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Polypathology and dementia after brain trauma: Does brain injury trigger distinct neurodegenerative diseases, or should they be classified together as traumatic encephalopathy?

Abstract

Neuropathological studies of human traumatic brain injury (TBI) cases have described amyloid plaques acutely after a single severe TBI, and tau pathology after repeat mild TBI (mTBI). This has helped drive the hypothesis that a single moderate to severe TBI increases the risk of developing late-onset Alzheimer's disease (AD), while repeat mTBI increases the risk of developing chronic traumatic encephalopathy (CTE). In this review we critically assess this position-examining epidemiological and case control human studies, neuropathological evidence, and preclinical data. Epidemiological studies emphasize that TBI is associated with the increased risk of developing multiple types of dementia, not just AD-type dementia, and that TBI can also trigger other neurodegenerative conditions such as Parkinson's disease. Further, human post-mortem studies on both single TBI and repeat mTBI can show combinations of amyloid, tau, TDP-43, and Lewy body pathology indicating that the neuropathology of TBI is best described as a 'polypathology'. Preclinical studies confirm that multiple proteins associated with the development of neurodegenerative disease accumulate in the brain after TBI. The chronic sequelae of both single TBI and repeat mTBI share common neuropathological features and clinical symptoms of classically defined neurodegenerative disorders. However, while the spectrum of chronic cognitive and neurobehavioral disorders that occur following repeat mTBI is viewed as the symptoms of CTE, the spectrum of chronic cognitive and neurobehavioral symptoms that occur after a single TBI is considered to represent distinct neurodegenerative diseases such as AD. These data support the suggestion that the multiple manifestations of TBI-induced neurodegenerative disorders be classified together as traumatic encephalopathy or trauma-induced neurodegeneration, regardless of the nature or frequency of the precipitating TBI.

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  • Authors+Show Affiliations

    ,

    Department of Pediatrics and Critical Care Medicine, Columbia University Medical Center, New York, NY, USA; Neurotrauma and Repair Laboratory, Department of Biomedical Engineering, Columbia University, New York, NY, USA.

    ,

    Laboratory for Brain Injury and Dementia, Department of Neuroscience, Georgetown University Medical Center, Washington, DC, USA.

    Laboratory for Brain Injury and Dementia, Department of Neuroscience, Georgetown University Medical Center, Washington, DC, USA. Electronic address: mpb37@georgetown.edu.

    Source

    Experimental neurology 275 Pt 3: 2016 Jan pg 381-388

    MeSH

    Alzheimer Disease
    Animals
    Brain
    Brain Injuries
    Brain Injury, Chronic
    Dementia
    Humans
    Neurodegenerative Diseases
    Plaque, Amyloid

    Pub Type(s)

    Journal Article
    Research Support, N.I.H., Extramural
    Review

    Language

    eng

    PubMed ID

    26091850

    Citation

    Washington, Patricia M., et al. "Polypathology and Dementia After Brain Trauma: Does Brain Injury Trigger Distinct Neurodegenerative Diseases, or Should They Be Classified Together as Traumatic Encephalopathy?" Experimental Neurology, vol. 275 Pt 3, 2016, pp. 381-388.
    Washington PM, Villapol S, Burns MP. Polypathology and dementia after brain trauma: Does brain injury trigger distinct neurodegenerative diseases, or should they be classified together as traumatic encephalopathy? Exp Neurol. 2016;275 Pt 3:381-388.
    Washington, P. M., Villapol, S., & Burns, M. P. (2016). Polypathology and dementia after brain trauma: Does brain injury trigger distinct neurodegenerative diseases, or should they be classified together as traumatic encephalopathy? Experimental Neurology, 275 Pt 3, pp. 381-388. doi:10.1016/j.expneurol.2015.06.015.
    Washington PM, Villapol S, Burns MP. Polypathology and Dementia After Brain Trauma: Does Brain Injury Trigger Distinct Neurodegenerative Diseases, or Should They Be Classified Together as Traumatic Encephalopathy. Exp Neurol. 2016;275 Pt 3:381-388. PubMed PMID: 26091850.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Polypathology and dementia after brain trauma: Does brain injury trigger distinct neurodegenerative diseases, or should they be classified together as traumatic encephalopathy? AU - Washington,Patricia M, AU - Villapol,Sonia, AU - Burns,Mark P, Y1 - 2015/06/16/ PY - 2015/02/13/received PY - 2015/06/06/revised PY - 2015/06/15/accepted PY - 2015/6/21/entrez PY - 2015/6/21/pubmed PY - 2016/4/26/medline KW - Alzheimer's disease (AD) KW - Amyloid (Aβ) KW - Chronic traumatic encephalopathy (CTE) KW - Dementia KW - Tau KW - Tauopathy KW - Traumatic brain injury (TBI) SP - 381 EP - 388 JF - Experimental neurology JO - Exp. Neurol. VL - 275 Pt 3 N2 - Neuropathological studies of human traumatic brain injury (TBI) cases have described amyloid plaques acutely after a single severe TBI, and tau pathology after repeat mild TBI (mTBI). This has helped drive the hypothesis that a single moderate to severe TBI increases the risk of developing late-onset Alzheimer's disease (AD), while repeat mTBI increases the risk of developing chronic traumatic encephalopathy (CTE). In this review we critically assess this position-examining epidemiological and case control human studies, neuropathological evidence, and preclinical data. Epidemiological studies emphasize that TBI is associated with the increased risk of developing multiple types of dementia, not just AD-type dementia, and that TBI can also trigger other neurodegenerative conditions such as Parkinson's disease. Further, human post-mortem studies on both single TBI and repeat mTBI can show combinations of amyloid, tau, TDP-43, and Lewy body pathology indicating that the neuropathology of TBI is best described as a 'polypathology'. Preclinical studies confirm that multiple proteins associated with the development of neurodegenerative disease accumulate in the brain after TBI. The chronic sequelae of both single TBI and repeat mTBI share common neuropathological features and clinical symptoms of classically defined neurodegenerative disorders. However, while the spectrum of chronic cognitive and neurobehavioral disorders that occur following repeat mTBI is viewed as the symptoms of CTE, the spectrum of chronic cognitive and neurobehavioral symptoms that occur after a single TBI is considered to represent distinct neurodegenerative diseases such as AD. These data support the suggestion that the multiple manifestations of TBI-induced neurodegenerative disorders be classified together as traumatic encephalopathy or trauma-induced neurodegeneration, regardless of the nature or frequency of the precipitating TBI. SN - 1090-2430 UR - https://www.unboundmedicine.com/medline/citation/26091850/Polypathology_and_dementia_after_brain_trauma:_Does_brain_injury_trigger_distinct_neurodegenerative_diseases_or_should_they_be_classified_together_as_traumatic_encephalopathy L2 - https://linkinghub.elsevier.com/retrieve/pii/S0014-4886(15)30025-X DB - PRIME DP - Unbound Medicine ER -