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Cited by 39Traumatic Brain Injury ResearchTraumatic Brain Injury and Neurovascular DisturbancesAlzheimer's disease research and treatments

Neurochemical Profile of Dementia Pugilistica

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Kokjohn, Tyler A., Maarouf, Chera L., Daugs, Ian D., Hunter, Jesse M., Whiteside, Charisse M., Malek-Ahmadi, Michael, Rodriguez, Emma, Kalback, Walter +4 more·2013·Journal of Neurotrauma
DOI 10.1089/neu.2012.2699PMC PMC3684215
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Abstract

Dementia pugilistica (DP), a suite of neuropathological and cognitive function declines after chronic traumatic brain injury (TBI), is present in approximately 20% of retired boxers. Epidemiological studies indicate TBI is a risk factor for neurodegenerative disorders including Alzheimer disease (AD) and Parkinson disease (PD). Some biochemical alterations observed in AD and PD may be recapitulated in DP and other TBI persons. In this report, we investigate long-term biochemical changes in the brains of former boxers with neuropathologically confirmed DP. Our experiments revealed biochemical and cellular alterations in DP that are complementary to and extend information already provided by histological methods. ELISA and one-dimensional and two dimensional Western blot techniques revealed differential expression of select molecules between three patients with DP and three age-matched non-demented control (NDC) persons without a history of TBI. Structural changes such as disturbances in the expression and processing of glial fibrillary acidic protein, tau, and α-synuclein were evident. The levels of the Aβ–degrading enzyme neprilysin were reduced in the patients with DP. Amyloid-β levels were elevated in the DP participant with the concomitant diagnosis of AD. In addition, the levels of brain-derived neurotrophic factor and the axonal transport proteins kinesin and dynein were substantially decreased in DP relative to NDC participants. Traumatic brain injury is a risk factor for dementia development, and our findings are consistent with permanent structural and functional damage in the cerebral cortex and white matter of boxers. Understanding the precise threshold of damage needed for the induction of pathology in DP and TBI is vital.

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  • Post mortem chronic traumatic encephalopathy studies reveal cerebral edema, perivascular hemosiderin-burdened macrophages, mural cell mineralization, enlarged perivascular spaces, and leukocyte infiltration.

    “Post mortem CTE studies reveal cerebral edema, perivascular hemosiderinburdened macrophages, mural cell mineralization, enlarged perivascular spaces, and leukocyte infiltration (149, 325, 454, 455)”

    From Blood-Brain Barrier: From Physiology to Disease and Back (2019) · cites this paper as [325]

    The Methods (Neuropathology; page not provided) report visibly dilated perivascular spaces in one dementia pugilistica case, supporting that part of the claim. The passages do not report cerebral edema, hemosiderin-burdened macrophages, mural cell mineralization, or leukocyte infiltration; searches for those features found no supporting passage. (LLM, conf=0.88)

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Cited by

Sorted by citations

Authors
Kokjohn, T. A., Maarouf, C. L., Daugs, I. D., Hunter, J. M., Whiteside, C. M., Malek-Ahmadi, M., Rodriguez, E., Kalback, W., Jacobson, S. A., Sabbagh, M. N., Beach, T. G., & Roher, A. E.
Affiliations
  • Midwestern University (US)
  • Banner Sun Health Research Institute (US)
  • Banner Sun Health Research Institute
Corresponding author
Roher, Alex E.
ORCID
Venue
Journal of Neurotrauma
Publisher
SAGE Publications
Published
2013-06
Volume
30
Issue
11
Pages
981-997
ISSN
  • 0897-7151 (ISSN-L)
  • 1557-9042
DOI
10.1089/neu.2012.2699
PMC
PMC3684215
OpenAlex
W1989378970
Cited by
39
References
15
Citations by year
2026: 1 · 2025: 2 · 2024: 2 · 2022: 3 · 2021: 2 · 2020: 3 · 2019: 5 · 2018: 2 · 2017: 4 · 2016: 1 · 2015: 8 · 2014: 5 · 2013: 1
FWCI
3.35
Type
journal article
Language
en
Open access
Licence
journals.sagepub.com/page/policies/text-and-data-mining-license (tdm)
Locations
  • Journal of Neurotrauma (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • U.S. Department of Veterans Affairs (AG13846, P30 AG13846)
  • Michael J. Fox Foundation for Parkinson's Research (05-901, 211002, P30 AG19610)
  • Massachusetts General Hospital (P50 AG005134)
  • Arizona Department of Health Services (P30 AG19610, 05-901, P50 AG005134, 211002, Contract 211002)
  • Arizona Biomedical Research Commission (P30 AG19610, 05–901, 4001, 011, 05-901, 211002)
  • National Institute on Aging (211002, P30-AG-19610, AG005134, AG 13846, R01AG019795, AG-19610, AG019795, P30AG019610, 05-901, P30AG013846, P50AG005134, P30-AG13846))
  • National Institute of Neurological Disorders and Stroke (211002, U24 NS0702026, 05-901, P30 AG19610)
Topics
  • Health Sciences › Medicine › Epidemiology › Traumatic Brain Injury Research
  • Health Sciences › Medicine › Neurology › Traumatic Brain Injury and Neurovascular Disturbances
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
Keywords
chronic traumatic encephalopathy, chronic traumatic brain injury, boxing, neurochemical changes, glial fibrillary acidic protein, tau protein, alpha-synuclein, neprilysin, amyloid-beta, brain-derived neurotrophic factor, kinesin, dynein, axonal transport, Alzheimer's disease, Parkinson's disease, neurodegeneration
MeSH terms
Aged, Aged, 80 and over, Athletic Injuries, Autopsy, Boxing, Brain, Brain Injuries, Chronic Disease, Dementia, Enzyme-Linked Immunosorbent Assay, Humans, Male, Blotting, Western

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