Abstract
Neurological compensatory mechanisms help our brain to adjust to neurodegeneration as in Parkinson’s disease. It is suggested that the compensation of the damaged striato-thalamo-cortical circuit is focused on the intact thalamo-rubro-cerebellar pathway as seen during presymptomatic Parkinson, paradoxical movement and sensorimotor rhythm (SMR). Indeed, the size of the red nucleus, connecting the cerebellum with the cerebral cortex, is larger in Parkinson’s disease patients suggesting an increased activation of this brain area. Therefore, the red nucleus was examined in MPTP-induced parkinsonian marmoset monkeys during the presymptomatic stage and after SMR activation by neurofeedback training. We found a reverse significant correlation between the early expression of parkinsonian signs and the size of the parvocellular part of the red nucleus, which is predominantly present in human and non-human primates. In quadrupedal animals it consists mainly of the magnocellular part. Furthermore, SMR activation, that mitigated parkinsonian signs, further increased the size of the red nucleus in the marmoset monkey. This plasticity of the brain helps to compensate for dysfunctional movement control and can be a promising target for compensatory treatment with neurofeedback technology, vibrotactile stimulation or DBS in order to improve the quality of life for Parkinson’s disease patients.
Highlights
Parkinson’s disease (PD) is a major progressive disorder affecting the central nervous system by specific degeneration of dopamine producing neurons in the substantia nigra, which govern the control of muscle movement
PD patients who are not able to walk can start a movement by external visual guidance such as lines drawn on the floor
We examined the effect of stimulation of a compensation mechanism by sensorimotor rhythm (SMR) brain training on the size of the red nucleus (RN)
Summary
Parkinson’s disease (PD) is a major progressive disorder affecting the central nervous system by specific degeneration of dopamine producing neurons in the substantia nigra, which govern the control of muscle movement Treatments against this motor disorder are still based on increasing dopamine neurotransmission capacity in the brain by pharmacological intervention, such as Levodopa (L-DOPA) that reduces the PD symptoms. This is explained by altered connectivity within the brain through which motor function can be maintained[3]. Compensatory pathways using external cues and gait are often making use of the cortico-parieto-frontal circuitry and cerebellum[6] Another mechanism to compensate for the damaged basal ganglia is stimulation of the sensorimotor rhythm (SMR)[7,8,9]. Again, targeting pathways involving a cerebellar circuit might be a promising strategy to prevent susceptibility for PD development and to bypass the dysfunctional basal ganglia in order to restore normal motor function (Fig. 1)
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