The experts believe that fixing congenital anosmia, which is medical language for not being able to smell anything, may eventually lead to curing similar medical issues which also come from the cilia or small hair-like pieces which reside on the outside of cells and are present in diseases involving the kidneys, eyes, and other parts of the body.
According to the report, it may take a while for the evidence to be able to help humans and it will eventually be extremely significant for individuals who have lost the ability to smell because of some type of medical problem, and not so much for people who can't smell because of trauma to the nose, or simply old age. However, the new findings help researchers to understand anosmia on the cellular level, which gives hope to anyone who does not have a sense of smell that someday their ability to smell may be restored.
Jeffery Martens, Ph.D., senior author of the study commented:
"Using gene therapy in a mouse model of cilia dysfunction, we were able to rescue and restore olfactory function, or sense of smell. Essentially, we induces the neurons that transmit the sense of smell to regrow the cilia they'd lost."
The rodents involved in the study possessed some genetic defect that affected a protein named IFT88. This defect made the individuals have less- than-normal amounts of cilia in their bodies. When this problem occurs in mice, it results in early death and poor feeding habits, while for humans it can be fatal.
IFT88 genes were implanted into the cells in the mice when the researchers gave them a common cold virus which had plenty of normal DNA. This made it easy for the virus to infect them, and therefore, the researchers could insert the virus into the cells of the mice.
After this, the experts were able to analyze the feeding habits of the mice, as well as how they were growing, and the neuron signals which assist in the smelling process.
14 days after the mice were treated with 3 day therapy, the researchers found the mice to have increased in body weight by 60%, which meant their feeding habits had improved. When the mice were exposed to amyl acetate, or banana oil, the experts were able to see that their neurons were also working correctly.
Martens said: "At the molecular level, function that had been absent was restored.
First author Jeremy McIntyre, Ph.D., added:
"By restoring the protein back into the olfactory neurons, we could give the cell the ability to regrow and extend cilia off the dendrite knob, which is what the olfactory neuron needs to detect odorants."
People who have ciliopathies, diseases caused by the dysfunction of cilia, may benefit greatly from these findings. Examples of ciliopathies include:
- primary ciliary
- Alström syndrome
- Bardet-Biedl syndrome
"We hope this stimulates the olfactory research community to look at asnosmia caused by other factors, such as head trauma and degenerative diseases. We know a lot about how this system works - now have to look at how to fix it when it malfunctions."
Written by Christine Kearney