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|Title:||Amyloid- and Tau Imaging in Chronic Traumatic Brain Injury: A Cross-sectional Study.||Austin Authors:||Hicks, Amelia;Ponsford, Jennie L;Spitz, Gershon;Doré, Vincent ;Krishnadas, Natasha ;Roberts, Caroline;Rowe, Christopher C||Affiliation:||Molecular Imaging and Therapy
The Florey Institute of Neuroscience and Mental Health
Monash-Epworth Rehabilitation Research Centre, Turner Institute for Brain and Mental Health, School of Psychological Sciences, Monash University, Clayton, 3168, Australia..
CSIRO Health and Biosecurity Flagship, The Australian e-Health Research Centre, Parkville, 3052, Australia..
|Issue Date:||15-Jun-2022||metadata.dc.date:||2022||Publication information:||Neurology 2022; online first: 15 June||Abstract:||Traumatic brain injury (TBI) has been promoted as a risk factor for Alzheimer's disease. There is evidence of elevated amyloid-β and tau, the pathological hallmarks of Alzheimer's disease, immediately following TBI. It is not clear whether amyloid-β and tau remain elevated in the chronic period. To address this issue, we assessed amyloid-β and tau burden in long-term TBI survivors and healthy controls using PET imaging. Using a cross-sectional design, we recruited individuals following a single moderate to severe TBI at least 10 years previously from an inpatient rehabilitation program. A demographically similar healthy control group was recruited from the community. PET data were acquired using 18F-NAV4694 (amyloid-β) and 18F-MK6240 (tau) tracers. Amyloid-β deposition was quantified using the Centiloid scale. Tau deposition was quantified using the standardized uptake value ratio (SUVR) in four regions of interest (ROI). As a secondary measure, PET scans were also visually read as positive or negative. We examined PET data in relation to time since injury and age at injury. PET data were analysed in a series of regression analyses. The sample comprised 87 individuals with TBI (71.3% male; 28.7% female; M = 57.53 years, SD = 11.53) and 59 controls (59.3% male; 40.7% female; M = 60.34 years, SD = 11.97). Individuals with TBI did not have significantly higher 18F-NAV4694 Centiloid values (p = 0.067) or 18F-MK6240 tau SUVRs in any ROI (p = ≤ 0.001; SUVR greater for controls). Visual assessment was consistent with the quantification; individuals with TBI were not more likely than controls to have a positive amyloid-β (p = 0.505) or tau scan (p = 0.221). No associations were identified for amyloid-β or tau burden with time since injury (p = 0.057 to 0.332) or age at injury. A single moderate to severe TBI was not associated with higher burden of amyloid-β or tau pathologies in the chronic period relative to healthy controls. Amyloid-β and tau burden did not show a significant increase with years since injury, and burden did not appear to be greater for those who were older at the time of injury.||URI:||https://ahro.austin.org.au/austinjspui/handle/1/30381||DOI:||10.1212/WNL.0000000000200857||ORCID:||https://orcid.org/0000-0002-1152-0576
|Journal:||Neurology||PubMed URL:||35705503||PubMed URL:||https://pubmed.ncbi.nlm.nih.gov/35705503/||Type:||Journal Article|
|Appears in Collections:||Journal articles|
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