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Potential Link between Brain Trauma and Alzheimer’s Disease

People who suffer just one or more serious brain trauma events (concussions) could face a greater risk of developing the same brain tissue abnormalities as those found in Alzheimer’s patients, according to a recent study. The study found that elderly test subjects who exhibited mild cognitive impairment and also have a history of head trauma showed higher amounts of the same protein deposits (plaques) that are associated with Alzheimer’s disease. The results, published in late December in the journal Neurology, suggest a potentially strong link between a history of concussions and cognitive deficits later in life.

Study Results Link Deficits with Once-Concussed Brains

Lead by author Michelle Mielke, a Mayo Clinic research team scanned the brains of 589 people ages 70 and older beginning back in 2004. Test subjects were also put through a battery of tests for cognition and memory. Of those enlisted, 141 subjects showed signs of mild cognitive impairment. All subjects were asked if they recalled suffering a concussion any time in the past. A roughly equal proportion of each group reported at least one concussion involving memory loss, unconsciousness or medical attention. The median age for a head trauma event was 21 for men and 32 for women.

The brain scans revealed that the subjects with cognition deficits and a history of head trauma had an average of 18 percent more amyloid beta plaques than those with no history of head trauma. These plaques are a key  indicator of Alzheimer’s disease. Study leader Mielke said in a public statement:

“Interestingly, in people with a history of concussion, a difference in the amount of brain plaques was found only in those with memory and thinking problems, not in those who were cognitively normal. Our results add merit to the idea that concussion and Alzheimer’s disease brain pathology may be related.”

Same Beta Plaques Found in Alzheimer’s Brains May Develop Years after Head Trauma

Researchers examined the relationship between head trauma and amyloid beta plaques in the brain. While the study wasn’t specifically able to prove causation, it does help to offer further insight into the possible long-term effects of one or more concussions. Brain scans revealed no differences among the test subjects without memory and cognition impairments, regardless of any occurrence of past head trauma.

Amyloid buildup has been long associated with neurological disorders, particularly Alzheimer’s disease. Only the brains of test subjects with cognitive impairment contained higher levels of amyloids, according to the study. Researchers suggested that higher amyloid levels within the cognitively impaired group could be a response to a higher level of damage to the myelin coating of the axons of neurons – the brain’s white matter. Despite the study’s indications, Mielke made a point of noting that any relationship between head trauma and amyloid plaque development is likely complex and dependent upon other unknown or unconfirmed variables.

Keith Fargo, the director of publications and outreach for the Alzheimer’s Association, referred to the recent study as “intriguing.” Fargo expressed a concern that the study raises more questions than it answers, placing an even stronger emphasis on follow-up research such as long-term studies that follow head trauma patients through the course of their natural lives starting with the day after the initial injury.

References

LA Times

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