A new study conducted by researchers at the Mayo Clinic has found that a history of concussion involving at least a momentary loss of consciousness may result in the development of Alzheimer’s disease. They published their findings online on December 26 in Neurology, the medical journal of the American Academy of Neurology.
“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,” noted study author Michelle Mielke, PhD.
The study group comprised 448 individuals without any signs of memory problems and 141 individuals with minor cognitive impairment (memory and thinking problems) who resided in Olmstead County, Minnesota. All participants were age 70 or older. They all underwent brain scans and were asked if they had ever experienced a brain injury that involved any loss of consciousness or memory. Among the 448 subjects without any thinking or memory problems, 17% reported a brain injury; among the 141 subjects with mild cognitive impairment, 18% reported a concussion or head trauma.
The investigators found no difference in any brain scan measures among the individuals without cognitive impairment, whether or not they had suffered head trauma. However, those with cognitive impairment and a history of head trauma had levels of amyloid plaques an average of 18% higher than those with no head trauma history. Amyloid plaques are indicative of Alzheimer’s disease. Dr. Mielke explained, “Our results add merit to the idea that concussion and Alzheimer’s disease brain pathology may be related. However, the fact that we did not find a relationship in those without memory and thinking problems suggests that any association between head trauma and amyloid is complex.”
The present study is in accord with a study published in June 2013 by researchers at the New York University School of Medicine, which reported that mild traumatic brain injury (MTBI) can have long-lasting health consequences. The researchers conducted a study to investigate changes over time in brain volume in patients one year after suffering MTBI; they correlated the changes with clinical and neurocognitive factors. The study group comprised 28 patients with MTBI (with 19 followed up at one year) with posttraumatic symptoms after injury and 22 matched control subjects (with 12 followed up at one year). Automated segmentation of brain regions to compute regional gray matter and white matter volumes was performed by using three-dimensional magnetic resonance imaging (MZRI); the results were correlated with clinical findings.
The investigators found that one year after MTBI, there was measurable global brain atrophy, larger than that in control subjects. The anterior cingulate white matter bilaterally and the left cingulate gyrus isthmus white, as well as the right precuneal gray matter, showed significant decreases in regional volume in patients with MTBI over the first year after injury; this was confirmed by means of cross-sectional comparison with data in control subjects. Left and right rostral anterior cingulum white matter volume loss correlated with changes in neurocognitive measures of memory and attention. At one-year follow-up, white matter volume in the left cingulate gyrus isthmus correlated with clinical scores of anxiety and postconcussive symptoms. The researchers found that white matter damage in the brains of people who had experienced concussions closely resembled the type of white matter damage found in patients with Alzheimer’s disease.
The authors concluded that their findings suggest that concussions set off a chain of neurological events that can cause long-term damage to the brain. They noted that their study demonstrated structural changes to the brain one year after injury after a single concussive episode. They stressed that regional brain atrophy is not exclusive to moderate and severe traumatic brain injury but may be seen after mild injury. In particular, the anterior part of the cingulum and the cingulate gyrus isthmus, as well as the precuneal gray matter, may be distinctively vulnerable one year after MTBI.