ArticleProceedings of the National Academy of Sciences of the United States of America2020
Mechanical injuries of neurons induce tau mislocalization to dendritic spines and tau-dependent synaptic dysfunction.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 49 citations in OpenAlex.
- Neuromechanobiology: Bridging Mechanobiology and Neuroscience Through Evidence and Open Questions.Cells · 2026Review
- Multimodal characterization of intracranial biomechanics in a 3D biofidelic head surrogate.Journal of the mechanical behavior of biomedical materials · 2026Article
- Concussive injuries induce neuronal stress-dependent tau mislocalization to dendritic spines with acrolein and functional network alteration in TBI-on-a-chip.Lab on a chip · 2025Article
- Soccer Heading Exposure-Dependent Microstructural Injury at Depths of Sulci in Adult Amateur Players.Neurology · 2025Article
- Pathological Calcium Signaling in Traumatic Brain Injury and Alzheimer's Disease: From Acute Neuronal Injury to Chronic Neurodegeneration.International journal of molecular sciences · 2025Review
- Adherent cells undergo rate softening mediated by actomyosin kinetics.Biophysical journal · 2025Article
- Protein kinases in neurodegenerative diseases: current understandings and implications for drug discovery.Signal transduction and targeted therapy · 2025Review
- Early cerebrospinal fluid elevations of pTau-217 in severe traumatic brain injury subjects.Frontiers in neurology · 2025Article
- Neurodegeneration in the cortical sulcus is a feature of chronic traumatic encephalopathy and associated with repetitive head impacts.Acta neuropathologica · 2024Article
- Actomyosin-II protects axons from degeneration induced by mild mechanical stress.The Journal of cell biology · 2024Article
- G272V and P301L Mutations Induce Isoform Specific Tau Mislocalization to Dendritic Spines and Synaptic Dysfunctions in Cellular Models of 3R and 4R Tau Frontotemporal Dementia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Super-Resolution Imaging of Tau Proteins in Isolated and Immobilized Brain Synaptosomes.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Cavitation in blunt impact traumatic brain injury.Experiments in fluids · 2024Review
- Recent insights from non-mammalian models of brain injuries: an emerging literature.Frontiers in neurology · 2024Review
- Neuronal tau pathology worsens late-phase white matter degeneration after traumatic brain injury in transgenic mice.Acta neuropathologica · 2023Article
- Chronic traumatic encephalopathy (CTE): criteria for neuropathological diagnosis and relationship to repetitive head impacts.Acta neuropathologica · 2023Review
- Characterization of material properties and deformation in the ANGUS phantom during mild head impacts using MRI.Journal of the mechanical behavior of biomedical materials · 2023Article
- Biomechanics of Traumatic Head and Neck Injuries on Women: A State-of-the-Art Review and Future Directions.Biology · 2023Review
- NMDA and AMPA Receptors at Synapses: Novel Targets for Tau and α-Synuclein Proteinopathies.Biomedicines · 2022Review
- Caspase-2 Inhibitor Blocks Tau Truncation and Restores Excitatory Neurotransmission in Neurons Modeling FTDP-17 Tauopathy.ACS chemical neuroscience · 2022Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Chronic traumatic encephalopathy (CTE) is associated with repeated traumatic brain injuries (TBI) and is characterized by cognitive decline and the presence of neurofibrillary tangles (NFTs) of the protein tau in patients' brains. Here we provide direct evidence that cell-scale mechanical deformation can elicit tau abnormalities and synaptic deficits in neurons. Using computational modeling, we find that the early pathological loci of NFTs in CTE brains are regions of high deformation during injury. The mechanical energy associated with high-strain rate deformation alone can induce tau mislocalization to dendritic spines and synaptic deficits in cultured rat hippocampal neurons. These cellular changes are mediated by tau hyperphosphorylation and can be reversed through inhibition of GSK3β and CDK5 or genetic deletion of tau. Together, these findings identify a mechanistic pathway that directly relates mechanical deformation of neurons to tau-mediated synaptic impairments and provide a possibly exploitable therapeutic pathway to combat CTE.
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Registered trials
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