title: A quantitative study of tau pathology in 11 cases of chronic traumatic encephalopathy.
abstract: OBJECTIVE
  To quantify tau pathology of chronic traumatic encephalopathy (CTE) and investigate influence of dot-like lesions (DL), brain region, comorbidity and sporting career length.
  
  
  METHODS
  Densities 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.
  
  
  RESULTS
  DL 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.
  
  
  CONCLUSIONS
  DL 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.
authors.affiliation: Vision Sciences, Aston University, Birmingham, UK.
authors.forename: R A
authors.initials: RA
authors.lastname: Armstrong
authors.affiliation: VA Boston HealthCare System, Boston, MA, USA.|Department of Neurology, Boston University School of Medicine, Boston, MA, USA.|Department of Pathology & Laboratory Medicine, Boston University School of Medicine, Boston, MA, USA.
authors.forename: A C
authors.initials: AC
authors.lastname: McKee
authors.affiliation: Department of Pathology & Laboratory Medicine, Boston University School of Medicine, Boston, MA, USA.|Department of Veterans Affairs Medical Center, Bedford, MA, USA.
authors.forename: T D
authors.initials: TD
authors.lastname: Stein
authors.affiliation: Department of Neurology, Boston University School of Medicine, Boston, MA, USA.|Department of Veterans Affairs Medical Center, Bedford, MA, USA.
authors.forename: V E
authors.initials: VE
authors.lastname: Alvarez
authors.affiliation: Departments of Neurology and Pathology & Immunology, Washington University School of Medicine, Saint Louis, MO, USA.
authors.forename: N J
authors.initials: NJ
authors.lastname: Cairns
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000070627:Chronic Traumatic Encephalopathy / Q000150:complications / Q000473:pathology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D016874:Neurofibrillary Tangles / Q000473:pathology; D058225:Plaque, Amyloid / Q000473:pathology; D024801:Tauopathies / Q000150:complications / Q000453:epidemiology* / Q000473:pathology; D016875:tau Proteins / Q000378:metabolism*
chemical_list: D016875:tau Proteins
keywords: astrocytic tangles; chronic traumatic encephalopathy; neurofibrillary tangles; principal components analysis; tau