Early Head Trauma Triggers Amyloid Buildup In SeniorsPublished: May 20, 2014 in Personal Injury, Traumatic Brain Injury
Early traumatic brain injuries experienced by Seniors, not only cause initial damage to the Central Nervous System, but increase the risk of additional neurologic problems and dramatically impact the ongoing costs associated with caring for the patient, says Alabama liability attorney Keith T. Belt.
Cognitively impaired older people who had previously experienced head injuries had a significantly greater burden of beta-amyloid protein plaque than did otherwise similar individuals without such a history, researchers found.
- Cognitively impaired seniors with a history of head injuries had a significantly greater burden of beta-amyloid protein plaque than did otherwise similar individuals without such a history.
- Point out that the study suggests that the etiology of cognitive impairment in individuals with mild cognitive impairment with head trauma is more likely to be Alzheimer’s disease pathology than in those with MCI but without head trauma.
Among 141 participants in the Mayo Clinic Study of Aging with mild cognitive impairment (MCI), the 25 who reported having experienced a significant head injury sometime in the past had significantly more extensive beta-amyloid plaques (mean difference 0.36 standardized uptake value ratio units, 95% CI 0.12-0.60,P=0.002), equating to about an 18% greater burden, according to Michelle M. Mielke, PhD, and colleagues at the Mayo Clinic’s locations in Rochester, Minn., and Scottsdale, Arizona.
Head injury history was unrelated to plaque burdens in 448 cognitively normal study participants the researchers reported online in Neurology.
The findings “suggest that the etiology of cognitive impairment in MCI individuals with head trauma is more likely to be Alzheimer’s disease (AD) pathology than in MCI individuals without head trauma,” Mielke and colleagues wrote.
“This is consistent with some human and animal data and deserves additional study because it would provide in vivo evidence for a cause and effect mechanistic link between prior head trauma and AD.”
On the other hand, the lack of association between head injury and plaque burden in cognitively normal individuals was “contradictory,” the researchers conceded.
They undertook the study to help sort out conflicting results from previous examinations of Alzheimer’s disease risk in people with head injuries. Some epidemiological studies had found such a link, but others including meta-analyses had not.
The Mayo Clinic Study of Aging is an ongoing, population-based, prospective study among nondemented individuals who were 70 to 89 years of age at enrollment. Mielke and colleagues analyzed data on 589 participants who underwent PET scans using the PiB tracer for beta-amyloid plaques and an agent (fluorodeoxyglucose or FDG) that provides a quantitative picture of brain metabolic activity. MRI scans had also been performed on the participants.
Just under 20% of both the cognitively normal and MCI participants had reported a history of head trauma that included either loss of consciousness or memory lapse. There was no difference between them and those without such a history in most characteristics, such as age, education level, APOE genotype, or scores on various measures of cognitive function.
FDG-PET results also did not differ by head injury history, either in the MCI subgroup or in those considered cognitively normal, indicating no difference in overall levels of brain activity.
However, in the MCI subgroup, PiB binding was significantly greater in those with previous head injuries. Also, MRI measures of hippocampal volume in the MCI subgroup showed a strong trend toward atrophy in those with the head injury history.
Among individuals reporting head injuries meeting study criteria, the median time since the first such injury was 58 years in the cognitively normal participants and 56 in the MCI subgroup. With no meaningful difference in this measure between the two subgroups, Mielke and colleagues suggested that the explanation for the differing neuroimaging findings must lie elsewhere.
One possible explanation is that the study had excluded patients with overt dementia, and “those most susceptible to the adverse effects of head trauma developed Alzheimer’s disease and thus were not included,” Mielke and colleagues suggested.
Alternatively, the amyloid accumulation may be a response to neuronal injury resulting in demyelination, they offered. “Therefore, the association between head trauma and amyloid appears only in the MCI group because amyloid is a byproduct of the myelin repair process and occurs only after a critical level of demyelination has occurred,” the researchers wrote, although they acknowledged that this hypothesis is controversial.
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