Abstract
BackgroundThe mechanisms leading to a loss of dopaminergic (DA) neurons from the substantia nigra pars compacta (SNc) in Parkinson's disease (PD) have multifactorial origins. In this context, nutrition is currently investigated as a modifiable environmental factor for the prevention of PD. In particular, initial studies revealed the deleterious consequences of vitamin A signaling failure on dopamine-related motor behaviors. However, the potential of vitamin A supplementation itself to prevent neurodegeneration has not been established yet.ObjectiveThe hypothesis tested in this study is that preventive vitamin A supplementation can protect DA neurons in a rat model of PD.MethodsThe impact of a 5-week preventive supplementation with vitamin A (20 IU/g of diet) was measured on motor and neurobiological alterations induced by 6-hydroxydopamine (6-OHDA) unilateral injections in the striatum of rats. Rotarod, step test and cylinder tests were performed up to 3 weeks after the lesion. Post-mortem analyses (retinol and monoamines dosages, western blots, immunofluorescence) were performed to investigate neurobiological processes.ResultsVitamin A supplementation improved voluntary movements in the cylinder test. In 6-OHDA lesioned rats, a marked decrease of dopamine levels in striatum homogenates was measured. Tyrosine hydroxylase labeling in the SNc and in the striatum was significantly decreased by 6-OHDA injection, without effect of vitamin A. By contrast, vitamin A supplementation increased striatal expression of D2 and RXR receptors in the striatum of 6-OHDA lesioned rats.ConclusionsVitamin A supplementation partially alleviates motor alterations and improved striatal function, revealing a possible beneficial preventive approach for PD.
Highlights
Parkinson’s disease (PD) is a neurodegenerative disease with multifactorial origins that involves interactions between genetic and environmental factors [1, 2]
Tyrosine hydroxylase labeling in the substantia nigra pars compacta (SNc) and in the striatum was significantly decreased by 6-OHDA injection, without effect of vitamin A
In 6-OHDA rats with supplemented diet, latency to fall was close to sham rats 1 week after the lesion, but was shorter at 2 and 3 weeks after the lesion. These results reveal that beneficial effect of vitamin A supplementation on motor impairments induced by unilateral 6-OHDA injection in the striatum is only observable in the cylinder test
Summary
Parkinson’s disease (PD) is a neurodegenerative disease with multifactorial origins that involves interactions between genetic and environmental factors [1, 2]. PD is characterized by disabling motor symptoms, such as akinesia, bradykinesia and tremor at rest, but these motor symptoms generally appear when a large proportion of DA neurons have already degenerated [4] In this context, nutrition has recently attracted attention as a potent modifiable environmental factor for the prevention of neurodegeneration in PD [5, 6]. Mice lacking ALDH1A1 enzyme or ALDH1A1+ neurons, exhibit motor impairments along with alterations of DA metabolism [17, 18] This evidence highlights a role for vitamin A signaling in dopamine-related motor behaviors. The mechanisms leading to a loss of dopaminergic (DA) neurons from the substantia nigra pars compacta (SNc) in Parkinson’s disease (PD) have multifactorial origins In this context, nutrition is currently investigated as a modifiable environmental factor for the prevention of PD. The potential of vitamin A supplementation itself to prevent neurodegeneration has not been established yet
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