With the baby boomer generation aging, Alzheimer’s disease is quickly becoming a debilitating illness that is affecting more and more people.
Doctors are constantly striving to find new ways to prevent or treat this devastating condition, which slowly strips a person of their memory. It is a disease that affects the mind and slowly causes mental deterioration to the point of dementia. Alzheimer’s attacks the nerve cells in the brain, causing the afflicted person to lose control of their emotions, movement, and memory.
As of right now, there is no treatment available for this devastating disease, but there is hope.
New research, conducted in genetically altered mice, has found that some memory can be restored if the disease is caught early enough.
It appears that the protein tau–which is actually a mutated protein–is playing a hand in the disease. This protein is thought to “poison brain cells.” By inhibiting this protein memory could potentially be restored.
According to the lead researcher, Karen Ashe, who is involved in the most recent findings surrounding tau, it appears as though neurons affected by Alzheimer’s are not dead.
There are a number of theories abounding from all the different research conducted on the disease–the most prevalent theory states that something is causing the protein beta amyloid to form abnormally, thereby clumping and coating the brain and causing the plaque that is seen in people suffering from Alzheimer’s disease. However, when mutated, tau causes “fibrous tangles in brain cells” in people diagnosed with Alzheimer’s–and this could lead to yet another type of dementia.
As of right now, all research pertaining to the tau protein has been conducted on mice. But, when the fibrous tangles were mimicked in mice during research, the more tangles there were the more brain cells died, leading to extreme loss of memory in the mouse. This was seen when the mice were placed in water. Mice do not like being immersed in water and therefore swim quite well in order to escape drowning. Researchers tested the memory and cognitive thinking of the mice when they were at one month of age.
At this stage, there was a hidden platform in a maze, which the mice located and then could return to each and every time. Then, researchers removed the platform and gauged how long it took for the mice to return to that same location. However, as the dementia set it, the mice were unable to find their way and just swam around, unable to recall where the platform was located.
The researchers conducted the study so that they would be able to turn off the protein tau in the mice before their neurons were lost. When they did this, much of the memory was restored in the mice.
However, this only occurred early on in the progress of dementia. The longer the researchers waited to shut off the protein, the lesser amount of memory could be recovered in the mice. Until now, much research has been done on another potential culprit–the protein beta amyloid.
With the latest research, printed in the journal Science, pointing to tau as a potential factor in the development of Alzheimer’s as well, it is hopeful that further research will start focusing on both beta amyloid and tau as factors.