Abstract
Recent clinical evidence supports a link between 25-hydroxyvitamin D insufficiency (serum 25-hydroxyvitamin D [25(OH)D] levels <30 ng/mL) and Parkinson’s disease. To investigate the effect of 25(OH)D depletion on neuronal susceptibility to toxic insult, we induced a state of 25(OH)D deficiency in mice and then challenged them with the dopaminergic neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). We found there was no significant difference between control and 25(OH)D-deficient animals in striatal dopamine levels or dopamine transporter and tyrosine hydroxylase expression after lesioning with MPTP. Additionally, we found no difference in tyrosine hydroxylase expression in the substantia nigra pars compacta. Our data suggest that reducing 25(OH)D serum levels in mice has no effect on the vulnerability of nigral dopaminergic neurons in vivo in this model system of parkinsonism.
Highlights
Multiple factors, including increased oxidative stresses, varying genetic susceptibility, mitochondrial dysfunction, proteasomal dysfunction, inflammation and premature apoptosis contribute to the pathophysiology of Parkinson’s disease (PD) [1]
We used serum 25(OH)D levels to define vitamin D status as it is done in most animal and human studies
Since changes in markers of dopamine neuron integrity can be seen in the absence of any behavioral deficit and are often changed when dopamine levels are altered, we investigated the effect of 25(OH)D depletion of expression of markers of dopamine neurons in the nigrostriatal system
Summary
Multiple factors, including increased oxidative stresses, varying genetic susceptibility, mitochondrial dysfunction, proteasomal dysfunction, inflammation and premature apoptosis contribute to the pathophysiology of Parkinson’s disease (PD) [1]. Such environmental factors as vitamin D status may modify PD risk and/or progression [2]. Whether 25(OH)D deficiency states are causal or merely correlative in PD remains poorly understood. Despite this knowledge limitation, many clinicians recommend vitamin D supplementation to patients as a means to prevent or delay progression of PD.
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