ArticleNeurobiology of aging2016
Metabolic changes may precede proteostatic dysfunction in a Drosophila model of amyloid beta peptide toxicity.
Article in Neurobiology of aging, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Role of Oxidative Stress in Human Neurodegenerative Pathologies: Lessons from theCurrent topics in medicinal chemistry · 2026Review
- Coordinated Regulation of Myelination by Growth Factor and Amino-acid Signaling Pathways.Neuroscience bulletin · 2023Review
- Recent insights into the role of glia and oxidative stress in Alzheimer's disease gained from Drosophila.Current opinion in neurobiology · 2022Review
- Muscle-to-Brain Signaling Via Myokines and Myometabolites.Brain plasticity (Amsterdam, Netherlands) · 2022Review
- Proteasome stress in skeletal muscle mounts a long-range protective response that delays retinal and brain aging.Cell metabolism · 2021Article
- Article
- Amyloid β42 peptide is toxic to non-neural cells inBiology open · 2017Article
- Metabolomic Studies inGenetics · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Amyloid beta (Aβ) peptide aggregation is linked to the initiation of Alzheimer's disease; accordingly, aggregation-prone isoforms of Aβ, expressed in the brain, shorten the lifespan of Drosophila melanogaster. However, the lethal effects of Aβ are not apparent until after day 15. We used shibire(TS) flies that exhibit a temperature-sensitive paralysis phenotype as a reporter of proteostatic robustness. In this model, we found that increasing age but not Aβ expression lowered the flies' permissive temperature, suggesting that Aβ did not exert its lethal effects by proteostatic disruption. Instead, we observed that chemical challenges, in particular oxidative stressors, discriminated clearly between young (robust) and old (sensitive) flies. Using nuclear magnetic resonance spectroscopy in combination with multivariate analysis, we compared water-soluble metabolite profiles at various ages in flies expressing Aβ in their brains. We observed 2 genotype-linked metabolomic signals, the first reported the presence of any Aβ isoform and the second the effects of the lethal Arctic Aβ. Lethality was specifically associated with signs of oxidative respiration dysfunction and oxidative stress.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.