Abstract
Alzheimer's (AD) and Parkinson's (PD) diseases are the two most common causes of dementia in aged population. Both are protein-misfolding diseases characterized by the presence of protein deposits in the brain. Despite growing evidence suggesting that oxidative stress is critical to neuronal death, its precise role in disease etiology and progression has not yet been fully understood. Budding yeast Saccharomyces cerevisiae shares conserved biological processes with all eukaryotic cells, including neurons. This fact together with the possibility of simple and quick genetic manipulation highlights this organism as a valuable tool to unravel complex and fundamental mechanisms underlying neurodegeneration. In this paper, we summarize the latest knowledge on the role of oxidative stress in neurodegenerative disorders, with emphasis on AD and PD. Additionally, we provide an overview of the work undertaken to study AD and PD in yeast, focusing the use of this model to understand the effect of oxidative stress in both diseases.
Highlights
Misfolded proteins are typically insoluble and tend to form long linear or fibrillar aggregates known as amyloid deposits
As outlined in this paper, several in vivo and in vitro studies point towards a role of oxidative stress in Alzheimer’s disease (AD) and Parkinson’s disease (PD) pathogenesis
Concerning AD, there are quite a few contradictory reports regarding the role of oxidative stress in the disease
Summary
Misfolded proteins are typically insoluble and tend to form long linear or fibrillar aggregates known as amyloid deposits. The generation of free radicals is closely linked with the involvement of trace metals, copper and irons [5, 6]. Whenever cells are subjected to stress conditions, an excess of superoxide anion radical acts as an oxidant of Fe-S clusters of several enzymes, releasing “free iron.”. Despite the absence of a nervous system in yeast, several studies have shown that this eukaryotic unicellular organism is a suitable model system to understand the molecular mechanisms underlying neurodegenerative diseases. The knowledge from those studies is summarized .
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