Background
Increasing evidence suggests that olfaction is largely preserved in multiple system atrophy while most patients with Parkinson's disease are hyposmic. Consistent with these observations, recent experimental studies demonstrated olfactory deficits in transgenic Parkinson's disease mouse models, but corresponding data are lacking for MSA models.
Conclusions
Our experimental data show preserved olfaction in a transgenic multiple system atrophy mouse model despite α-synucleinopathy in the olfactory bulb. These findings are in line with the human disorder supporting the concept of a primary oligodendrogliopathy with variable neuronal involvement.
Methods
Olfactory function and underlying neuropathological changes were investigated in a transgenic multiple system atrophy mouse model based on targeted oligodendroglial overexpression of α-synuclein as well as wild-type controls. The study was divided into (1) a pilot study investigating olfactory preference testing and (2) a long-term study characterizing changes in the olfactory bulb of aging transgenic multiple system atrophy mice.
Results
In our pilot behavioral study, we observed no significant differences in investigation time in the olfactory preference test comparing transgenic with wild-type animals. These findings were accompanied by unaffected tyrosine hydroxylase-positive cell numbers in the olfactory bulb. Similarly, although a significant age-related increase in the amount of α-synuclein within the olfactory bulb was detected in the long-term study, progressive degeneration of the olfactory bulb could not be verified. Conclusions: Our experimental data show preserved olfaction in a transgenic multiple system atrophy mouse model despite α-synucleinopathy in the olfactory bulb. These findings are in line with the human disorder supporting the concept of a primary oligodendrogliopathy with variable neuronal involvement.