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@INPROCEEDINGS{Bathe:283145,
      author       = {Bathe, Tim and Salomasova, Svetlana and Lalia, Manvir and
                      Kunze, Lea and Palumbo, Giovanna and Oos, Rosel and Joseph,
                      Emanuel and Brendel, Matthias},
      title        = {{M}ulti‐tracer {PET} monitoring of an immunomodulatory
                      therapy in 4{R} tauopathy: {E}valuating a novel drug's
                      impact on glial function and protein pathology},
      journal      = {Alzheimer's and dementia},
      volume       = {21},
      number       = {S2},
      issn         = {1552-5260},
      reportid     = {DZNE-2026-00041},
      pages        = {e104796},
      year         = {2025},
      abstract     = {The prevalence of neurodegenerative diseases (ND),
                      including Alzheimer's disease (AD) and non-AD tauopathies,
                      is projected to rise significantly by 2050 due to an aging
                      global population. Chronic neuroinflammation, driven by
                      glial activation in response to protein pathologies, is a
                      major contributor to disease progression. Targeting glial
                      dysfunction through immunomodulatory therapies offers a
                      promising approach to mitigate the effects of tauopathies
                      and other ND.PS19 mice receive chronic treatment with GV1001
                      over 5 months. Serial neuroimaging techniques, including PET
                      scans targeting tau protein, microglial activation, and
                      astrocytic responses, are employed to assess treatment
                      effects in vivo (Figure 1). Postmortem validation is
                      performed using immunohistochemistry and biochemical
                      methods, comparing treated mice to placebo and
                      non-transgenic controls.The research scope is to monitor the
                      efficacy of GV1001 in a transgenic tau mouse model (PS19)
                      with an early-intervention biomarker study using molecular
                      biology and neuroimaging techniques including TSPO
                      (microglia) PET, deprenyl (astroglia) PET, tau PET
                      (perfusion and retention) and CSF markers of inflammation
                      (e.g. sTREM2) and neurodegeneration (NfL). Preliminary
                      findings, expected to be presented at the conference, will
                      provide insights into the drug's ability to modulate glial
                      activity, restore homeostasis, and reduce tau pathology.This
                      study highlights the potential of monitoring
                      immunomodulatory strategies to address the complex interplay
                      between chronic neuroinflammation and protein aggregation in
                      ND. If successful, these findings could inform the
                      development of novel therapeutic approaches for AD and
                      related disorders, bridging the gap between preclinical
                      research and clinical application.},
      month         = {Jul},
      date          = {2025-07-27},
      organization  = {Alzheimer’s Association
                       International Conference, Toronto
                       (Canada), 27 Jul 2025 - 31 Jul 2025},
      keywords     = {Animals / Biomarkers: cerebrospinal fluid / Biomarkers:
                      metabolism / Mice / Mice, Transgenic / Disease Models,
                      Animal / Alzheimer Disease: drug therapy / Positron-Emission
                      Tomography / tau Proteins: metabolism / Humans / Brain:
                      metabolism / Brain: pathology / Brain: diagnostic imaging /
                      Brain: drug effects / Tauopathies: drug therapy / Microglia:
                      metabolism / Biomarkers (NLM Chemicals) / tau Proteins (NLM
                      Chemicals)},
      cin          = {AG Haass},
      ddc          = {610},
      cid          = {I:(DE-2719)1110007},
      pnm          = {352 - Disease Mechanisms (POF4-352)},
      pid          = {G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)1 / PUB:(DE-HGF)16},
      doi          = {10.1002/alz70856_104796},
      url          = {https://pub.dzne.de/record/283145},
}