MedicalResearch: What are the main findings of the study?
Dr. Farr: We found that reducing the conversion of amyloid precursor protein (APP) to beta amyloid with an antisense targeting the beta amyloid portion of amyloid precursor protein in the Tg2576 mouse which overexpresses human beta amyloid, improves learning and memory and reduces neuroinflammatory cytokine (inflammation in the brain).
MedicalResearch: Were any of the findings unexpected?
Dr. Farr: No, we had found that this occurred in the SAMP8 mouse model of Alzheimer’s disease. The SAMP8 overproduces mouse beta amyloid so we wanted to confirm that the compound would work in a mouse model that overproduced human beta amyloid. We anticipated it would work because the structure for mouse and human beta amyloid are homologus at the site that is involved in learning and memory.
MedicalResearch: What should clinicians and patients take away from your report?
Dr. Farr: The study is a preclinical study so it will not be in the clinic any time soon. It is important to note that reducing beta amyloid results in improved learning and memory so beta amyloid does not need to be eliminated. In fact we have shown in a previous study that reducing beta amyloid in a normal mouse impairs learnind and memory. It also suggests that antisense therapies are worth developing in conditions where total blockage of compound would be harmful.
MedicalResearch: What recommendations do you have for future research as a result of this study?
- Looking at therapies that reduce, but not eliminate beta amyloid.
- Exploring antisense therapies.
Farr S, Erickson M, Niehoff M, Banks W, Morley J. Central and Peripheral Administration of Antisense Oligonucleotide Targeting Amyloid-β Protein Precursor Improves Learning and Memory and Reduces Neuroinflammatory Cytokines in Tg2576 (AβPPswe) Mice. Journal of Alzheimer’s Disease. 2014.