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Original research
Clinical and neuropsychological profile of patients with dementia and chronic traumatic encephalopathy
  1. Christian LoBue1,2,
  2. Jeff Schaffert1,
  3. C. Munro Cullum1,2,3,
  4. Matthew E. Peters4,
  5. Nyaz Didehbani1,
  6. John Hart1,3,5,
  7. Charles L. White6
  1. 1Psychiatry, UT Southwestern Medical Center, Dallas, Texas, USA
  2. 2Neurological Surgery, UT Southwestern Medical Center, Dallas, Texas, USA
  3. 3Neurology and Neurotherapeutics, UT Southwestern Medical Center, Dallas, Texas, USA
  4. 4Psychiatry and Behavioral Sciences, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
  5. 5Callier Center, School of Behavioral and Brain Sciences, University of Texas at Dallas, Dallas, Texas, USA
  6. 6Pathology, UT Southwestern Medical Center, Dallas, Texas, USA
  1. Correspondence to Dr Christian LoBue, UT Southwestern Medical, Dallas, TX 75390-8570, USA; christian.lobue{at}utsw.edu

Abstract

Objective To determine whether subjects with chronic traumatic encephalopathy (CTE) and dementia have distinct clinical features compared to subjects with pathologically confirmed Alzheimer’s disease (AD).

Methods Among 339 subjects assessed for CTE in the National Alzheimer’s Coordinating Center dataset, 6 subjects with CTE and 25 subjects with AD neuropathologic change matched for age (±5 years) and sex were identified. All subjects had a clinical diagnosis of dementia. Neurological examination, neuropsychological testing and emotional/behavioural data were compared between CTE and AD subjects at the time of dementia diagnosis and last clinical visit near death.

Results A history of traumatic brain injury with loss of consciousness (LOC) was reported in one CTE and one AD subject; information about injuries without LOC or multiple injuries was unavailable. CTE and AD subjects did not differ significantly at the time of diagnosis or last visit on the Unified Parkinson’s Disease Rating Scale—Motor Exam, global measures of cognitive functioning (Mini-Mental State Exam and Clinical Dementia Rating Scale), emotional/behaviour symptoms as assessed with the Neuropsychiatric Inventory questionnaire or across neuropsychological measures. All CTE participants had co-occurring neuropathologic processes, including AD and most had TAR DNA-binding protein 43 (TDP-43) neuropathology.

Conclusions CTE pathology was rare in a large multicentre national dataset, and when present, was accompanied by AD and TDP-43 pathologies. CTE was not associated with a different clinical presentation from AD or with greater cognitive impairment or neurobehavioral symptoms. These findings suggest that CTE may not have a distinct clinical profile when other neuropathologic processes are coexistent with CTE pathology.

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Footnotes

  • Contributors CL and JS designed and conceptualised the study, analysed and interpreted the data and drafted the manuscript for intellectual content. MC, MP, ND, JH and CW interpreted the data and revised the manuscript for intellectual content.

  • Funding Financial support for this work was provided in part by the Texas Alzheimer’s Research and Care Consortium (TARCC) and the Texas Institute for Brain Injury and Repair (TIBIR) in the Peter O’Donnell Brain Institute at University of Texas Southwestern Medical Center. The NACC database is funded by NIA/NIH Grant U01 AG016976. NACC data are contributed by the NIA-funded ADCs: P30 AG019610 (PI Eric Reiman, MD), P30 AG013846 (PI Neil Kowall, MD), P50 AG008702 (PI Scott Small, MD), P50 AG025688 (PI Allan Levey, MD, PhD), P50 AG047266 (PI Todd Golde, MD, PhD), P30 AG010133 (PI Andrew Saykin, PsyD), P50 AG005146 (PI Marilyn Albert, PhD), P50 AG005134 (PI Bradley Hyman, MD, PhD), P50 AG016574 (PI Ronald Petersen, MD, PhD), P50 AG005138 (PI Mary Sano, PhD), P30 AG008051 (PI Thomas Wisniewski, MD), P30 AG013854 (PI M. Marsel Mesulam, MD), P30 AG008017 (PI Jeffrey Kaye, MD), P30 AG010161 (PI David Bennett, MD), P50 AG047366 (PI Victor Henderson, MD, MS), P30 AG010129 (PI Charles DeCarli, MD), P50 AG016573 (PI Frank LaFerla, PhD), P50 AG005131 (PI James Brewer, MD, PhD), P50 AG023501 (PI Bruce Miller, MD), P30 AG035982 (PI Russell Swerdlow, MD), P30 AG028383 (PI Linda Van Eldik, PhD), P30 AG053760 (PI Henry Paulson, MD, PhD), P30 AG010124 (PI John Trojanowski, MD, PhD), P50 AG005133 (PI Oscar Lopez, MD), P50 AG005142 (PI Helena Chui, MD), P30 AG012300 (PI Roger Rosenberg, MD), P30 AG049638 (PI Suzanne Craft, PhD), P50 AG005136 (PI Thomas Grabowski, MD), P50 AG033514 (PI Sanjay Asthana, MD, FRCP), P50 AG005681 (PI John Morris, MD) and P50 AG047270 (PI Stephen Strittmatter, MD, PhD).

  • Competing interests None declared.

  • Patient consent for publication Not required.

  • Provenance and peer review Not commissioned; externally peer reviewed.

  • Data availability statement Data are available in a public, open access repository. Documented data, materials, and methods from NACC’s dataset used to conduct the research in the article are carefully documented. The NACC dataset is freely available to all researchers and can be obtained by visiting https://www.alz.washington.edu/.

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