Forskning

February 15, 2012

Delayed caffeine treatment prevents nigral dopamine neuron loss in a progressive rat model of Parkinson’s disease

P K Sonsalla et al, Delayed caffeine treatment prevents nigral dopamine neuron loss in a progressive rat model of Parkinson’s disease, Experimental Neurology, 2012, Article in Press

ABSTRACT

Parkinson’s disease (PD) is characterized by a prominent degeneration of nigrostriatal dopamine (DA) neuons with an accompanying neuroinflammation. Despite clinical and preclinical studies of neuroprotective strategies for PD, there is no effective treatment for preventing or slowing the progression of neurodegeneration. The inverse correlation between caffeine consumption and risk of PD suggests that caffeine may exert neuroprotection. Whether caffeine is neuroprotective in a chronic progressive model of PD has not been eval uated nor is it known if delayed caffeine treatment can stop DA neuronal loss. We show that a chronic unilateral intra-cerebroventricular infusion of 1-methyl-4-phenylpyridinium in the rat brain for 28 days  produces a progressive loss of DA and tyrosine hydroxylase in the ipsilateral striatum and a loss of DA cell  bodies and microglial activation in the ipsilateral substantia nigra. Chronic caffeine consumption prevented  the degeneration of DA cell bodies in the substantia nigra. Importantly, neuroprotection was still apparent  when caffeine was introduced after the onset of the neurodegenerative process. These results add to the clinical relevance for adenosine receptors as a disease-modifying drug target for PD.