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@ARTICLE{LamannaRama:307448,
      author       = {N. Lamanna-Rama and M. Casquero-Veiga and C. Ceron and G.
                      Sobrino and I. Fernandez-Nueda and S. Kossatz$^*$ and D.
                      Sehlin and M. Desco and B. Salinas and M. Cortes-Canteli},
      title        = {{A}lzheimer's {I}maging {C}onsortium.},
      journal      = {Alzheimer's and dementia},
      volume       = {21 Suppl 8},
      number       = {Suppl 8},
      issn         = {1552-5260},
      address      = {Hoboken, NJ},
      publisher    = {Wiley},
      reportid     = {DKFZ-2025-03047},
      pages        = {e109958},
      year         = {2025},
      note         = {Poster presentation / PMID: 41434183},
      abstract     = {Alzheimer's disease (AD) is the most common form of
                      dementia[1]. Despite the advances in the understanding of
                      its main neuropathological hallmarks, a significant gap
                      remains in comprehending this multifactorial
                      neurodegenerative disorder. Contributing factors to AD
                      include chronic vascular dysregulation and a prothrombotic
                      milieu, promoting fibrin accumulation in brain vessels[2].
                      Fibrin, the main protein component of blood clots, is
                      significantly increased in $60\%$ of AD-patients' brains[3].
                      Furthermore, its strong interaction with amyloid-β promotes
                      the production of degradation-resistant clots[2]. This
                      prothrombotic milieu intensifies hypoperfusion,
                      neurodegeneration and blood-brain barrier (BBB)
                      disruption[4], but not in all patients. Early detection
                      could help identify patients which might benefit from
                      anticoagulant therapies[5]. The BioClotAD Project aims to
                      develop an imaging biomarker based on a fibrin binding probe
                      (FBP)[6] to non-invasively identify AD's pro-coagulant
                      state.BioClotAD involves four partners in three European
                      countries with complementary expertise, using extensive in
                      vitro, ex vivoand in vivo assays, including AD animal models
                      and human AD brain samples. Our project is based on three
                      blocks: 1) Testing the FBP to in vivo detect the cerebral
                      occlusions by nuclear imaging. 2) Detecting fibrin deposits
                      inside the brain parenchyma with FBP coupled to a
                      transferrin receptor antibody (FBP-TfR) to facilitate BBB
                      crossing[7]. FBP-TfR will be labelled for optical and
                      nuclear imaging. 3) Validating the most promising FBP probes
                      in frozen brain samples of AD patients by autoradiography or
                      fluorescence microscopy.BioClotAD provides feasible
                      neuroimaging strategies to in vivo detect the fibrin
                      cerebral accumulation of AD models and identify the specific
                      regional distribution in the brain. Our project will set the
                      basis for future clinical trials on neuroimaging of the
                      cerebral fibrin accumulation in AD.BioClotAD neuroimaging
                      biomarkers will allow the early detection of the
                      pro-thrombotic state in AD, opening a window of opportunity
                      to delay the disease progression by personalized
                      anticoagulant therapies. References: 1. Alzheimer's
                      Association. 2021.
                      https://www.alz.org/media/documents/alzheimers-facts-and-figures.pdf.
                      2. Cortes-Canteli et al. 2020. 10.1016/j.jacc.2019.10.062 3.
                      Cortes-Canteli, et al. 2015.
                      https://doi.org/10.1016/j.neurobiolaging.2014.10.030 4.
                      Cortes-Canteli, et al. 2012.
                      https://doi.org/10.3233/JAD-2012-120820 5. Cortes-Canteli,
                      et al. 2019. https://doi.org/10.1016/j.jacc.2019.07.081 6.
                      Oliveira, Caravan. 2017. https://doi.org/10.1039/c7dt02634j
                      7. Sehlin, et al. 2019.
                      https://doi.org/10.1007/s00259-019-04426-0.},
      subtyp        = {Other},
      keywords     = {Humans / Alzheimer Disease: diagnostic imaging / Alzheimer
                      Disease: metabolism / Alzheimer Disease: pathology / Animals
                      / Fibrin: metabolism / Brain: diagnostic imaging / Brain:
                      metabolism / Brain: pathology / Biomarkers / Disease Models,
                      Animal / Fibrin (NLM Chemicals) / Biomarkers (NLM
                      Chemicals)},
      cin          = {MU01},
      ddc          = {610},
      cid          = {I:(DE-He78)MU01-20160331},
      pnm          = {899 - ohne Topic (POF4-899)},
      pid          = {G:(DE-HGF)POF4-899},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:41434183},
      pmc          = {pmc:PMC12726136},
      doi          = {10.1002/alz70862_109958},
      url          = {https://inrepo02.dkfz.de/record/307448},
}