ArticleJournal of Alzheimer's disease : JAD2014
Proteins recruited to exosomes by tau overexpression implicate novel cellular mechanisms linking tau secretion with Alzheimer's disease.
Article in Journal of Alzheimer's disease : JAD, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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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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Who cites it
45 citing papers in PubMed, 70 citations in OpenAlex.
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- The Role of Extracellular Vesicles and Microparticles in Central Nervous System Disorders: Mechanisms, Biomarkers, and Therapeutic Potential.Cellular and molecular neurobiology · 2024Review
- Frontotemporal dementia-like disease progression elicited by seeded aggregation and spread of FUS.Molecular neurodegeneration · 2024Article
- APP mediates tau uptake and its overexpression leads to the exacerbated tau pathology.Cellular and molecular life sciences : CMLS · 2023Article
- Salivary Exosomes in Health and Disease: Future Prospects in the Eye.International journal of molecular sciences · 2023Review
- Unconventional protein secretion (UPS): role in important diseases.Molecular biomedicine · 2023Review
- Contribution of Extracellular Vesicles and Molecular Chaperones in Age-Related Neurodegenerative Disorders of the CNS.International journal of molecular sciences · 2023Review
- Traumatic brain injury and the pathways to cerebral tau accumulation.Frontiers in neurology · 2023Review
- Can Soluble Immune Checkpoint Molecules on Exosomes Mediate Inflammation?Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2022Review
- Systems Genetic Identification of Mitochondrion-Associated Alzheimer's Disease Genes and Implications for Disease Risk Prediction.Biomedicines · 2022Article
- Slingshot homolog-1 mediates the secretion of small extracellular vesicles containing misfolded proteins by regulating autophagy cargo receptors and actin dynamics.Frontiers in aging neuroscience · 2022Article
- Alzheimer's disease is an inherent, natural part of human brain aging: an integrated perspective.Free neuropathology · 2022Article
- The prion-like transmission of tau oligomersFrontiers in aging neuroscience · 2022Review
- The Emerging Role of the Interaction of Extracellular Vesicle and Autophagy-Novel Insights into Neurological Disorders.Journal of inflammation research · 2022Review
- Decrease of neuronal FKBP4/FKBP52 modulates perinuclear lysosomal positioning and MAPT/Tau behavior during MAPT/Tau-induced proteotoxic stress.Autophagy · 2021Article
- Netrin-1 in Glioblastoma Neovascularization: The New Partner in Crime?International journal of molecular sciences · 2021Review
- Extracellular Vesicles under Oxidative Stress Conditions: Biological Properties and Physiological Roles.Cells · 2021Review
- Circulating exosomes repair endothelial cell damage by delivering miR-193a-5p.Journal of cellular and molecular medicine · 2021Article
- Roles of Exosomes and Exosomal MicroRNAs in Postoperative Sleep Disturbance.Nature and science of sleep · 2021Review
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Tau misprocessing to form aggregates and other toxic species has emerged as a major feature in our developing understanding of the etiology and pathogenesis of Alzheimer's disease (AD). The significance of tau misprocessing in AD has been further emphasized by recent studies showing that tau can be secreted from neurons via exosomes and may itself be an important agent in the spreading of neurofibrillary lesions within the brain. Tau secretion occurs most readily under disease-associated conditions in cellular models, suggesting that cellular changes responsible for secretion, possibly including tau oligomerization, could play a key role in the propagation of neurofibrillary lesions in neurodegenerative disease. Here we show that overexpression of 4R0N human tau in neuroblastoma cells recruits mitochondrial and axonogenesis-associated proteins relevant to neurodegeneration into the exosomal secretion pathway via distinct mechanisms. The recruitment of mitochondrial proteins appears to be linked to autophagy disruption (exophagy) in multiple neurodegenerative conditions but has few known direct links to AD and tau. By contrast, the involvement of synaptic plasticity and axonogenesis markers is highly specific to both tau and AD and may be relevant to the reactivation of developmental programs involving tau in AD and the recently demonstrated ability of secreted tau to establish tissue distribution gradients in CNS neuropil. We also found a highly significant correlation between genes that are significantly downregulated in multiple forms of AD and proteins that have been recruited to exosomes by tau, which we interpret as strong evidence for the central involvement of tau secretion in AD cytopathogenesis. Our results suggest that multiple cellular mechanisms may link tau secretion to both toxicity and neurofibrillary lesion spreading in AD and other tauopathies.
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