The olfactory bulb is significantly smaller in Parkinson’s disease patients compared to healthy individuals, a new study found, providing an anatomical explanation for the loss of the sense of smell in the early stages of the disease.
The discovery, “A ventral glomerular deﬁcit in Parkinson’s disease revealed by whole olfactory bulb reconstruction,” was published in the journal Brain. It results from joint work of two research teams, one based in New Zealand and other from Germany.
In the study, the team compared the olfactory bulbs of Parkinson’s disease patients with those of healthy subjects. They found that the glomeruli distribution was significantly altered. While 70 percent of the glomerular component was in the bottom part of the olfactory bulb in normal cases, this dropped to 44 percent in Parkinson’s patients.
Additionally, the volume taken up by the glomeruli was reduced by more than half in Parkinson’s patients.
Results support the theory that Parkinson’s disease begins with viruses, bacteria, or environmental toxins entering the brain via the nose, affecting the olfactory bulb first. According to this hypothesis, the disease then gradually spreads through other regions of the brain.
The team also calculated the joint volume of all glomeruli in the olfactory bulb. They then compared the values between olfactory bulbs from people with and without Parkinson’s disease. Findings showed that the number of glomeruli in Parkinson’s patients was reduced by more than half.
Following up on the study, researchers are already working to unravel what causes glomeruli deterioration in Parkinson’s disease and whether there are any other changes in the olfactory bulb in this neurodegenerative disease.