ArticleFrontiers in cellular neuroscience2018
The Involvement of Aβ42 and Tau in Nucleolar and Protein Synthesis Machinery Dysfunction.
Article in Frontiers in cellular neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 41 citations in OpenAlex.
- A proteomic analysis of the PHF-forming tau fragment (tau297-391) following uptake into differentiated human neuronal SHSY5Y cells.Bioscience reports · 2026Article
- Beyond the Ribosome: The Expanding Role of the Nucleolus in Neurodegenerative Pathways.Molecular neurobiology · 2026Review
- Nucleolar aggregation of key neuropathological proteins in the postmortem neurodegenerative brain.Acta neuropathologica · 2025Article
- Mutant MAPT Induces rDNA Transcriptional Hyperactivation and Nucleolar Stress in Cellular Models.Research square · 2025Article
- Modified tau leads to neuronal and global ribosome dysfunction inbioRxiv : the preprint server for biology · 2025Article
- Investigating Connectivity Deficits in Alzheimer's Disease Using a Novel 3D Bioprinted Model Designed to Quantify Neurite Outgrowth.Bioengineering (Basel, Switzerland) · 2025Article
- Organelle abnormalities in Alzheimer's disease.Organelle (Tucson, Ariz.) · 2025Article
- Novel avenues of tau research.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Review
- Translational profiling identifies sex-specific metabolic and epigenetic reprogramming of cortical microglia/macrophages in APPPS1-21 mice with an antibiotic-perturbed-microbiome.Molecular neurodegeneration · 2023Article
- CRISPRi screening reveals regulators of tau pathology shared between exosomal and vesicle-free tau.Life science alliance · 2023Article
- Dityrosine cross-linking and its potential roles in Alzheimer's disease.Frontiers in neuroscience · 2023Review
- Ribosomal proteins are blood biomarkers and associated with CD4+ T cell activation in Alzheimer's disease: a study based on machine learning strategies and scRNA-Seq data validation.American journal of translational research · 2023Article
- SMN-deficient cells exhibit increased ribosomal DNA damage.Life science alliance · 2022Article
- Tau mRNA Metabolism in Neurodegenerative Diseases: A Tangle Journey.Biomedicines · 2022Review
- Nicotinic receptor components of amyloid beta 42 proteome regulation in human neural cells.PloS one · 2022Article
- Non-Canonical Roles of Tau and Their Contribution to Synaptic Dysfunction.International journal of molecular sciences · 2021Review
- Nuclear dynamics and stress responses in Alzheimer's disease.Molecular neurodegeneration · 2021Review
- Altered ribosomal function and protein synthesis caused by tau.Acta neuropathologica communications · 2021Article
- Tau Modulates mRNA Transcription, Alternative Polyadenylation Profiles of hnRNPs, Chromatin Remodeling and Spliceosome Complexes.Frontiers in molecular neuroscience · 2021Article
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Alzheimer's disease (AD) is the most common form of dementia and is distinguished from other dementias by observation of extracellular Amyloid-β (Aβ) plaques and intracellular neurofibrillary tangles, comprised of fibrils of Aβ and tau protein, respectively. At early stages, AD is characterized by minimal neurodegeneration, oxidative stress, nucleolar stress, and altered protein synthesis machinery. It is generally believed that Aβ oligomers are the neurotoxic species and their levels in the AD brain correlate with the severity of dementia suggesting that they play a critical role in the pathogenesis of the disease. Here, we show that the incubation of differentiated human neuroblastoma cells (SHSY5Y) with freshly prepared Aβ42 oligomers initially resulted in oxidative stress and subtle nucleolar stress in the absence of DNA damage or cell death. The presence of exogenous Aβ oligomers resulted in altered nuclear tau levels as well as phosphorylation state, leading to altered distribution of nucleolar tau associated with nucleolar stress. These markers of cellular dysfunction worsen over time alongside a reduction in ribosomal RNA synthesis and processing, a decrease in global level of newly synthesized RNA and reduced protein synthesis. The interplay between Aβ and tau in AD remains intriguing and Aβ toxicity has been linked to tau phosphorylation and changes in localization. These findings provide evidence for the involvement of Aβ42 effects on nucleolar tau and protein synthesis machinery dysfunction in cultured cells. Protein synthesis dysfunction is observed in mild cognitive impairment and early AD in the absence of significant neuronal death.
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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.