The Down syndrome brain in the presence and absence of fibrillar β-amyloidosis

NEUROBIOLOGY OF AGING

卷:53

Article

Annus, Tiina¹  Wilson, Liam R.¹  Acosta-Cabronero, Julio^2,3  Cardenas-Blanco, Arturo²  Hong, Young T.⁴  Fryer, Tim D.⁴  Coles, Jonathan P.⁵  Menon, David K.⁵  Zaman, Shahid H.^1,6  Holland, Anthony J.^1,6  Nestor, Peter J.² 

[1] Univ Cambridge, Dept Psychiat, Cambridge Intellectual & Dev Disabil Res Grp, Douglas House,18b Trumpington Rd, Cambridge CB2 8AH, England

[2] German Ctr Neurodegenerat Dis DZNE, Magdeburg, Germany

[3] UCL, Wellcome Trust Ctr Neuroimaging, Inst Neurol, London, England

[4] Univ Cambridge, Wolfson Brain Imaging Ctr, Dept Clin Neurosci, Cambridge, England

[5] Univ Cambridge, Dept Med, Div Anaesthesia, Cambridge, England

[6] Fulbourn Hosp, Cambridgeshire & Peterborough NHS Fdn Trust, Elizabeth House, Cambridge, England

关键词: Alzheimer's disease;    Amyloid;    Cortical thickness;    Down syndrome;    Gray matter volume;   

DOI  :  10.1016/j.neurobiolaging.2017.01.009

来源: Elsevier

【 摘 要 】

People with Down syndrome (DS) have a neurodevelopmentally distinct brain and invariably developed amyloid neuropathology by age 50. This cross-sectional study aimed to provide a detailed account of DS brain morphology and the changes occuring with amyloid neuropathology. Forty-six adults with DS underwent structural and amyloid imagingdthe latter using Pittsburgh compound B (PIB) to stratify the cohort into PIB-positive (n = 19) and PIB-negative (n = 27). Age-matched controls (n = 30) underwent structural imaging. Group differences in deep gray matter volumetry and cortical thickness were studied. PIB-negative people with DS have neurodevelopmentally atypical brain, characterized by disproportionately thicker frontal and occipitoparietal cortex and thinner motor cortex and temporal pole with larger putamina and smaller hippocampi than controls. In the presence of amyloid neuropathology, the DS brains demonstrated a strikingly similar pattern of posterior dominant cortical thinning and subcortical atrophy in the hippocampus, thalamus, and striatum, to that observed in non-DS Alzheimer's disease. Care must be taken to avoid underestimating amyloid-associated morphologic changes in DS due to disproportionate size of some subcortical structures and thickness of the cortex. (C) 2017 The Authors. Published by Elsevier Inc. This is an open access article under the CC BY license.

【 授权许可】

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