Upstream deregulation of calcium signaling in Parkinson's disease

Front Mol Neurosci. 2014 Jun 17;7:53. doi: 10.3389/fnmol.2014.00053. eCollection 2014.

Abstract

Parkinson's disease (PD) is a major health problem affecting millions of people worldwide. Recent studies provide compelling evidence that altered Ca(2) (+) homeostasis may underlie disease pathomechanism and be an inherent feature of all vulnerable neurons. The downstream effects of altered Ca(2) (+) handling in the distinct subcellular organelles for proper cellular function are beginning to be elucidated. Here, we summarize the evidence that vulnerable neurons may be exposed to homeostatic Ca(2) (+) stress which may determine their selective vulnerability, and suggest how abnormal Ca(2) (+) handling in the distinct intracellular compartments may compromise neuronal health in the context of aging, environmental, and genetic stress. Gaining a better understanding of the varied effects of Ca(2) (+) dyshomeostasis may allow novel combinatorial therapeutic strategies to slow PD progression.

Keywords: Golgi; Parkinson’s disease; calcium; dopamine; endoplasmic reticulum; lysosomes; mitochondria.

Publication types

  • Review