Editor's Summary
28 June 2007
Tackling Parkinson's
Although several regions of the brain display signs of pathology in Parkinson's disease, it is the death of dopaminergic (DA) neurons in the substantia nigra pars compacta that causes the motor symptoms characteristic of the disease. Why these neurons are vulnerable is not clear, but it has been thought that a rising tide of intracellular calcium could be a major factor. Work by Chan et al. now shows that DA neurons rely on Ca2+ channels to maintain their rhythmic activity, and that this reliance increases with age. But the adult neurons can be made to revert to using the Na+/HCN channels, as younger neurons do, by treatment with isradipine, a calcium antagonist used to treat hypertension and stroke. In mouse models of Parkinson's disease this 'rejuvenation' protects DA neurons, suggesting that it might slow or stop disease progression. Current antiparkinson's drugs treat only the symptoms of the disease, so there will be intense interest in the progress of this new approach in clinical trials.
News and Views: Neurophysiology: Stressful pacemaking
In Parkinson's disease, dopamine-secreting neurons die — perhaps because unrelenting calcium entry during spontaneous electrical activity puts them under unusual pressure.
Bruce P. Bean
doi:10.1038/4471059a
Article: 'Rejuvenation' protects neurons in mouse models of Parkinson's disease
C. Savio Chan, Jaime N. Guzman, Ema Ilijic, Jeff N. Mercer, Caroline Rick, Tatiana Tkatch, Gloria E. Meredith & D. James Surmeier
doi:10.1038/nature05865
Abstract | Full Text | PDF (1,458K) | Supplementary information