Losing Your Sense of Smell can be a Sign of Alzheimer's
A weak sense of smell can be an early indicator of Alzheimer’s disease, especially in the elderly. For the longest time, it was not certain what played such a major role in determining how the disease progressed, but now researchers have discovered that the culprit behind the smell loss could be beta-amyloid, which is a protein that can build up in a toxic form in those who have the disease.
In order to determine the extended repercussions of smell loss and how it could be linked with Alzheimer's, scientists performed extensive tests with laboratory mice in order to develop a disease that could resemble Alzheimer's in humans. Researchers found that the plaque-forming protein was able to restore the sense of smell in the animals, though they also believe that the smell centers of the brain were among the first affected by toxic beta-amyloid as the disease unfolded. This resulted in a fascinating duality that scientists observed in determining how to control the illness. Because critical thinking and memory areas of the brain were often the next to go, scientists were confident that the presence of smell loss could be a sure potential indicator of Alzheimer's.
However, the loss of smell can be difficult for doctors to diagnose because it can also be caused by numerous other conditions other than Alzheimer’s disease. Sometimes viral illnesses, brain injuries and even side effects from medications can all be to blame for the condition. The research that the scientists conducted, however, indicates that it is possible that a general poor sense of smell can be recognized as a sign of Alzheimer's development. If the sense of smell loss is paired with other mild cognitive impairments or some other form of memory loss, the link to Alzheimer's becomes stronger and stronger.
The new research based on the mice shows where and how the loss of smell occurs in the brain, and the way that the impairment develops show that it is also likely to be much more treatable in the future. The mice that were exposed to a small amount of beta-amyloid were unable to detect odors. In these instances, the plaques largely made up of these toxic proteins had appeared in the brain sections responsible for smell before making their way to the sections responsible for memory. In these developed cases, the mice had spent much more time sniffing for odors than usual, but also were unable to remember the smells or tell the differences between odors in different lab experiments.
When the research team then aimed to reverse the effects, the results were definitive. The mice were put on a long-term drug that cleared the presence of the beta-amyloid from inside the brain. After just two weeks on the drug, the mice were able to resume smelling as normal. After withdrawal from the drug for a week, however, the impairments returned. This research could provide individuals with promising results in reversing the effects of Alzheimer's.
