ArticleBrain communications2020
Tumour necrosis factor induces increased production of extracellular amyloid-β- and α-synuclein-containing aggregates by human Alzheimer's disease neurons.
Article in Brain communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 31 citations in OpenAlex.
- The Role of TNF-α in Neuropathic Pain: An Immunotherapeutic Perspective.Life (Basel, Switzerland) · 2025Review
- Interplay of Neuroinflammation and Gut Microbiota Dysbiosis in Alzheimer's Disease Using Diffusion Kurtosis Imaging Biomarker in 3 × Tg-AD Mouse Models.ACS chemical neuroscience · 2025Article
- Molecular Determinants of Protein Pathogenicity at the Single-Aggregate Level.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Clearance of beta-amyloid and tau aggregates is size dependent and altered by an inflammatory challenge.Brain communications · 2025Article
- Disable 2, A Versatile Tissue Matrix Multifunctional Scaffold Protein with Multifaceted Signaling: Unveiling Role in Breast Cancer for Therapeutic Revolution.Cell biochemistry and biophysics · 2024Review
- Neuropathological and sociodemographic factors associated with the cortical amyloid load in aging and Alzheimer's disease.GeroScience · 2024Article
- Adeno-associated virus (AAV) 9-mediated gene delivery of Nurr1 and Foxa2 ameliorates symptoms and pathologies of Alzheimer disease model mice by suppressing neuro-inflammation and glial pathology.Molecular psychiatry · 2023Article
- Multiomic prediction of therapeutic targets for human diseases associated with protein phase separation.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Neutrophil activation may trigger tau burden contributing to cognitive progression of chronic sleep disturbance in elderly individuals not living with dementia.BMC medicine · 2023Article
- Identification of the molecular mechanism of insulin-like growth factor-1 (IGF-1): a promising therapeutic target for neurodegenerative diseases associated with metabolic syndrome.Cell & bioscience · 2023Review
- Review
- Low-grade peripheral inflammation affects brain pathology in the AppActa neuropathologica communications · 2021Article
- Broader Insights into Understanding Tumor Necrosis Factor and Neurodegenerative Disease Pathogenesis Infer New Therapeutic Approaches.Journal of Alzheimer's disease : JAD · 2021Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
In addition to increased aberrant protein aggregation, inflammation has been proposed as a key element in the pathogenesis and progression of Alzheimer's disease. How inflammation interacts with other disease pathways and how protein aggregation increases during disease are not clear. We used single-molecule imaging approaches and membrane permeabilization assays to determine the effect of chronic exposure to tumour necrosis factor, a master proinflammatory cytokine, on protein aggregation in human-induced pluripotent stem cell-derived neurons harbouring monogenic Alzheimer's disease mutations. We report that exposure of Alzheimer's disease neurons, but not control neurons, to tumour necrosis factor induces substantial production of extracellular protein aggregates. Aggregates from Alzheimer's disease neurons are composed of amyloid-β and α-synuclein and induce significant permeabilization of lipid membranes in an assay of pathogenicity. These findings provide support for a causal relationship between two crucial processes in Alzheimer's disease pathogenesis and suggest that targeting inflammation, particularly tumour necrosis factor, may have beneficial downstream effects on ameliorating aberrant protein aggregation and accumulation.
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Registered trials
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