ArticleBrain pathology (Zurich, Switzerland)2021
Contribution of the astrocytic tau pathology to synapse loss in progressive supranuclear palsy and corticobasal degeneration.
Article in Brain pathology (Zurich, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 35 citations in OpenAlex.
- Using iPSC models to examine neuron-glia interactions in neurodegenerative diseases.Bioscience reports · 2026Review
- Cell Cycle Dysfunction and Metabolic Alterations Consistent With Pathological Tau in Progressive Supranuclear Palsy Derived Fibroblasts.Molecular neurobiology · 2026Article
- Tau conformation, distribution and PET imaging correlations in progressive supranuclear palsy.Translational neurodegeneration · 2026Review
- From Neuron-Centric to Glia-Centric: How Aging Glial Networks Drive Neurodegenerative Disease.Journal of neurochemistry · 2026Review
- Glutamatergic and GABAergic Synapses in the Human Spinal Dorsal Horn Revealed With Immunohistochemistry.The Journal of comparative neurology · 2025Article
- Tau-Targeted Therapeutic Strategies: Mechanistic Targets, Clinical Pipelines, and Analysis of Failures.Cells · 2025Review
- A Spanish-Portuguese GWAS of progressive supranuclear palsy reveals a novel risk locus in NFASC.European journal of human genetics : EJHG · 2025Article
- Astrocyte-driven vasoconstriction impairs glymphatic clearance in a human tauopathy-on-chip model.APL bioengineering · 2025Article
- Pathomechanisms of neuropsychiatric disturbances in atypical parkinsonian disorders: a current view.Journal of neural transmission (Vienna, Austria : 1996) · 2025Review
- The Spectrum of Cognitive Impairment in Atypical Parkinsonism Syndromes: A Comprehensive Review of Current Understanding and Research.Diseases (Basel, Switzerland) · 2025Review
- DYRK1A in the physiology and pathology of the neuron-astrocyte axis.Frontiers in neuroscience · 2025Review
- Selective cellular and regional vulnerability in frontotemporal lobar degeneration: a scoping review.Free neuropathology · 2025Review
- A human Tau expressing zebrafish model of progressive supranuclear palsy identifies Brd4 as a regulator of microglial synaptic elimination.Nature communications · 2024Article
- Article
- Loss and microglia phagocytosis of synaptic proteins in frontotemporal lobar degeneration with TDP-43 proteinopathy.Neurochemistry international · 2024Article
- Pathomechanisms of cognitive and behavioral impairment in corticobasal degeneration.Journal of neural transmission (Vienna, Austria : 1996) · 2023Review
- Pathological Impact of Tau Proteolytical Process on Neuronal and Mitochondrial Function: a Crucial Role in Alzheimer's Disease.Molecular neurobiology · 2023Review
- Pathomechanisms of depression in progressive supranuclear palsy.Journal of neural transmission (Vienna, Austria : 1996) · 2023Review
- Intracellular accumulation of tau oligomers in astrocytes and their synaptotoxic action rely on Amyloid Precursor Protein Intracellular Domain-dependent expression of Glypican-4.Progress in neurobiology · 2023Article
- Pathomechanisms of cognitive impairment in progressive supranuclear palsy.Journal of neural transmission (Vienna, Austria : 1996) · 2023Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Primary 4-repeat tauopathies with frontotemporal lobar degeneration (FTLD) like Progressive Supranuclear Palsy (PSP) or Corticobasal Degeneration (CBD) show diverse cellular pathology in various brain regions. Besides shared characteristics of neuronal and oligodendroglial cytoplasmic inclusions of accumulated hyperphosphorylated tau protein (pTau), astrocytes in PSP and CBD contain pathognomonic pTau aggregates - hence, lending the designation tufted astrocytes (TA) or astrocytic plaques (AP), respectively. pTau toxicity is most commonly assigned to neurons, whereas the implications of astrocytic pTau for maintaining neurotransmission within the tripartite synapse of human brains is not well understood. We performed immunofluorescent synapse labeling and automated puncta quantification in the medial frontal gyrus (MFG) and striatal regions from PSP and CBD postmortem samples to capture morphometric synaptic alterations. This approach indicated general synaptic losses of both, excitatory and inhibitory bipartite synapses in the frontal cortex of PSP cases, whereas in CBD lower synapse densities were only related to astrocytic plaques. In contrast to tufted astrocytes in PSP, affected astrocytes in CBD could not preserve synaptic integrity within their spatial domains, when compared to non-affected internal astrocytes or astrocytes in healthy controls. These findings suggest a pTau pathology-associated role of astrocytes in maintaining connections within neuronal circuits, considered as the microscopic substrate of cognitive dysfunction in CBD. By contrasting astrocytic-synaptic associations in both diseases, we hereby highlight astrocytic pTau as an important subject of prospective research and as a potential cellular target for therapeutic approaches in the primary tauopathies PSP and CBD.
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