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

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Apr 9th, 11:15 AM

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.