Parkinson's disease is a common neurodegenerative disorder of unknown cause. 
There is no cure or proven strategy for slowing the progression of the disease. 
Although there are signs of pathology in many brain regions, the core symptoms 
of Parkinson's disease are attributable to the selective degeneration of 
dopaminergic neurons in the substantia nigra pars compacta. A potential clue to 
the vulnerability of these neurons is their increasing reliance on Ca(2+) 
channels to maintain autonomous activity with age. This reliance could pose a 
sustained metabolic stress on mitochondria, accelerating cellular ageing and 
death. The Ca(2+) channels underlying autonomous activity in dopaminergic 
neurons are closely related to the L-type channels found in the heart and smooth 
muscle. Systemic administration of isradipine, a dihydropyridine blocker of 
L-type channels, forces dopaminergic neurons in rodents to revert to a juvenile, 
Ca(2+)-independent mechanism to generate autonomous activity. More importantly, 
reversion confers protection against toxins that produce experimental 
parkinsonism, pointing to a potential neuroprotective strategy for Parkinson's 
disease with a drug class that has been used safely in human beings for decades. 
These studies also suggest that, although genetic and environmental factors can 
hasten its onset, Parkinson's disease stems from a distinctive neuronal design 
common to all human beings, making its appearance simply a matter of time.