ArticleFrontiers in molecular neuroscience2017
Interplay of Energetics and ER Stress Exacerbates Alzheimer's Amyloid-β (Aβ) Toxicity in Yeast.
Article in Frontiers in molecular neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Microbial Pathogenesis and Pathophysiology of Alzheimer's Disease: A Systematic Assessment of Microorganisms' Implications in the Neurodegenerative Disease.Frontiers in neuroscience · 2021Pooled it
- Combinatorial engineering approaches for improved lipid production in Saccharomyces cerevisiae.FEMS yeast research · 2026Article
- Simple model systems reveal conserved mechanisms of Alzheimer's disease and related tauopathies.Molecular neurodegeneration · 2023Review
- Alzheimer's Disease: Significant Benefit from the Yeast-Based Models.International journal of molecular sciences · 2023Review
- Dataset for suppressors of amyloid-β toxicity and their functions in recombinant protein production in yeast.Data in brief · 2022Article
- UBBAging · 2021Article
- A Toxic Synergy between Aluminium and Amyloid Beta in Yeast.International journal of molecular sciences · 2021Article
- Protein Homeostasis Networks and the Use of Yeast to Guide Interventions in Alzheimer's Disease.International journal of molecular sciences · 2020Review
- FMN reduces Amyloid-β toxicity in yeast by regulating redox status and cellular metabolism.Nature communications · 2020Article
- An Apoptotic and Endosymbiotic Explanation of the Warburg and the Inverse Warburg Hypotheses.International journal of molecular sciences · 2018Review
- Global rewiring of cellular metabolism renders Saccharomyces cerevisiae Crabtree negative.Nature communications · 2018Article
- Recent Insights on Alzheimer's Disease Originating from Yeast Models.International journal of molecular sciences · 2018Review
- Different Expression Levels of Human Mutant Ubiquitin BFrontiers in molecular neuroscience · 2018Article
- The Impact of ESCRT on AβFrontiers in molecular neuroscience · 2018Article
- Exploiting Post-mitotic Yeast Cultures to Model Neurodegeneration.Frontiers in molecular neuroscience · 2018Review
- Calcium Dysregulation in Alzheimer's Disease: A Target for New Drug Development.Journal of Alzheimer's disease & Parkinsonism · 2017Article
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is a progressive neurodegeneration. Oligomers of amyloid-β peptides (Aβ) are thought to play a pivotal role in AD pathogenesis, yet the mechanisms involved remain unclear. Two major isoforms of Aβ associated with AD are Aβ40 and Aβ42, the latter being more toxic and prone to form oligomers. Here, we took a systems biology approach to study two humanized yeast AD models which expressed either Aβ40 or Aβ42 in bioreactor cultures. Strict control of oxygen availability and culture pH, strongly affected chronological lifespan and reduced variations during cell growth. Reduced growth rates and biomass yields were observed upon Aβ42 expression, indicating a redirection of energy from growth to maintenance. Quantitative physiology analyses furthermore revealed reduced mitochondrial functionality and ATP generation in Aβ42 expressing cells, which matched with observed aberrant mitochondrial structures. Genome-wide expression level analysis showed that Aβ42 expression triggered strong ER stress and unfolded protein responses. Equivalent expression of Aβ40, however, induced only mild ER stress, which resulted in hardly affected physiology. Using AD yeast models in well-controlled cultures strengthened our understanding on how cells translate different Aβ toxicity signals into particular cell fate programs, and further enhance their potential as a discovery platform to identify possible therapies.
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