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Head injury linked to amyloid deposition decades later



A history of head injury is associated with increased amyloid deposition in the brain, both globally and in the frontal cortex, according to PET imaging in 329 older adults without dementia.

Previous studies have found an association between head injury and later dementia, but the mechanism isn’t understood. The importance of the new investigation is that it “hints at pathophysiology. We were very excited” to find amyloid in the frontal cortex, “which is also associated with Alzheimer’s disease,” said lead investigator Andrea Schneider, MD, PhD, a neurology resident at Johns Hopkins University, Baltimore.

Increased amyloid deposition was not found in other areas associated with the disease, but frontal cortex involvement “does suggest perhaps a common” denominator, she noted.

Dr. Andrea Schneider M. Alexander Otto/Frontline Medical News

Dr. Andrea Schneider

Although there’s no intervention to prevent amyloid deposition, perhaps there will be someday. “That’s the hope,” Dr. Schneider said at the annual meeting of the American Neurological Association.

The older adults in the study were all participants in the Atherosclerosis Risk in Communities (ARIC) cohort, a group of over 15,000 community-dwelling adults who have been followed since the late 1980s. All 329 had brain amyloid deposition assessed by florbetapir (Amyvid) PET scans in 2011-2013; mean age was 76 years.

Sixty-six (20%) reported a history of head trauma at a median of about 25 years before the scan, with self-reports correlating well with hospitalization billing codes collected as part of ARIC. The cause of the head trauma was not known.

Head injury was associated with elevated standardized uptake value ratios (SUVRs, greater than 1.2). Head injury patients had a 1.31-fold increased prevalence of elevated global amyloid deposition (95% confidence interval, 1.07-1.60) as well as a 1.24-fold increased prevalence of elevated deposition in the orbitofrontal cortex (95% CI, 1.02-1.50) and prefrontal cortex (95% CI, 1.03-1.49), and 1.29-fold increased prevalence in the superior frontal cortex (95% CI, 1.06-1.56).

There were no differences in the prevalence of elevated SUVRs in the anterior cingulate, posterior cingulate, precuneus, or the lateral temporal, parietal, or occipital lobes (all P greater than .05) Dr. Schneider reported.

The model was adjusted for age, sex, race, total intracranial volume, and cardiovascular disease, among other things.

Thirty percent of the participants had either one or two APOE4 alleles, and 27% had mild cognitive impairment; neither correlated with increased amyloid deposition.

Head injuries were more common among participants who were men (43%) or white (57%). There was a trend for a slightly stronger link between head injury and increased amyloid deposition among black individuals (P for interaction 0.169).

Dr. Schneider is continuing her work to illuminate the connection between head trauma and dementia. She plans to integrate more detailed cognitive data from ARIC into the analysis, and perhaps emergency department and outpatient data. She also wants to look at more acute imaging after head trauma.

The work was funded by the National Institutes of Health. Avid Radiopharmaceuticals provided the florbetapir. Dr. Schneider did not have any relevant disclosures.

SOURCE: Schneider A et al. ANA 2017 abstract M336WIP

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