Friday, December 26, 2014

UCD: Brain changes in football players differ from Alzheimer’s

July 28, 2011 |

Special to The Enterprise

SACRAMENTO — The brain damage found in a growing number of professional football players has been described in detail by a UC Davis Medical Center researcher and colleagues in the July issue of Neurosurgery.

The pattern of protein tangles and plaques in chronic traumatic encephalopathy, or CTE, is distinct from those in Alzheimer’s patients, they report, pointing the way toward an objective diagnosis of the disease.

“The first thing is to identify the disease, give it a name, and identify its pathology. We’ve done that,” said Bennet Omalu, associate clinical professor of pathology at the UCD Medical Center and co-director of the Brain Injury Research Institute at West Virginia University.

Omalu was the first to describe CTE in 2002, after examining the brain of former Pittsburgh Steelers football player Mike Webster.

CTE is thought to be caused by blunt force impacts to the head. It can take years to manifest as behavioral and personality changes, including memory loss and mood disorders. These can progress to serious cognitive impairment, culminating in early dementia.

“We’re seeing CTE in any activity that subjects your brain to repeated acceleration and deceleration,” Omalu said.

In the current study, Omalu and colleagues detailed histological examinations of the brains of 17 athletes who played contact sports, including eight professional football players, four professional wrestlers and three high school football players. All had died suddenly from suicide, drug abuse or in accidents.

The researchers diagnosed CTE in 10 of the 14 professional athletes, and one high school football player.

The study revealed important differences between CTE and Alzheimer’s disease. Subjects with CTE had tangles of tau proteins in their brains that were similar to those seen in later-stage Alzheimer’s patients. However, these tangles occurred in a very different pattern.

While the tangles in Alzheimer’s patients are scattered throughout the brain, those in the athletes exhibited a “skip phenomenon:” The tangles occurred in some areas of the cerebral cortex but were absent in others within the same lobe. In addition, the brains of the athletes did not show the classic neuritic amyloid plaques or the widespread cerebral atrophy characteristic of Alzheimer’s disease.

Finally, the subjects diagnosed with CTE ranged from 18 to 52 years old, whereas Alzheimer’s disease typically does not occur until after age 60.

The study also questions the connection between CTE and a variant of the apolipoprotein E gene.

Previous researchers have linked the ApoE4 allele to a predisposition for Alzheimer’s disease and the behavior changes of CTE. However, the CTE-positive subjects in this study were more likely to have the ApoE3 genotype, which is associated with tangle-only dementia. The CTE also produces tangle-only brain abnormalities.

Identifying the genotypes associated with CTE could help patients evaluate the risks they face when playing high contact sports.

“Although we do not have the capability now, it may one day be possible to develop a battery of genetic tests to identify individuals at high, medium or low risk for CTE. Knowing whether you had these certain types of genes, you may be advised not to play football,” Omalu said.

At present, CTE can only be diagnosed during autopsy. Omalu and his colleagues are now focusing their research on ways to identify the disease in the living and to develop potential drug treatments.

In the meantime, “parents need to be aware of the dangers of repeated blows to the head sustained by children in football, wrestling and hockey. The younger you are when you start playing, the greater risk you have of permanent brain damage,” Omalu said.

“We need to embark on an aggressive education of physicians and parents, so people are able to make informed judgments before they decide to play or not to play.”

— UC Davis Health News Office



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