SAN DIEGO — Patients with a history of head injury show significant increases in amyloid deposition in key parts of the brain, including the frontal cortex, a finding that further supports evidence linking head injury with dementia later in life.
“Our study found associations between prior head injury and increased amyloid deposition both globally and within the frontal cortex, including orbitofrontal, prefrontal, and superior frontal cortices,” Andrea Schneider, MD, PhD, from Johns Hopkins University, Baltimore, Maryland, told Medscape Medical News.
“Our findings suggest that the frontal cortex may be particularly susceptible to the damaging effects of head injury.”
The findings were presented here at the ANA 2017: 48th Annual Meeting of the American Neurological Association.
Head injury has been linked to dementia in previous epidemiologic studies, and while the mechanisms are not well understood, amyloid and tau depositions are speculated to be likely factors.
To take a closer look at the association, Dr Schneider and her colleagues identified 329 participants in the Atherosclerosis Risk and Communities (ARIC) study who underwent positron emission tomography assessing brain amyloid deposition between 2011 and 2013.
The patients had a mean age of 76 years, 57% were female, 43% were black, and 20% had a history of head injury, defined by self-report or hospitalization International Classification of Diseases, Ninth Revision, codes. Approximately one third (27%) of patients had mild cognitive impairment; however, patients with dementia were excluded.
Dr Schneider noted that patients with head injuries had sustained the injuries a mean of approximately 25 years earlier.
Those with a history of head injury showed elevated (greater than 1.2) standard uptake value ratios (SUVRs) indicating the presence of amyloid deposition, in global assessments (prevalence ratio [PR], 1.31; 95% confidence interval [CI], 1.07 – 1.60).
The elevated levels were specifically in the orbitofrontal cortex (PR, 1.24; 95% CI, 1.02 – 1.50), the prefrontal cortex (PR, 1.24; 95% CI, 1.03 – 1.49), and the superior frontal cortex (PR, 1.29; 95% CI, 1.06 – 1.56).
Meanwhile, there were no significant differences in the prevalence of elevated SUVR in the anterior cingulate, posterior cingulate, precuneus, lateral temporal, parietal, or occipital lobes (all P > .05).
“It was exciting to see that the frontal cortex was particularly associated with increased amyloid deposition among those with prior head injury,” Dr Schneider said.
“We had also hypothesized that the posterior cingulate and precuneus areas would have elevated amyloid deposition, as these areas, along with the frontal cortex, have been shown to have early amyloid deposition in Alzheimer’s dementia — but this hypothesis was not validated in our sample.”
The findings add to ongoing speculation of a link between traumatic brain injury (TBI) and Alzheimer’s disease, Dr Schneider added.
“Overall, our study is consistent with the conclusion that there is some overlap in areas with amyloid deposition in TBI and in early Alzheimer’s pathology,” she said.
Additional research is needed to better understand how amyloid deposition with head injury relates to dementia, Dr Schneider noted.
“Further work is needed to determine if this increased amyloid deposition contributes to dementia and cognitive decline following head injury in this population — this is an area of active research within the ARIC cohort study.”
Insight on Mechanism
The study offers important insights on the possible mechanisms that could explain how TBI and amyloid relate, said Ramon Diaz-Arrastia, MD, PhD, presidential professor of neurology and attending neurologist at the Penn Presbyterian Medical Center Hospital of the University of Pennsylvania, in Philadelphia.
“It’s been known for a long time that TBI, particularly more moderate or severe injury, is associated with an increased risk of dementia — approximately two- or threefold or so,” he told Medscape Medical News.
“But little is known about the mechanism, and there is some [speculation] that TBI accelerates Alzheimer’s disease pathology, and another view is that it accelerates perhaps another type of pathology, such as tau-related pathology or vascular dementia,” he explained.
“So I think this is an important study because it is among the few that have looked at amyloid deposition in people with a history with TBI.”
The location of the amyloid disposition that was identified “is also intriguing in that it is different from that expected with Alzheimer’s disease,” Dr Diaz-Arrastia said.
“The increased amyloid deposition is not in the canonical Alzheimer’s disease regions but rather in these areas in the frontal lobes, which is important because the indications are that the features of dementia in people with TBI are not exactly like those we see with Alzheimer’s disease.”
The authors and Dr Diaz-Arrastia have disclosed no relevant financial relationships.
ANA 2017: 48th Annual Meeting of the American Neurological Association. Abstract M336WIP. Presented October 16, 2017.
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