Does cellular iron dysregulation play a causative role in Parkinson's disease?Ageing research reviews, Vol. 3, No. 3. (July 2004), pp. 327-343.
|
Reviews
[Write a review of this article]
There are no reviews of this article
Find related articles from these CiteULike users
Find related articles with these CiteULike tags
AbstractSelective dopaminergic cell loss in Parkinson's disease is correlated with increased levels of cellular iron. It is still hotly debated as to whether the increase in iron is an upstream event which acts to promote neurodegeneration via formation of oxidative stress or whether iron accumulates as a by-product of the neuronal cell loss. Here we review evidence for loss of iron homeostasis as a causative factor in disease-associated neurodegeneration and the primary players which may be involved. A series of recent studies suggest that iron regulatory proteins (IRPs) coordinate both cellular iron levels and energy metabolism, both of which are disrupted in Parkinson's disease (PD) and may in turn contribute to increased levels of oxidative stress associated with the disease. Iron has also been recently been implicated in promotion of alpha-synuclein aggregation either directly or via increasing levels of oxidative stress suggesting an important role for it in Lewy body formation, another important hallmark of the disease.
BibTeX record
RIS record