Spatial Patterns of Amyloid Deposition in Patients with Chronic Focal or Diffuse Traumatic Brain Injury Using

PET amyloid deposition chronic diffuse axonal injury focal injury

Journal

Neuropsychiatric disease and treatment
ISSN: 1176-6328
Titre abrégé: Neuropsychiatr Dis Treat
Pays: New Zealand
ID NLM: 101240304

Informations de publication

Date de publication:
2020
Historique:
received: 01 07 2020
accepted: 12 10 2020
entrez: 19 11 2020
pubmed: 20 11 2020
medline: 20 11 2020
Statut: epublish

Résumé

Amyloid-β (Aβ) accumulation, accelerated by traumatic brain injury (TBI), may play a crucial role in neurodegeneration in chronic-stage TBI. The injury type could influence Aβ dynamics because of TBI's complex, heterogeneous nature. We, therefore, investigated spatial patterns of amyloid deposition according to injury type after TBI using 5-(5-(2-(2-(2-[F]-fluoroethoxy)ethoxy)ethoxy)benzofuran-2-yl)- Altogether, 20 patients with chronic TBI [12 with focal injury, 8 with diffuse axonal injury (DAI)] underwent Standardized uptake value ratio (SUVR) on PET images and regional brain volumes were measured in four cortical (frontal, parietal, occipital, temporal) and subcortical (combined caudate, putamen, pallidum, thalamus) regions. Patients with DAI showed significantly increased (compared with controls) SUVR in occipital and temporal cortices and decreased brain volume in occipital cortex (corrected p < 0.05). Although patients with focal injury showed decreased SUVR in all regions except occipital cortex, there were no significant differences (compared with controls) in the SUVR in any regions. There were no significant correlations between increased SUVR and neuropsychological impairments in patients with DAI. Varying spatial patterns of amyloid deposition suggest amyloid pathology diversity depending on the injury type in chronic-TBI patients.

Identifiants

pubmed: 33209027
doi: 10.2147/NDT.S268504
pii: 268504
pmc: PMC7669502
doi:

Types de publication

Journal Article

Langues

eng

Pagination

2719-2732

Informations de copyright

© 2020 Ubukata et al.

Déclaration de conflit d'intérêts

Toshihiko Aso reports grants from Japan Society for the Promotion of Science, during the conduct of the study. The authors have no other potential conflicts of interest to declare.

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Auteurs

Shiho Ubukata (S)

Department of Psychiatry, Graduate School of Medicine, Kyoto University, Kyoto, Japan.
Medical Innovation Center, Graduate School of Medicine, Kyoto University, Kyoto, Japan.

Naoya Oishi (N)

Medical Innovation Center, Graduate School of Medicine, Kyoto University, Kyoto, Japan.

Tatsuya Higashi (T)

Shiga Medical Center Research Institute, Moriyama, Japan.
Department of Molecular Imaging and Theranostics, National Institute of Radiological Sciences (NIRS), National Institutes for Quantum and Radiological Science and Technology (QST), Chiba, Japan.

Shinya Kagawa (S)

Shiga Medical Center Research Institute, Moriyama, Japan.

Hiroshi Yamauchi (H)

Shiga Medical Center Research Institute, Moriyama, Japan.

Chio Okuyama (C)

Shiga Medical Center Research Institute, Moriyama, Japan.

Hiroyuki Watanabe (H)

Department of Patho-Functional Bioanalysis, Graduate School of Pharmaceutical Sciences, Kyoto University, Kyoto, Japan.

Masahiro Ono (M)

Department of Patho-Functional Bioanalysis, Graduate School of Pharmaceutical Sciences, Kyoto University, Kyoto, Japan.

Hideo Saji (H)

Department of Patho-Functional Bioanalysis, Graduate School of Pharmaceutical Sciences, Kyoto University, Kyoto, Japan.

Toshihiko Aso (T)

Department of Psychiatry, Graduate School of Medicine, Kyoto University, Kyoto, Japan.

Toshiya Murai (T)

Department of Psychiatry, Graduate School of Medicine, Kyoto University, Kyoto, Japan.

Keita Ueda (K)

Department of Psychiatry, Graduate School of Medicine, Kyoto University, Kyoto, Japan.

Classifications MeSH