Funding agencies: The authors' own work described in this article was supported by the Medical Research Council, UK (grant no.: U138164490), Parkinson's UK (grant nos.: G-0601 and K-1103), and the European Community (FP7: HEALTH-F2-2008-201716).
Article first published online: 24 SEP 2012
Copyright © 2012 Movement Disorder Society
Volume 27, Issue 12, pages 1478–1483, October 2012
How to Cite
Bolam, J. P. and Pissadaki, E. K. (2012), Living on the edge with too many mouths to feed: Why dopamine neurons die. Mov. Disord., 27: 1478–1483. doi: 10.1002/mds.25135
Relevant conflicts of interest/financial disclosures: Nothing to report.
Full financial disclosures and author roles may be found in the online version of this article.
- Issue published online: 18 OCT 2012
- Article first published online: 24 SEP 2012
- Manuscript Accepted: 17 JUL 2012
- Manuscript Revised: 2 JUL 2012
- Manuscript Received: 24 APR 2012
- Medical Research Council, UK. Grant Number: U138164490
- Parkinson's UK. Grant Numbers: G-0601, K-1103
- European Community. Grant Number: FP7: HEALTH-F2-2008-201716
- dopamine neurons;
Although genes, protein aggregates, environmental toxins, and other factors associated with Parkinson's disease (PD) are widely distributed in the nervous system and affect many classes of neurons, a consistent feature of PD is the exceptional and selective vulnerability of dopamine (DA) neurons of the SNc. What is it about these neurons, among all other neurons in the brain, that makes them so susceptible in PD? We hypothesize that a major contributory factor is the unique cellular architecture of SNc DA neuron axons. Their large, complex axonal arbour puts them under such a tight energy budget that it makes them particularly susceptible to factors that contribute to cell death, including unique molecular characteristics associated with SNc DA neurons and nonspecific, nervous-system–wide factors. © 2012 Movement Disorder Society