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@ARTICLE{Brown:140199,
      author       = {Brown, Rosalind and Benveniste, Helene and Black, Sandra E
                      and Charpak, Serge and Dichgans, Martin and Joutel, Anne and
                      Nedergaard, Maiken and Smith, Kenneth J and Zlokovic,
                      Berislav V and Wardlaw, Joanna M},
      title        = {{U}nderstanding the role of the perivascular space in
                      cerebral small vessel disease.},
      journal      = {Cardiovascular research},
      volume       = {114},
      number       = {11},
      issn         = {0008-6363},
      address      = {Oxford},
      publisher    = {Oxford University Press},
      reportid     = {DZNE-2020-06521},
      pages        = {1462-1473},
      year         = {2018},
      abstract     = {Small vessel diseases (SVDs) are a group of disorders that
                      result from pathological alteration of the small blood
                      vessels in the brain, including the small arteries,
                      capillaries and veins. Of the 35-36 million people that are
                      estimated to suffer from dementia worldwide, up to $65\%$
                      have an SVD component. Furthermore, SVD causes $20-25\%$ of
                      strokes, worsens outcome after stroke and is a leading cause
                      of disability, cognitive impairment and poor mobility. Yet
                      the underlying cause(s) of SVD are not fully understood.
                      Magnetic resonance imaging has confirmed enlarged
                      perivascular spaces (PVS) as a hallmark feature of SVD. In
                      healthy tissue, these spaces are proposed to form part of a
                      complex brain fluid drainage system which supports
                      interstitial fluid exchange and may also facilitate
                      clearance of waste products from the brain. The
                      pathophysiological signature of PVS and what this infers
                      about their function and interaction with cerebral
                      microcirculation, plus subsequent downstream effects on
                      lesion development in the brain has not been established.
                      Here we discuss the potential of enlarged PVS to be a unique
                      biomarker for SVD and related brain disorders with a
                      vascular component. We propose that widening of PVS suggests
                      presence of peri-vascular cell debris and other waste
                      products that form part of a vicious cycle involving
                      impaired cerebrovascular reactivity, blood-brain barrier
                      dysfunction, perivascular inflammation and ultimately
                      impaired clearance of waste proteins from the interstitial
                      fluid space, leading to accumulation of toxins, hypoxia, and
                      tissue damage. Here, we outline current knowledge, questions
                      and hypotheses regarding understanding the brain fluid
                      dynamics underpinning dementia and stroke through the common
                      denominator of SVD.},
      subtyp        = {Review Article},
      keywords     = {Animals / Blood-Brain Barrier: physiopathology / Cerebral
                      Small Vessel Diseases: diagnostic imaging / Cerebral Small
                      Vessel Diseases: pathology / Cerebral Small Vessel Diseases:
                      physiopathology / Glymphatic System: diagnostic imaging /
                      Glymphatic System: pathology / Glymphatic System:
                      physiopathology / Humans / Magnetic Resonance Imaging /
                      Microvessels: diagnostic imaging / Microvessels: pathology /
                      Microvessels: physiopathology / Prognosis},
      cin          = {Clinical Dementia Research München},
      ddc          = {610},
      cid          = {I:(DE-2719)1111016},
      pnm          = {344 - Clinical and Health Care Research (POF3-344)},
      pid          = {G:(DE-HGF)POF3-344},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:29726891},
      pmc          = {pmc:PMC6455920},
      doi          = {10.1093/cvr/cvy113},
      url          = {https://pub.dzne.de/record/140199},
}