(dailyRx News) When an individual begins developing the early signs of Alzheimer's disease, one of the earliest symptoms is the loss of smell. Scientists have found a way to reverse this symptom in a lab.
In a study involving a mouse model of the disease, researchers found that the impairment could be reversed by removing a plaque-forming protein called amyloid beta, a hallmark of Alzheimer's. This also confirmed that amyloid beta caused the inability to smell.
Daniel Wesson, lead researcher and assistant professor of neuroscience at Case Western Reserve University, said the evidence suggests that sense of smell could be used to determine if someone might develop Alzheimer's disease.
Doctors could then use those changes in the sense of smell to begin treatments instead of waiting until memory problems develop. He said it also could be used as a barometer to see if therapies are working.
Loss of the ability to smell was first associated with Alzheimer's in the 1970s. Researchers now think it may hold clues about how to slow progression of the neurodegenerative disease.
During the study researchers found that a tiny amount of amyloid beta -- too small to be seen on brain scans -- caused smell loss in a mouse model. They determined that amyloid beta accumulated in parts of the brain associated with smell much earlier than areas of the brain related to cognition and memory.
They found that the olfactory bulb, where odor information from the nose is processed, became hyperactive, yet over time it slowed as amyloid beta accumulated in the brain.
Though mice began spending more time sniffing, they could not remember scents and had difficulty telling the difference between odors even though the rest of the brain continued to act normally.
This is the same pattern that occurs as humans develop Alzheimer's.
Investigators were able to reverse the loss of smell by giving mice a synthetic liver x-receptor agonist, a drug that clears amyloid beta from the brain. Two weeks later the mice could process smells normally. However, a week after taking away the drug, the impairment returned.
Researchers plan to use the finding to determine how amyloid beta spreads through the brain in order to pinpoint methods for slowing the progression of the disease.
The research was recently published in The Journal of Neuroscience.