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@ARTICLE{Schreiber:273915,
      author       = {Schreiber, Stefanie and Ulbrich, Philipp and Morton, Lorena
                      and Garza, Alejandra P and Müller, Patrick and Neumann,
                      Katja and Mattern, Hendrik and Dörner, Marc and Bernal,
                      Jose and Vielhaber, Stefan and Meuth, Sven G and Dunay,
                      Ildiko R and Dityatev, Alexander and Henneicke, Solveig},
      title        = {{I}mmune system activation and cognitive impairment in
                      arterial hypertension.},
      journal      = {American journal of physiology / Cell physiology},
      volume       = {327},
      number       = {6},
      issn         = {0363-6143},
      address      = {Bethesda, Md.},
      publisher    = {American Physiological Society},
      reportid     = {DZNE-2024-01389},
      pages        = {C1577 - C1590},
      year         = {2024},
      abstract     = {Chronic arterial hypertension disrupts the integrity of the
                      cerebral microvasculature, doubling the risk of age-related
                      dementia. Despite sufficient antihypertensive therapy in
                      still a significant proportion of individuals blood pressure
                      lowering alone does not preserve cognitive health.
                      Accumulating evidence highlights the role of inflammatory
                      mechanisms in the pathogenesis of hypertension. In this
                      review, we introduce a temporal framework to explore how
                      early immune system activation and interactions at
                      neurovascular-immune interfaces pave the way to cognitive
                      impairment. The overall paradigm suggests that
                      prohypertensive stimuli induce mechanical stress and
                      systemic inflammatory responses that shift peripheral and
                      meningeal immune effector mechanisms toward a
                      proinflammatory state. Neurovascular-immune interfaces in
                      the brain include a dysfunctional blood-brain barrier,
                      crossed by peripheral immune cells; the perivascular space,
                      in which macrophages respond to cerebrospinal fluid- and
                      blood-derived immune regulators; and the meningeal immune
                      reservoir, particularly T cells. Immune responses at these
                      interfaces bridge peripheral and neurovascular unit
                      inflammation, directly contributing to impaired brain
                      perfusion, clearance of toxic metabolites, and synaptic
                      function. We propose that deep immunophenotyping in
                      biofluids together with advanced neuroimaging could aid in
                      the translational determination of sequential immune and
                      brain endotypes specific to arterial hypertension. This
                      could close knowledge gaps on how and when immune system
                      activation transits into neurovascular dysfunction and
                      cognitive impairment. In the future, targeting specific
                      immune mechanisms could prevent and halt hypertension
                      disease progression before clinical symptoms arise,
                      addressing the need for new interventions against one of the
                      leading threats to cognitive health.},
      subtyp        = {Review Article},
      keywords     = {Humans / Hypertension: immunology / Hypertension:
                      physiopathology / Cognitive Dysfunction: immunology /
                      Cognitive Dysfunction: physiopathology / Animals /
                      Blood-Brain Barrier: immunology / Brain: immunology / Brain:
                      physiopathology / Brain: metabolism / Brain: pathology /
                      Immune System: immunology / Immune System: physiopathology /
                      Immune System: metabolism / Cognition: physiology /
                      Inflammation: immunology / arterial hypertension (Other) /
                      cerebral small vessel disease (Other) / cognitive impairment
                      (Other) / cytokines (Other) / immune system (Other)},
      cin          = {AG Schreiber / AG Dityatev / AG Düzel},
      ddc          = {000},
      cid          = {I:(DE-2719)1310010 / I:(DE-2719)1310007 /
                      I:(DE-2719)5000006},
      pnm          = {353 - Clinical and Health Care Research (POF4-353) / 351 -
                      Brain Function (POF4-351)},
      pid          = {G:(DE-HGF)POF4-353 / G:(DE-HGF)POF4-351},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:39495252},
      doi          = {10.1152/ajpcell.00219.2024},
      url          = {https://pub.dzne.de/record/273915},
}