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Neurosci Biobehav Rev. 2015 Sep;56:276-93. doi: 10.1016/j.neubiorev.2015.05.008. Epub 2015 Jul 14.

A critical review of chronic traumatic encephalopathy.

Author information

1
Department of Physical Medicine and Rehabilitation, Harvard Medical School, Spaulding Rehabilitation Hospital, MassGeneral Hospital for Children Sports Concussion Program, & Red Sox Foundation and Massachusetts General Hospital Home Base Program, Boston, MA, USA. Electronic address: giverson@mgh.harvard.edu.
2
Hunter New England Local Health District Sports Concussion Program; & Centre for Translational Neuroscience and Mental Health, School of Medicine and Public Health, University of Newcastle, Callaghan, NSW, Australia.
3
The Florey Institute of Neuroscience and Mental Health, Melbourne Brain Centre - Austin Campus, Heidelberg, Victoria, Australia.
4
Department of Physical Medicine and Rehabilitation, Harvard Medical School; Spaulding Rehabilitation Hospital; Brigham and Women's Hospital; & Red Sox Foundation and Massachusetts General Hospital Home Base Program, Boston, MA, USA.
5
Division of Neuropathology, University of Maryland School of Medicine, USA.

Abstract

Chronic traumatic encephalopathy (CTE) has been described in the literature as a neurodegenerative disease with: (i) localized neuronal and glial accumulations of phosphorylated tau (p-tau) involving perivascular areas of the cerebral cortex, sulcal depths, and with a preference for neurons within superficial cortical laminae; (ii) multifocal axonal varicosities and axonal loss involving deep cortex and subcortical white matter; (iii) relative absence of beta-amyloid deposits; (iv) TDP-43 immunoreactive inclusions and neurites; and (v) broad and diverse clinical features. Some of the pathological findings reported in the literature may be encountered with age and other neurodegenerative diseases. However, the focality of the p-tau cortical findings in particular, and the regional distribution, are believed to be unique to CTE. The described clinical features in recent cases are very similar to how depression manifests in middle-aged men and with frontotemporal dementia as the disease progresses. It has not been established that the described tau pathology, especially in small amounts, can cause complex changes in behavior such as depression, substance abuse, suicidality, personality changes, or cognitive impairment. Future studies will help determine the extent to which the neuropathology is causally related to the diverse clinical features.

KEYWORDS:

Athletes; Brain injury; Concussion; Dementia; Dementia pugilistica

PMID:
26183075
DOI:
10.1016/j.neubiorev.2015.05.008
[Indexed for MEDLINE]

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