An anatomical link for the loss of the sense of smell in Parkinson’s disease has been found by researchers at University of Auckland. Loss of the sense of smell is an often overlooked but remarkably prevalent early symptom of Parkinson’s disease.
Parkinson’s disease is a progressive, degenerative disorder of the brain. Symptoms include tremors, stiffness or rigidity, and slowness of movement. There is no cure so treatment will normally focus on managing symptoms, typically with medication.
“A complete loss of smell or a diminished sense of smell often precedes the usual motor symptoms of this neurodegenerative disease by several years, and has a prevalence of 90 per cent in early-stage patients,”
says Associate Professor Maurice Curtis, of the Centre for Brain Research at the University’s Faculty of Medical and Health Sciences.
Olfactory Bulb Glomeruli
The olfactory bulb is a part of the brain that acts as a primary relay station for smell signals from olfactory sensory neurons that detect smells in the nose. These neurons identify smells in the environment.
Smell signals are transmitted via axons – the long thread-like part of a nerve cell – of the sensory neurons, which terminate and come together into thousands of structures called glomeruli. The odor-induced signals are processed in the olfactory bulb and relayed to several other parts of the brain including the olfactory cortex.
Associate Professor Maurice Curtis. Credit: University of Auckland
The researchers compared the olfactory bulbs from people with and without Parkinson’s disease and found that the volume taken up by the glomeruli (the functional units of the olfactory bulb) was reduced by more than half in Parkinson’s patients.
The researchers discovered that the distribution of the glomeruli was greatly altered. The olfactory bulbs of normal cases had 70 per cent of their glomerular component in the bottom half of the olfactory bulb, but the olfactory bulbs of Parkinson’s disease cases had only 44 per cent in the bottom half.
This reduction is consistent with the hypothesis that Parkinson’s disease begins with bacteria, viruses or environmental toxins entering the brain via the nose and affecting first the olfactory bulb, where the neurodegenerative disease is triggered and gradually spreads through other parts of the brain.
The New Zealand-based researchers were able to collect olfactory bulbs fit for an in-depth quantitative study.
In a globe-spanning project, the researchers processed the post mortem olfactory bulbs, cut thousands of ten-micrometer thin sections throughout its entire length, and stained the sections with fluorescently labeled antibodies. The labeled sections were then scanned in Frankfurt, and the images reconstructed in 3-D allowing for quantitative whole-olfactory bulb analyses.
As glomeruli of the human olfactory bulb are difficult to count unambiguously, the researchers came up with a new, quantitative parameter: the global glomerular voxel volume. This quantity is the sum of the volume of all the glomeruli in the olfactory bulb.
Having defined this new parameter, the researchers compared the values between olfactory bulbs from normal and Parkinson’s disease cases, and found that it was reduced by more than half. Whether the decrease is the result of Parkinson’s patients having fewer or smaller glomeruli, or is due to a combination of these two effects, remains to be seen.
The research will be followed up with further work, already underway, to understand what causes the glomeruli to deteriorate in Parkinson’s disease and to demonstrate what other changes occur in the olfactory bulb in Parkinson’s disease.