No Evidence of Increased Chronic Traumatic Encephalopathy Pathology or Neurodegenerative Proteinopathy in Former Military Service Members: A Preliminary Study
Affiliations: [a]
Center for Neuropathology, Western Michigan University Homer Stryker MD School of Medicine, Kalamazoo, MI, USA
| [b]
College of Sciences, University of Texas at San Antonio, San Antonio, TX, USA
| [c]
Departments of Pathology and Neuroscience, West Virginia University School of Medicine, Rockefeller Neuroscience Institute, Morgantown, WV, USA
Correspondence:
[*]
Correspondence to: Rudy J. Castellani, MD, 64 Medical Center Drive, Morgantown, WV 26506, USA. Tel.: +1 304 293 1625; Fax: +1 304 293 1627; E-mail: Rudolph.castellani@hsc.wvu.edu.
Abstract: It is presently unknown whether military service members are at risk for chronic traumatic encephalopathy (CTE) or Alzheimer’s disease (AD) pathology, due to traumatic brain injury (TBI). Studies with respect to AD have had mixed results with respect to mild TBI, although an increased risk of clinical AD with moderate and severe TBI is more consistently demonstrated. No studies to date have demonstrated a longitudinal progression from TBI to autopsy. We therefore initiated a cross-sectional survey of former military service members. 18 brain specimens have been examined to date, with a mean age of 68.9±16 years (range 32–94). Twelve had a history of psychiatric problems; 10 had a history of PTSD specifically. Five had neurological problems including stroke and seizures. One subject had early-onset AD. Two subjects had a history of TBI and two had a history of blast exposure. Age-related proteinopathy, ranging from AD neuropathologic change A0B1C0 to A3B3C3 by NIA-AA guidelines, was identified. None of the cases showed changes specific for CTE pathology. There was no relationship between p-tau in the amygdala and psychiatric signs. There was no significant difference in phosphorylated tau (p-tau) or amyloid-β burden compared to age-matched controls. These preliminary data suggest that military service per se is not a risk factor for CTE pathology or neurodegenerative proteinopathy. More research is needed to study the relationship, if any, between TBI and neurodegenerative proteinopathy.
