Review

PET imaging of the neurovascular interface in cerebrovascular disease

  • Nature Reviews Neurology 13, 676688 (2017)
  • doi:10.1038/nrneurol.2017.129
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Abstract

Cerebrovascular disease encompasses a range of pathologies that affect different components of the cerebral vasculature and brain parenchyma. Large artery atherosclerosis, acute cerebral ischaemia, and intracerebral small vessel disease all demonstrate altered metabolic processes that are key to their pathogenesis. Although structural imaging techniques such as MRI are the mainstay of clinical care and research in cerebrovascular disease, they have limited ability to detect these pathophysiological processes in vivo. By contrast, PET can detect and quantify metabolic processes that are relevant to each facet of cerebrovascular disease. Information obtained from PET studies has helped to shape the understanding of key concepts in cerebrovascular medicine, including vulnerable atherosclerotic plaque, salvageable ischaemic penumbra, neuroinflammation and selective neuronal loss after ischaemic insult. PET has also helped to elucidate the relationships between chronic hypoxia, neuroinflammation, and amyloid-β deposition in cerebral small vessel disease. This Review describes how PET-based imaging of metabolic processes at the neurovascular interface has contributed to our understanding of cerebrovascular disease.

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Acknowledgements

N.R.E. is supported by a research training fellowship from The Dunhill Medical Trust (grant number RTF44/0114). J.M.T. is supported by a Wellcome Trust research training fellowship (104492/Z/14/Z). J.H.F.R. is part-supported by the Higher Education Funding Council for England (HEFCE), the British Heart Foundation, and the Wellcome Trust. H.S.M. is supported by the Medical Research Council (MRC) as a National Institute for Health Research (NIHR) Senior Investigator. E.A.W. is supported by the British Heart Foundation. H.S.M., J.H.F.R., and E.A.W. are supported by the NIHR Cambridge Biomedical Research Centre.

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  1. Department of Clinical Neurosciences, University of Cambridge, Box 83, Addenbrooke's Hospital, Hills Road, Cambridge CB2 0QQ, UK.

    • Nicholas R. Evans
    • , Hugh S. Markus
    •  & Elizabeth A. Warburton
  2. Division of Cardiovascular Medicine, Department of Medicine, University of Cambridge, Box 157, Addenbrooke's Hospital, Hills Road, Cambridge CB2 0QQ, UK.

    • Jason M. Tarkin
    •  & James H. F. Rudd
  3. Department of Nuclear Medicine, Box 219, Cambridge University Hospitals NHS Foundation Trust, Hills Road, Cambridge CB2 0QQ, UK.

    • John R. Buscombe

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Contributions

N.R.E. wrote the manuscript. N.R.E., J.M.T. and J.H.F.R. researched data for the article. All authors (N.R.E., J.M.T., J.R.B., H.S.M., J.H.F.R. & E.A.W.) contributed substantially to discussions of the article content and undertook review and/or editing of the manuscript before submission.

Competing interests

The authors declare no competing financial interests.

Corresponding author

Correspondence to Nicholas R. Evans.