While pharmaceutical company Biogen for their much-discussed Alzheimer's drug , a new drug may actually present a better option. Researchers at Nankai University and Peking Union Medical College recently showed that a not only stops the physical manifestations of Alzheimer’s disease, but also restores the damage it causes to the brain in mice.
is a type of dementia that impacts brain structure, shape and function, to the point that patients lose significant portions of their memory and struggle to perform daily activities. As we still , developing treatments remains difficult, notably in how to stop the disease and restore brain function, instead of only slowing the progressive memory loss.
The scientists of this study created 9i from the base structure of tacrine, a compound previously sold under the name to treat mild to moderate Alzheimer's disease. Scientists eventually realized that tacrine caused fatal liver damage. Though , researchers occasionally use it to develop new compounds that they hope will keep the same positive effects but lose the negative effects. One daughter compound, 9i, seems to be following in its parent’s footsteps but with a .
The researchers fed 9i in low doses to Alzheimer’s disease-afflicted mice. Even at these low doses, they saw that the mice remembered new objects and navigated water mazes, two behavioral tests that evaluate object and spatial memory, significantly better than the placebo group. In addition, when examining the brains of these mice, 9i significantly decreased the number and severity of , one of the physical signatures of Alzheimer’s. Most importantly, 9i boosted the amount of synapse-related proteins that are typically decreased in Alzheimer's and encouraged a greater density of dendritic spines, cell structures that contribute to memory.
In essence, 9i seems to do what Aducanumab can, but with the added bonus of restoring the cellular structure of memory.
These preliminary results show that it is possible to stop the disease and recover from its adverse effects. However, the real test will be if human clinical trails can replicate these findings and provide hope for those affected by Alzheimer’s disease.