Individuals who were not born by having an olfactory sense, or who lost the ability to smell as a result of disease, could someday once more eat the sweet smells all around them courtesy of new research in the University of Michigan Medical School.

Dr. Jeffery Martens, an associate professor of pharmacology, and colleagues were, the very first time, capable of curing the condition, known as congenital anosmia, and restore a feeling of smell in mice using gene therapy, the university said in a September 2 statement. They learned that the mice were lacking in a protein known as IFT88, which resulted in a lack of cilia the hair-shaped structures on the surface of a cell throughout the body.

“The researchers were able to insert normal IFT88 genes into the cells of the mice by providing them a typical cold virus loaded with the normal DNA sequence, and allowing the virus to infect them and insert the DNA into the mouse’s own cells,” based on the statement. “Then they monitored cilia growth, feeding habits, and well as signals within and between your nerve cells, called neurons, which are active in the olfaction.”

The treatment lasted for three days, and just two weeks after its completion, the mice experienced a 60% increase in bodyweight, suggesting that they had been consuming more food than before the treatment. Furthermore, the researchers discovered that cell-level indicators suggested that neurons related to smelling were functioning correctly once the rodent subjects were subjected to the pungent chemical amyl acetate.

Their findings have been published online within the journal Nature Medicine.

“The researchers caution that it’ll take some time for their work to affect human treatment, which will be most important for people who have lost their olfaction as a result of genetic disorder, rather than those who lose it because of aging, head trauma, or chronic sinus problems,” the university said. “However their work paves the way for a better understanding of anosmia at the cellular level.”

“Using gene therapy in a mouse type of cilia dysfunction, we were able to rescue and restore olfactory function, or feeling of smell“¦ Essentially, we induced the neurons that transmit a feeling of smell to regrow the cilia they’d lost,” added Dr. Martens. “At the molecular level, function that had been absent was restored.”

Martens added the research could also be important in treating other diseases caused by cilia dysfunction, including polycystic kidney disease, retinitis pigmentosa, and rare inherited disorders such as Alström syndrome and nephronopthisis. Next he said he and the team continues to consider additional cilia-related genetic causes of anosmia, including head trauma and degenerative diseases.

The research was funded by four National Institutes of Health (NIH) divisions, and researchers from Duke University, the Baylor College of drugs, the University of Alabama-Birmingham, the NIH Intramural Sequencing Center, the Université Paris Descartes; St. James’s University Hospital in the UK, and University College London were also credited as authors around the study.