Tuesday, August 17, 2010

Athlete's Head Injuries Linked to ALS

Full Article at: Report: Scientists link ALS, athlete head injuries
"Dr. Ann McKee said in an interview with the television magazine show that she found toxic proteins in the spinal cords of three athletes who had suffered head injuries and then later died of Lou Gehrig's disease, or ALS. Those same proteins have been found in the brains of athletes with chronic traumatic encephalopathy (CTE), a disease linked to head injuries that causes cognitive decline, abnormal behavior and dementia."

The findings are to be published in the Journal of Neuropathology and Experimental Neurology, Abstract Abstractpubmed, see below.

"McKee, a neurology professor at Boston University who has studied CTE in athletes, noticed that an unusually high number of football players seemed to be affected by ALS. The disease attacks nerve cells in the brain and spinal cord, and destroys the ability to move and speak.?

Abstractpubmed
J Neuropathol Exp Neurol. 2009 Jul;68(7):709-35.
Chronic traumatic encephalopathy in athletes: progressive tauopathy after repetitive head injury.

McKee AC, Cantu RC, Nowinski CJ, Hedley-Whyte ET, Gavett BE, Budson AE, Santini VE, Lee HS, Kubilus CA, Stern RA.

Department of Neurology, Center for the Study of Traumatic Encephalopathy, Boston University School of Medicine, Boston, MA, USA. amckee@bu.edu
Abstract

Since the 1920s, it has been known that the repetitive brain trauma associated with boxing may produce a progressive neurological deterioration, originally termed dementia pugilistica, and more recently, chronic traumatic encephalopathy (CTE). We review 48 cases of neuropathologically verified CTE recorded in the literature and document the detailed findings of CTE in 3 profession althletes, 1 football player and 2 boxers. Clinically, CTE is associated with memory disturbances, behavioral and personality changes, parkinsonism, and speech and gait abnormalities. Neuropathologically, CTE is characterized by atrophy of the cerebral hemispheres, medial temporal lobe, thalamus, mammillary bodies, and brainstem, with ventricular dilatation and a fenestrated cavum septum pellucidum. Microscopically, there are extensive tau-immunoreactive neurofibrillary tangles, astrocytic tangles, and spindle-shaped and threadlike neurites throughout the brain. The neurofibrillary degeneration of CTE is distinguished from other tauopathies by preferential involvement of the superficial cortical layers, irregular patchy distribution in the frontal and temporal cortices, propensity for sulcal depths, prominent perivascular, periventricular, and subpial distribution, and marked accumulation of tau-immunoreactive astrocytes. Deposition of beta-amyloid, most commonly as diffuse plaques, occurs in fewer than half the cases. Chronic traumatic encephalopathy is a neuropathologically distinct slowly progressive tauopathy with a clear environmental etiology.

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