Our “Olfaction in Parkinson’s disease” themed session: Michaela Johnson, Postdoc at Van Andel Institute, presents on “Deficits in olfactory sensitivity in a mouse model of Parkinson’s disease” and Aishwarya Kulkarni, PhD student at University of Florida, discusses “α-Synuclein perturbs in vivo neural activity following seeding in the olfactory bulb”.

Michaela’s presentation features:
Braak and colleagues proposed that early in Parkinson’s disease α-synuclein pathology is present in the dorsal motor nucleus of the vagus, olfactory bulb and anterior olfactory nucleus. We bilaterally injected α-synuclein preformed fibrils into the olfactory bulb. Six-months after injection, the anterior olfactory nucleus and the piriform cortex displayed a high α-synuclein pathology load. We evaluated olfactory perceptual function by monitoring odor-evoked sniffing behavior in a plethysmograph at one-, three- and six-months after injection. At all-time points, females injected with fibrils exhibited reduced odor detection sensitivity, which was detectable with the semi-automated plethysmography apparatus, but not a buried pellet test.

Aishwarya’s presentation discusses:
Aggregation of a-synuclein in the olfactory bulb (OB) is observed during prodromal Parkinson’s disease (PD). Whether this influences neural activity, in manners which may be responsible for olfactory perceptual deficits observed in PD is unknown. To address this void, we injected pathogenic a-Syn fibrils into the OB and used local field potential recordings to monitor neural activity in awake mice as they were delivered odors. We uncovered that a-Syn pathology in the olfactory system impacts in vivo neural activity in specific manners. This work provides initial insights into the effects of a-Syn aggregation on neural activity in awake mice.