Abstract

ObjectivesAn observational study to compare the laminar distributions in frontal and temporal cortex of the tau-immunoreactive pathologies in chronic traumatic encephalopathy (CTE) and Alzheimer’s disease neuropathologic change (ADNC).PatientsPost-mortem material of (1) four cases of CTE without ADNC, (2) seven cases of CTE with ADNC (CTE/ADNC), and (3) seven cases of ADNC alone.ResultsIn CTE and CTE/ADNC, neurofibrillary tangles (NFT), neuropil threads (NT), and dot-like grains (DLG) were distributed either in upper cortex or across all layers. Low densities of astrocytic tangles (AT) and abnormally enlarged neurons (EN) were not localized to any specific layer. Surviving neurons exhibited peaks of density in both upper and lower cortex, and vacuole density was greatest in superficial layers. In ADNC, neuritic plaques (NP) were more frequent, AT rare, NFT and NT were more widely distributed, NT affected lower layers more frequently, and surviving neurons were less frequently bimodal than in CTE and CTE/ADNC.ConclusionTau pathology in CTE and CTE/ADNC consistently affected the upper cortex but was more widely distributed in ADNC. The presence of CTE may encourage the development of ADNC pathology later in the course of the disease.

Highlights

  • Chronic traumatic encephalopathy (CTE) is a neurodegenerative disorder associated with repetitive traumatic brain injuryVision Sciences, Aston University, Birmingham B4 7ET, UKVA Boston HealthCare System, Boston, MA 02130, USADepartment of Neurology, Boston University School of Medicine, Boston, MA 02118, USADepartment of Pathology & Laboratory Medicine, Boston UniversitySchool of Medicine, Boston, MA 02118, USADepartment of Veterans Affairs Medical Center, Bedford, MA 01730, USADepartments of Neurology and Pathology & Immunology, Washington University School of Medicine, Saint Louis, MO 63110, USA (TBI) [1]

  • Surviving neurons exhibited peaks of density in both upper and lower cortex, and vacuole density was greatest in superficial layers

  • The presence of CTE may encourage the development of Alzheimer’s disease neuropathologic change (ADNC) pathology later in the course of the disease

Read more

Summary

Introduction

VA Boston HealthCare System, Boston, MA 02130, USA. Departments of Neurology and Pathology & Immunology, Washington University School of Medicine, Saint Louis, MO 63110, USA (TBI) [1]. Clinical symptoms include impairment of memory and executive function, behavioral change, and motor dysfunction [2]. A spectrum of tau-immunoreactive pathology is present including neurofibrillary tangles (NFT) and neuropil threads (NT) [3], dot-like grains (DLG) [5], and astrocytic tangles (AT) [2, 6]. Alzheimer’s disease neuropathologic change (ADNC) is characterized by the presence of β-amyloid (Aβ) deposits in the form of neuritic plaques (NP) and tau-immunoreactive NFT without an extensive glial pathology [7, 8]. ADNC often occurs as a co-pathology with CTE but the relationship between

Objectives
Methods
Results
Conclusion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call