ArticleNeuropathology and applied neurobiology2017
A quantitative study of tau pathology in 11 cases of chronic traumatic encephalopathy.
Article in Neuropathology and applied neurobiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
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Who cites it
13 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Neuropathology in chronic traumatic encephalopathy: a systematic review of comparative post-mortem histology literature.Acta neuropathologica communications · 2022Pooled it
- Cortical circuit principles predict patterns of trauma induced tauopathy in humans.Cerebral cortex (New York, N.Y. : 1991) · 2025Article
- 'Knock down the brain': a nonlinear analysis of electroencephalography to study the effects of sub-concussion in boxers.European journal of neurology · 2025Article
- Tau Pathology in Chronic Traumatic Encephalopathy is Primarily Neuronal.Journal of neuropathology and experimental neurology · 2022Article
- Tau seeding in chronic traumatic encephalopathy parallels disease severity.Acta neuropathologica · 2021Article
- Chronic Traumatic Encephalopathy and Neuropathological Comorbidities.Seminars in neurology · 2020Review
- Astroglial tau pathology alone preferentially concentrates at sulcal depths in chronic traumatic encephalopathy neuropathologic change.Brain communications · 2020Article
- Mild Chronic Traumatic Encephalopathy Neuropathology in People With No Known Participation in Contact Sports or History of Repetitive Neurotrauma.Journal of neuropathology and experimental neurology · 2019Article
- Cortical degeneration in chronic traumatic encephalopathy and Alzheimer's disease neuropathologic change.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2019Article
- Postmortem Autopsy-Confirmation of Antemortem [F-18]FDDNP-PET Scans in a Football Player With Chronic Traumatic Encephalopathy.Neurosurgery · 2018Article
- Higher exosomal tau, amyloid-beta 42 and IL-10 are associated with mild TBIs and chronic symptoms in military personnel.Brain injury · 2018Article
- Clustering of tau-immunoreactive pathology in chronic traumatic encephalopathy.Journal of neural transmission (Vienna, Austria : 1996) · 2017Article
- Role of Tau Acetylation in Alzheimer's Disease and Chronic Traumatic Encephalopathy: The Way Forward for Successful Treatment.Journal of neurology and neurosurgery · 2017Article
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5 authors.
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Abstract
aimsTo quantify tau pathology of chronic traumatic encephalopathy (CTE) and investigate influence of dot-like lesions (DL), brain region, comorbidity and sporting career length.
methodsDensities of neurofibrillary tangles (NFT), astrocytic tangles (AT), DL, oligodendroglial inclusions (GI), neuropil threads (NT), vacuoles, neurons and enlarged neurons (EN) were measured in tau-immunoreactive sections of upper cortical laminae of frontal and temporal lobes, hippocampus (HC), amygdala and substantia nigra (SN) in 11 cases of CTE.
resultsDL were a consistent finding in CTE. Densities of NFT, NT and DL were greatest in sectors CA1 and CA2 of the HC. Densities of AT were lower than NFT, small numbers of GI were recorded in temporal lobe and low densities of vacuoles and EN were consistently present. β-Amyloid-containing neuritic plaques (NP) also occurred at low density. Densities of NFT, NT, DL and AT were greater in sulci than gyri, while vacuole density was greater in gyri. Principal components analysis (PCA) suggested that sporting career length and densities of NFT in entorhinal cortex, NT in CA2 and SN and vacuolation in the DG were significant sources of variation among cases.
conclusionDL are frequent in CTE suggesting affinity with argyrophilic grain disease (AGD) and Parkinson's disease dementia (PD-Dem). Densities of AT in all regions and NT/DL in sectors CA2/4 were consistent features of CTE. The 11 cases are neuropathologically heterogeneous which may result from genetic diversity, and variation in anatomical pathways subjected to trauma.
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