Cerebellar atrophy in a non-human primate model of Parkinson’s disease
Department, Center, or Institute
Biology
Secondary Department, Center, or Institute
Neuroscience
Presentation Format
Department Organized Oral Session
Presentation Type
Off-campus research
Description
Parkinson's disease (PD) is a chronic progressive neurodegenerative disorder characterized by resting tremor, slowness of movements, rigidity, gait disturbance and postural instability. Since the discovery of markedly decreased dopamine concentrations in the striatum in 1960s [1], the basal ganglia (BG) are the major clinical research targets in PD. At the same time, pathological changes in the cerebellum following dopaminergic degeneration have been reported in patients with PD and animal models, and anatomical, pathophysiological and clinical evidence suggest that the cerebellum may contribute substantially to the clinical symptoms of PD [2,3,4]. To further understand the possible cerebellar pathology in PD we have used the MPTP-treated rhesus monkey, a well-established non-human primate model of PD, to study possible anatomical changes in the cerebellum of one control and one parkinsonian MPTP-treated monkey. The volume (Cavalieri analysis), and the total number of Purkinje (PK) neurons in the motor areas of the cerebellum have been estimated using serial sagittal sections, calbindin immunostaining, and an unbiased stereological approach (optical fractionator; StereoInvestigator). In this analysis, we have found a 38% reduction in the volume, and a 20% decrease in the number of the PK neurons in the cerebellum of the parkinsonian monkey compared with the control. Although additional analysis (increasing the number of animals) are needed, these preliminary results suggest anatomical changes in structure of the cerebellum, and potential pathological changes in the cerebellar-thalamic-cortical functional network in parkinsonian animals.
Department Organized Oral Session Title
Neuroscience Program Talks Session II
Moderator/Professor
Linnea Freeman, Biology and Neuroscience
Session Number
2
Start Date and Time
4-9-2019 11:15 AM
Location
Johns Hall 208
Recommended Citation
Chaney, Bernadette, "Cerebellar atrophy in a non-human primate model of Parkinson’s disease" (2019). Furman Engaged!. 314.
https://scholarexchange.furman.edu/furmanengaged/2019/all/314
Cerebellar atrophy in a non-human primate model of Parkinson’s disease
Johns Hall 208
Parkinson's disease (PD) is a chronic progressive neurodegenerative disorder characterized by resting tremor, slowness of movements, rigidity, gait disturbance and postural instability. Since the discovery of markedly decreased dopamine concentrations in the striatum in 1960s [1], the basal ganglia (BG) are the major clinical research targets in PD. At the same time, pathological changes in the cerebellum following dopaminergic degeneration have been reported in patients with PD and animal models, and anatomical, pathophysiological and clinical evidence suggest that the cerebellum may contribute substantially to the clinical symptoms of PD [2,3,4]. To further understand the possible cerebellar pathology in PD we have used the MPTP-treated rhesus monkey, a well-established non-human primate model of PD, to study possible anatomical changes in the cerebellum of one control and one parkinsonian MPTP-treated monkey. The volume (Cavalieri analysis), and the total number of Purkinje (PK) neurons in the motor areas of the cerebellum have been estimated using serial sagittal sections, calbindin immunostaining, and an unbiased stereological approach (optical fractionator; StereoInvestigator). In this analysis, we have found a 38% reduction in the volume, and a 20% decrease in the number of the PK neurons in the cerebellum of the parkinsonian monkey compared with the control. Although additional analysis (increasing the number of animals) are needed, these preliminary results suggest anatomical changes in structure of the cerebellum, and potential pathological changes in the cerebellar-thalamic-cortical functional network in parkinsonian animals.