Abstract
Parkinson’s disease (PD) is a major health problem affecting millions of people worldwide. Recent studies provide compelling evidence that altered Ca2+ homeostasis may underlie disease pathomechanism and be an inherent feature of all vulnerable neurons. The downstream effects of altered Ca2+ 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 Ca2+ stress which may determine their selective vulnerability, and suggest how abnormal Ca2+ 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 Ca2+ dyshomeostasis may allow novel combinatorial therapeutic strategies to slow PD progression.
Highlights
Parkinson’s disease (PD) is a major health problem affecting millions of people worldwide
WHICH NEURONS DIE IN PD? Parkinson’s disease (PD) is an incurable late-onset neurodegenerative disorder which is strongly associated with aging, as evidenced by the exponential increase in incidence above the age of 65
Since not all dopaminergic neurons are at risk in PD, and since elevating DA levels in PD patients by L-DOPA administration does not accelerate the progression of PD (Fahn, 2005), DA unlikely is the principal culprit, even though its effects may further worsen the cellular deficits related to oxidant stress and/or protein aggregation triggered by other means
Summary
Parkinson’s disease (PD) is a major health problem affecting millions of people worldwide. The increased metabolic demand of SNc neurons may give rise to an increase in the basal level of mitochondrial oxidant stress, as high rates of metabolic activity cause increased ROS production (Figure 1; Lee et al, 2001).
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