In this experimental trial, 272 patients with mild to moderate AD received an infusion every four weeks for two years. The experimental group received donanemab, while the control group received a placebo. Those in the experimental group had a 32% deceleration in the rate of decline of AD and within 6 to 12 months, no longer had plaques. This trial was formulated on the grounds of the amyloid hypothesis, which states that Alzheimer's is linked with amyloid accumulation, and if this can be prevented, then the disease may be prevented or cured. Deceleration of the rate of decline was measured through performance on mental tests that dealt with reasoning and memory, as well as evaluating how participants performed on tasks in their daily lives. One effect of the drug was that 30% of patients had an accumulation of fluid in the brain (Kolata, 2021).
Similarly, in research done by Dr. Catherine Kaczorowski, she wanted to understand the genetics component that relates to the regulation of cognitive aging. Previous research has shown that around 50%-80% of AD is heritable. To figure this out, they set up an experiment with genetically diverse mice. These mice had genetic variants that related to memory and were identical to human mutations. They performed a forward genetic study, where mice were inbred with the B6 mouse and the D2 mouse. The mice underwent contextual fear conditioning in order to measure memory capabilities. Mice who had a better memory of the context with the foot shoot would have exhibit freezing and thus have a higher percentage of memory index. What they found was that the mice who inherited the B6 strain expressed Hp1bp3 and had better contextual fear memory. After this finding, they made sure the expression of the Hp1bp3 could be translated into humans. What they found was that it was possible to use AD mouse models to help study human AD (Neuner, 2019).
Both of these findings will ultimately help develop treatment and potentially cures for AD. In the current state, I think that these findings could be put together, to further advance what we know about AD. While one hypothesis is testing the correlation between amyloid accumulation and cognitive decline, the other hypothesis is testing for the influence of genetic makeup in AD. Since expression of Hp1bp3 has been shown to slow cognitive decline (Neuner, 2019), and the trial donanemab has also shown slowing cognitive decline (Kolata, 2021), researchers could potentially use donanemab on genetically diverse mice to see if donanemab also affects the expression of Hp1bp3.
References:
Neuner, S. M. et al. (2019). Harnessing Genetic Complexity to Enhance Translatability of Alzheimer’s Disease Mouse Models: A Path toward Precision Medicine. Neuron. Vol. 10, 399-411. https://doi.org/10.1016/j.neuron.2018.11.040.
Kolata, G. (2021, Jan. 11). Alzheimer’s Drug Shows Promise in Small Trial. The New York Times. https://www.nytimes.com/2021/01/11/health/alzheimers-amyloid-lilly.html?searchResultPosition=8.
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