ArticleThe Journal of biological chemistry2012
Paired helical filaments from Alzheimer disease brain induce intracellular accumulation of Tau protein in aggresomes.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.
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Who cites it
79 citing papers in PubMed, 152 citations in OpenAlex.
- Excited-State Intramolecular Proton Transfer Enables Self-Reporting Fluorescent Photoaffinity Labeling in Live Cells.Journal of the American Chemical Society · 2026Article
- Extracellular Protein Quality Control in Tau Pathology.Molecular neurobiology · 2026Review
- Targeting ASK1 signaling in neurodegeneration: molecular insights and therapeutic promise.Apoptosis : an international journal on programmed cell death · 2025Review
- Neocortical tau propagation is a mediator of clinical heterogeneity in Alzheimer's disease.Molecular psychiatry · 2025Article
- Protein aggregation and neurodegenerative disease: Structural outlook for the novel therapeutics.Proteins · 2025Review
- Differential roles of human tau isoforms in the modulation of inflammation and development of neuropathology.Neurobiology of disease · 2025Article
- Therapeutic Potential of Dexmedetomidine in Neuropsychiatric Disorders: From the Bench to the Clinic.Current neuropharmacology · 2025Review
- Recent advances in therapeutic strategies for Alzheimer's and Parkinson's disease using protein/peptide co-modified polymer nanoparticles.Neuroprotection (Chichester, England) · 2024Review
- Proteomic Analysis Reveals Physiological Activities of Aβ Peptide for Alzheimer's Disease.International journal of molecular sciences · 2024Article
- Simple modeling of familial Alzheimer's disease using human pluripotent stem cell-derived cerebral organoid technology.Stem cell research & therapy · 2024Article
- Binge ethanol exposure in advanced age elevates neuroinflammation and early indicators of neurodegeneration and cognitive impairment in female mice.Brain, behavior, and immunity · 2024Article
- Modulation of Tau Pathology in Alzheimer's Disease by Dietary Bioactive Compounds.International journal of molecular sciences · 2024Review
- Loss of calcium/calmodulin-dependent protein kinase kinase 2, transferrin, and transferrin receptor proteins in the temporal cortex of Alzheimer's patients postmortem is associated with abnormal iron homeostasis: implications for patient survival.Frontiers in cell and developmental biology · 2024Article
- Inducing aggresome and stable tau aggregation in Neuro2a cells with an optogenetic tool.Biophysics and physicobiology · 2024Article
- Hypothesis review: Alzheimer's overture guidelines.Brain pathology (Zurich, Switzerland) · 2023Review
- The Adult Neurogenesis Theory of Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2023Article
- Extracellular vesicles in the study of Alzheimer's and Parkinson's diseases: Methodologies applied from cells to biofluids.Journal of neurochemistry · 2022Review
- Alzheimer's Disease: Challenges and a Therapeutic Opportunity to Treat It with a Neurotrophic Compound.Biomolecules · 2022Review
- Extensive accumulation of misfolded protein aggregates during natural aging and senescence.Frontiers in aging neuroscience · 2022Article
- Alzheimer's disease is an inherent, natural part of human brain aging: an integrated perspective.Free neuropathology · 2022Article
19 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
Abnormal folding of tau protein leads to the generation of paired helical filaments (PHFs) and neurofibrillary tangles, a key neuropathological feature in Alzheimer disease and tauopathies. A specific anatomical pattern of pathological changes developing in the brain suggests that once tau pathology is initiated it propagates between neighboring neuronal cells, possibly spreading along the axonal network. We studied whether PHFs released from degenerating neurons could be taken up by surrounding cells and promote spreading of tau pathology. Neuronal and non-neuronal cells overexpressing green fluorescent protein-tagged tau (GFP-Tau) were treated with isolated fractions of human Alzheimer disease-derived PHFs for 24 h. We found that cells internalized PHFs through an endocytic mechanism and developed intracellular GFP-Tau aggregates with attributes of aggresomes. This was particularly evident by the perinuclear localization of aggregates and redistribution of the vimentin intermediate filament network and retrograde motor protein dynein. Furthermore, the content of Sarkosyl-insoluble tau, a measure of abnormal tau aggregation, increased 3-fold in PHF-treated cells. An exosome-related mechanism did not appear to be involved in the release of GFP-Tau from untreated cells. The evidence that cells can internalize PHFs, leading to formation of aggresome-like bodies, opens new therapeutic avenues to prevent propagation and spreading of tau pathology.
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