Saido
