Abstract
In this review article, yeast model-based research advances regarding the role of Amyloid-β (Aβ), Tau and frameshift Ubiquitin UBB+1 in Alzheimer’s disease (AD) are discussed. Despite having limitations with regard to intercellular and cognitive AD aspects, these models have clearly shown their added value as complementary models for the study of the molecular aspects of these proteins, including their interplay with AD-related cellular processes such as mitochondrial dysfunction and altered proteostasis. Moreover, these yeast models have also shown their importance in translational research, e.g., in compound screenings and for AD diagnostics development. In addition to well-established Saccharomyces cerevisiae models, new upcoming Schizosaccharomyces pombe, Candida glabrata and Kluyveromyces lactis yeast models for Aβ and Tau are briefly described. Finally, traditional and more innovative research methodologies, e.g., for studying protein oligomerization/aggregation, are highlighted.
Highlights
Alzheimer’s disease (AD) is the most common neurodegenerative disease worldwide. It accounts for approximately 60–70% of all dementia cases and affects about 6% of the population aged over 65, whereas 2–10% of patients suffer from early-onset AD [1,2]
In another article [184], the same yeast model was used to study the effects of native Aβ and in addition to previously shown lower growth rate, a reduced respiratory rate and elevated levels of reactive oxygen species (ROS) were exhibited
Uses fluorescence as quantifiable reporter. It is clear from the above discussed articles that yeast has proven its value in modern AD research
Summary
Alzheimer’s disease (AD) is the most common neurodegenerative disease worldwide. It accounts for approximately 60–70% of all dementia cases and affects about 6% of the population aged over 65 (late-onset AD), whereas 2–10% of patients suffer from early-onset AD [1,2]. Widespread experimental evidence suggests that AD is characterized by synaptic dysfunction early on in the disease process, disrupting communication within neural circuits important for memory formation and other cognitive functions such as intellectuality and comprehensive capacity [5,6,7] Damage to these brain structures results in memory loss, language difficulties and learning deficits that are typically observed within early stages of clinical manifestation of AD. The neuronal damage is related to the accumulation of misfolded proteins into extracellular and intracellular aggregates, consisting of Aβ peptides or protein Tau, respectively [9,10] It is not yet clear whether the presence of these two hallmarks is the cause of AD or mainly the result of a cascade of cellular events including oxidative stress, mitochondrial dysfunction and apoptosis. The exact mechanism by which these proteins damage neurons is still unknown
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