ArticleFrontiers in aging neuroscience2014
Lithium suppresses Aβ pathology by inhibiting translation in an adult Drosophila model of Alzheimer's disease.
Article in Frontiers in aging neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
34 citing papers in PubMed, 103 citations in OpenAlex.
- Blood and cerebrospinal fluid biomarker changes in patients with HIV-associated neurocognitive impairment treated with lithium: analysis from a randomised placebo-controlled trial.Journal of neurovirology · 2023Trial
- Article
- Dietary sucrose determines the regulatory activity of lithium on gene expression and lifespan inAging · 2024Article
- Molecular mechanisms and therapeutic potential of lithium in Alzheimer's disease: repurposing an old class of drugs.Frontiers in pharmacology · 2024Review
- The Role of the Transcription Factor Nrf2 in Alzheimer's Disease: Therapeutic Opportunities.Biomolecules · 2023Review
- Using Optogenetics to Model Cellular Effects of Alzheimer's Disease.International journal of molecular sciences · 2023Review
- Article
- Editorial for the Special Issue "Adaptation, Aging, and Cell Death in Yeast Stress Response: Models, Mechanisms and Applications".Microorganisms · 2022Article
- The Effect of Lithium on the Budding YeastMicroorganisms · 2022Article
- Potential mechanisms underlying lithium treatment for Alzheimer's disease and COVID-19.European review for medical and pharmacological sciences · 2022Review
- Age-related GSK3β overexpression drives podocyte senescence and glomerular aging.The Journal of clinical investigation · 2022Article
- Article
- Lithium Benzoate Exerts Neuroprotective Effect by Improving Mitochondrial Function, Attenuating Reactive Oxygen Species, and Protecting Cognition and Memory in an Animal Model of Alzheimer's Disease.Journal of Alzheimer's disease reports · 2022Article
- LiCl attenuates impaired learning and memory of APP/PS1 mice, which in mechanism involves α7 nAChRs and Wnt/β-catenin pathway.Journal of cellular and molecular medicine · 2021Article
- Review
- Article
- Lithium Chloride Sensitivity in Yeast and Regulation of Translation.International journal of molecular sciences · 2020Article
- The quest to slow ageing through drug discovery.Nature reviews. Drug discovery · 2020Review
- Pharmacological Treatment of Alzheimer's Disease: Insights fromInternational journal of molecular sciences · 2020Review
- Drug synergy as a strategy for compression of morbidity in a Caenorhabditis elegans model of Alzheimer's disease.GeroScience · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
The greatest risk factor for Alzheimer's disease (AD) is age, and changes in the ageing nervous system are likely contributors to AD pathology. Amyloid beta (Aβ) accumulation, which occurs as a result of the amyloidogenic processing of amyloid precursor protein (APP), is thought to initiate the pathogenesis of AD, eventually leading to neuronal cell death. Previously, we developed an adult-onset Drosophila model of AD. Mutant Aβ42 accumulation led to increased mortality and neuronal dysfunction in the adult flies. Furthermore, we showed that lithium reduced Aβ42 protein, but not mRNA, and was able to rescue Aβ42-induced toxicity. In the current study, we investigated the mechanism/s by which lithium modulates Aβ42 protein levels and Aβ42 induced toxicity in the fly model. We found that lithium caused a reduction in protein synthesis in Drosophila and hence the level of Aβ42. At both the low and high doses tested, lithium rescued the locomotory defects induced by Aβ42, but it rescued lifespan only at lower doses, suggesting that long-term, high-dose lithium treatment may have induced toxicity. Lithium also down-regulated translation in the fission yeast Schizosaccharomyces pombe associated with increased chronological lifespan. Our data highlight a role for lithium and reduced protein synthesis as potential therapeutic targets for AD pathogenesis.
Indexed as
Identifiers
What OpenQuestion holds
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.