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[PMID]: | 26843562 |
[Au] Autor: | Scott G; Ramlackhansingh AF; Edison P; Hellyer P; Cole J; Veronese M; Leech R; Greenwood RJ; Turkheimer FE; Gentleman SM; Heckemann RA; Matthews PM; Brooks DJ; Sharp DJ |
[Ad] Endereço: | From the Division of Brain Sciences (G.S., A.F.R., P.E., P.H., J.C., R.L., S.M.G., R.A.H., P.M.M., D.J.B., D.J.S.), Department of Medicine, Imperial College London; Institute of Psychiatry, Psychology & Neuroscience (P.H., M.V., F.E.T.), King's College London; Institute of Neurology (R.J.G.), Un |
[Ti] Título: | Amyloid pathology and axonal injury after brain trauma. |
[So] Source: | Neurology;86(9):821-8, 2016 Mar 01. | [Is] ISSN: | 1526-632X |
[Cp] País de publicação: | United States |
[La] Idioma: | eng |
[Ab] Resumo: | OBJECTIVE: To image ß-amyloid (Aß) plaque burden in long-term survivors of traumatic brain injury (TBI), test whether traumatic axonal injury and Aß are correlated, and compare the spatial distribution of Aß to Alzheimer disease (AD). METHODS: Patients 11 months to 17 years after moderate-severe TBI underwent (11)C-Pittsburgh compound B ((11)C-PiB)-PET, structural and diffusion MRI, and neuropsychological examination. Healthy aged controls and patients with AD underwent PET and structural MRI. Binding potential (BPND) images of (11)C-PiB, which index Aß plaque density, were computed using an automatic reference region extraction procedure. Voxelwise and regional differences in BPND were assessed. In TBI, a measure of white matter integrity, fractional anisotropy, was estimated and correlated with (11)C-PiB BPND. RESULTS: Twenty-eight participants (9 with TBI, 9 controls, 10 with AD) were assessed. Increased (11)C-PiB BPND was found in TBI vs controls in the posterior cingulate cortex and cerebellum. Binding in the posterior cingulate cortex increased with decreasing fractional anisotropy of associated white matter tracts and increased with time since injury. Compared to AD, binding after TBI was lower in neocortical regions but increased in the cerebellum. CONCLUSIONS: Increased Aß burden was observed in TBI. The distribution overlaps with, but is distinct from, that of AD. This suggests a mechanistic link between TBI and the development of neuropathologic features of dementia, which may relate to axonal damage produced by the injury. |
[Mh] Termos MeSH primário: |
Neuropatias Amiloides/diagnóstico Neuropatias Amiloides/etiologia Peptídeos beta-Amiloides/metabolismo Axônios/patologia Lesões Encefálicas/complicações Lesões Encefálicas/diagnóstico
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[Mh] Termos MeSH secundário: |
Adulto Neuropatias Amiloides/metabolismo Biomarcadores/metabolismo Lesões Encefálicas/metabolismo Imagem de Tensor de Difusão/métodos Feminino Seres Humanos Estudos Longitudinais Masculino Meia-Idade Imagem Multimodal/métodos Tomografia por Emissão de Pósitrons/métodos Reprodutibilidade dos Testes Sensibilidade e Especificidade Distribuição Tecidual
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[Pt] Tipo de publicação: | JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T |
[Nm] Nome de substância:
| 0 (Amyloid beta-Peptides); 0 (Biomarkers) |
[Em] Mês de entrada: | 1607 |
[Cu] Atualização por classe: | 171110 |
[Lr] Data última revisão:
| 171110 |
[Sb] Subgrupo de revista: | AIM; IM |
[Da] Data de entrada para processamento: | 160205 |
[St] Status: | MEDLINE |
[do] DOI: | 10.1212/WNL.0000000000002413 |
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