Tau immunohistochemistry in acute brain injury

Authors

  • C. Smith,

    1. Department of Neuropathology, University of Glasgow, Institute of Neurological Sciences, Southern General Hospital, Glasgow,
    2. Neuropathology Laboratory, Department of Pathology, University of Edinburgh, Western General Hospital, Edinburgh,
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  • D. I. Graham,

    1. Department of Neuropathology, University of Glasgow, Institute of Neurological Sciences, Southern General Hospital, Glasgow,
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  • L. S. Murray,

    1. Department of Medicine and Therapeutics, University of Glasgow, Western Infirmary, Glasgow, and
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  • J. A. R. Nicoll

    1. Department of Neuropathology, University of Glasgow, Institute of Neurological Sciences, Southern General Hospital, Glasgow,
    2. Division of Clinical Neurosciences, University of Southampton, Southampton General Hospital, Southampton, UK
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C. Smith, Neuropathology Laboratory, Department of Pathology, University of Edinburgh, Western General Hospital, Edinburgh, EH4 2XU, UK. Tel: 0131–537 1975; Fax: 0131–537 1013: E-mail: col.smith@ed.ac.uk

Abstract

Epidemiological studies have identified a history of head injury as a risk factor for Alzheimer's disease. However, the neuropathological mechanism underlying this relationship is as yet unclear. Neuronal cytoskeletal changes in the form of neurofibrillary tangles and neuropil threads have recently been demonstrated in young men who had sustained repetitive head injury and subsequently died in their 20s. In addition, recent experimental studies have found accumulation of tau within neuronal somata and damaged axons following diffuse brain injury. We hypothesized that tau-immunoreactive tangles may be present in the brains of patients who died after a single acute blunt head injury. A total of 45 cases of fatal head injury were immunostained for tau. They comprised nine groups (n = 5 for each group) separated by age (0–19 years, 20–50 years, 50 + years) and survival time (< 24 h, 24 h−1 week, 1 week−1 month) and were compared with age-matched controls. Subtle alterations in tau immunoreactivity, for example, in oligodendrocytes, were present in some head injury cases but not controls. However, neurofibrillary tangles did not appear more prevalent after traumatic brain injury (TBI) when compared with age-matched controls. Although alterations in tau immunoreactivity may occur which warrant further study, neurofibrillary tangles were not more prevalent after a single fatal episode of TBI.

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