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Calcium, cellular aging, and selective neuronal vulnerability in Parkinson's disease
D James Surmeier1, Jaime N Guzman, Javier Sanchez-Padilla
1Department of Physiology, Feinberg School of Medicine, Northwestern University, 303 E. Chicago Ave., Chicago, IL 60611, USA. j-surmeier@northwestern.edu
Cell Calcium
|January 8, 2010
Summary
Parkinson's disease involves dopamine neuron loss. Sustained calcium channel activity may increase neuron vulnerability to toxins, contributing to Parkinson's disease progression.
Area of Science:
- Neuroscience
- Neurodegenerative Diseases
Background:
- Parkinson's disease (PD) is a prevalent neurodegenerative disorder.
- Motor symptoms stem from dopamine neuron loss in the substantia nigra pars compacta (SNc).
- The selective vulnerability of these neurons remains unclear.
Purpose of the Study:
- To review the hypothesis that metabolic stress from calcium (Ca2+) entry contributes to PD pathogenesis.
- To explore the role of L-type Ca2+ channels in SNc dopamine neuron vulnerability.
Main Methods:
- Review of existing literature on PD, dopamine neuron function, and calcium channel activity.
- Analysis of studies linking L-type Ca2+ channels to PD risk and animal models.
- Examination of the interplay between Ca2+ entry, mitochondrial function, and neuroprotection.
Main Results:
- L-type Ca2+ channel engagement during pacemaking sensitizes SNc dopamine neurons to mitochondrial toxins.
- Epidemiological data suggests a correlation between L-type Ca2+ channels and PD risk.
- Sustained Ca2+ entry may induce metabolic stress, exacerbating neurodegeneration.
Conclusions:
- The primary driver of PD neurodegeneration may be metabolic stress induced by sustained Ca2+ entry.
- This stress is amplified by compromised oxidative defenses or proteostasis.
- Targeting L-type Ca2+ channels could be a potential therapeutic strategy for PD.
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