Abstract
It is now increasingly appreciated that glial cells play a critical role in the regulation of iron homeostasis. Impairment of these properties might lead to dysfunction of iron metabolism and neurodegeneration of neurons. We have previously shown that dysfunction of glia could cause iron deposit and enhance iron-induced degeneration of dopamine (DA) neurons in Parkinson’s disease (PD). There also has been a substantial growth of knowledge regarding the iron metabolism of glia and their effects on iron accumulation and degeneration of DA neurons in PD in recent years. Here, we attempt to describe the role of iron metabolism of glia and the effect of glia on iron accumulation and degeneration of DA neurons in the substantia nigra of PD. This could provide evidence to reveal the mechanisms underlying nigral iron accumulation of DA neurons in PD and provide the basis for discovering new potential therapeutic targets for PD.
Highlights
Parkinson’s disease (PD) is a common neurodegenerative disorder characterized by resting tremor, rigidity, and bradykinesia
Evidence has shown that Cp could potentiate LPSinduced activation of microglia and increase the production of IL-6 (Lazzaro et al, 2014). These findings provide powerful evidence that the cooperative effect of neuroinflammation and iron accumulation may enhance the degeneration of DA neurons in PD
Immunohistochemical studies of PD patients revealed an increase of LfR on substantia nigra pars compacta (SNpc) neurons and microvessels (Faucheux et al, 1995). These findings indicate a possible role of Lf/LfR in nigral iron accumulation and the subsequent degeneration of dopaminergic neurons in PD
Summary
Parkinson’s disease (PD) is a common neurodegenerative disorder characterized by resting tremor, rigidity, and bradykinesia. Increased iron and DMT1 expression were observed in post-mortem PD patients (Salazar et al, 2008) This indicated that abnormal expression of iron transporters caused iron accumulation and enhanced iron-induced neurotoxicity in PD. Astrocytes are of vital importance for iron transport across BBB and maintain brain iron homeostasis (Dringen et al, 2007) This might be the main source of iron for neurons and microglia (Figure 2). Studies found that iron overload could activate microglia and astrocytes and promote the release inflammatory factor and neurotrophic factors, which were involved in the regulation of iron metabolism of DA neurons (Wang J. et al, 2013; Zhang H.Y. et al, 2014).
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