‘Anosmia’ is the inability to smell, which is more harmful than it sounds, primarily because it could lead to a tendency to eat less, often leading to starvation and weight loss in mice. Anosmia can be caused by a number of factors, one of which is ciliopathy—when there are problems with the tiny protuberances on sensory cells called cilia. Among other cells, these cilia are found on the neurons that function in odor perception, and serve as ‘antennae’.
Scientists at the University of Michigan have treated mice that had genetic defects in a protein IFT88, which causing them to have no cilia across the body. They injected a common virus into these mice carrying DNA with the normal version of this gene. As the virus inserted itself into the genomes of these mice, they started producing cilia and their feeding patterns were found to change considerably. Moreover, the mice showed a 60% increase in body weight. “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,” says postdoctoral fellow and first author Jeremy McIntyre, Ph.D.
This is only a starting point for ciliary disorders, primarily because a mutation in IFT88 in humans is fatal, and does not cause the same defects as in mice. Thus, though this research has some way to go before it could be extended to humans, it shows promise in treating olfactory diseases that are genetic and due to malfunctioning cilia. Moreover, cilia perform important functions in diseases that aren’t just related to smell perception. Polycystic kidney disease and a disease called retinitis pigmentosa in the eye also result from a problem with the cilia.
You can read about this research here.