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@ARTICLE{Malpetti:272854,
      author       = {Malpetti, Maura and Roemer, Sebastian N and Harris,
                      Stefanie and Gross, Mattes and Gnoerich, Johannes and
                      Stephens, Andrew and Dewenter, Anna and Steward, Anna and
                      Biel, Davina and Dehsarvi, Amir and Wagner, Fabian and
                      Müller, Andre and Koglin, Norman and Weidinger, Endy and
                      Palleis, Carla and Katzdobler, Sabrina and Rupprecht, Rainer
                      and Perneczky, Robert and Rauchmann, Boris Stephan and
                      Levin, Johannes and Höglinger, Günter U and Brendel,
                      Matthias and Franzmeier, Nicolai},
      title        = {{N}euroinflammation {P}arallels 18{F}-{PI}-2620 {P}ositron
                      {E}mission {T}omography {P}atterns in {P}rimary 4-{R}epeat
                      {T}auopathies.},
      journal      = {Movement disorders},
      volume       = {39},
      number       = {9},
      issn         = {0885-3185},
      address      = {New York, NY},
      publisher    = {Wiley},
      reportid     = {DZNE-2024-01272},
      pages        = {1480 - 1492},
      year         = {2024},
      abstract     = {Preclinical, postmortem, and positron emission tomography
                      (PET) imaging studies have pointed to neuroinflammation as a
                      key pathophysiological hallmark in primary 4-repeat (4R)
                      tauopathies and its role in accelerating disease
                      progression.We tested whether microglial activation (1)
                      progresses in similar spatial patterns as the primary
                      pathology tau spreads across interconnected brain regions,
                      and (2) whether the degree of microglial activation
                      parallels tau pathology spreading.We examined in vivo
                      associations between tau aggregation and microglial
                      activation in 31 patients with clinically diagnosed 4R
                      tauopathies, using 18F-PI-2620 PET and 18F-GE180
                      (translocator protein [TSPO]) PET. We determined tau
                      epicenters, defined as subcortical brain regions with
                      highest tau PET signal, and assessed the connectivity of tau
                      epicenters to cortical regions of interest using a 3-T
                      resting-state functional magnetic resonance imaging template
                      derived from age-matched healthy elderly controls.In 4R
                      tauopathy patients, we found that higher regional tau PET
                      covaries with elevated TSPO-PET across brain regions that
                      are functionally connected to each other (β = 0.414, P <
                      0.001). Microglial activation follows similar distribution
                      patterns as tau and distributes primarily across brain
                      regions strongly connected to patient-specific tau
                      epicenters (β = -0.594, P < 0.001). In these regions,
                      microglial activation spatially parallels tau distribution
                      detectable with 18F-PI-2620 PET.Our findings indicate that
                      the spatial expansion of microglial activation parallels tau
                      distribution across brain regions that are functionally
                      connected to each other, suggesting that tau and
                      inflammation are closely interrelated in patients with 4R
                      tauopathies. The combination of in vivo tau and inflammatory
                      biomarkers could therefore support the development of
                      immunomodulatory strategies for disease-modifying treatments
                      in these conditions. © 2024 The Author(s). Movement
                      Disorders published by Wiley Periodicals LLC on behalf of
                      International Parkinson and Movement Disorder Society.},
      keywords     = {Humans / Tauopathies: diagnostic imaging / Tauopathies:
                      metabolism / Positron-Emission Tomography: methods / Male /
                      Female / Aged / Middle Aged / tau Proteins: metabolism /
                      Neuroinflammatory Diseases: diagnostic imaging /
                      Neuroinflammatory Diseases: metabolism / Brain: diagnostic
                      imaging / Brain: metabolism / Brain: pathology / Microglia:
                      metabolism / Receptors, GABA: metabolism / 4R tauopathies
                      (Other) / PET (Other) / Tau (Other) / fMRI (Other) /
                      inflammation (Other) / tau Proteins (NLM Chemicals) /
                      Receptors, GABA (NLM Chemicals) / TSPO protein, human (NLM
                      Chemicals)},
      cin          = {Clinical Research (Munich) / AG Haass / AG Höglinger},
      ddc          = {610},
      cid          = {I:(DE-2719)1111015 / I:(DE-2719)1110007 /
                      I:(DE-2719)1110002},
      pnm          = {353 - Clinical and Health Care Research (POF4-353) / 352 -
                      Disease Mechanisms (POF4-352)},
      pid          = {G:(DE-HGF)POF4-353 / G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:39022835},
      doi          = {10.1002/mds.29924},
      url          = {https://pub.dzne.de/record/272854},
}