Researchers, more than a decade ago, launched a project to develop a new mouse model that would allow more accurate evaluation of therapies for the disease.
Dr. Saido led project developed the first mice model (NL-F/NL-F), which knocked in with two mutations found in human familial Alzheimer's disease. The mice showed early accumulation of Abeta peptides, and importantly, were found to undergo cognitive dysfunction similar to the progression of AD seen in human patients.
A second model, with the addition of a further mutation that had been discovered in a family in Sweden, showed even faster initiation of memory loss.
These new models could help in two major areas. The first model, which expresses high levels of the Abeta peptides, seems to realistically model the human form of AD, and could be used for elucidating the mechanism of Abeta deposition.
The second model, which demonstrates AD pathology very early on, could be used to examine factors downstream of Abeta-40 and Abeta-42 deposition, such as tauopathy, which are believed to be involved in the neurodegeneration.
These results may eventually contribute to drug development and to the discovery of new biomarkers for Alzheimer's disease.
