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@ARTICLE{Franzmeier:266772,
      author       = {Franzmeier, Nicolai and Dehsarvi, Amir and Steward, Anna
                      and Biel, Davina and Dewenter, Anna and Roemer, Sebastian
                      Niclas and Wagner, Fabian and Groß, Mattes and Brendel,
                      Matthias and Moscoso, Alexis and Arunachalam, Prithvi and
                      Blennow, Kaj and Zetterberg, Henrik and Ewers, Michael and
                      Schöll, Michael},
      title        = {{E}levated {CSF} {GAP}-43 is associated with accelerated
                      tau accumulation and spread in {A}lzheimer's disease.},
      journal      = {Nature Communications},
      volume       = {15},
      number       = {1},
      issn         = {2041-1723},
      address      = {[London]},
      publisher    = {Nature Publishing Group UK},
      reportid     = {DZNE-2024-00035},
      pages        = {202},
      year         = {2024},
      abstract     = {In Alzheimer's disease, amyloid-beta (Aβ) triggers the
                      trans-synaptic spread of tau pathology, and aberrant
                      synaptic activity has been shown to promote tau spreading.
                      Aβ induces aberrant synaptic activity, manifesting in
                      increases in the presynaptic growth-associated protein 43
                      (GAP-43), which is closely involved in synaptic activity and
                      plasticity. We therefore tested whether Aβ-related GAP-43
                      increases, as a marker of synaptic changes, drive tau
                      spreading in 93 patients across the aging and Alzheimer's
                      spectrum with available CSF GAP-43, amyloid-PET and
                      longitudinal tau-PET assessments. We found that (1) higher
                      GAP-43 was associated with faster Aβ-related tau
                      accumulation, specifically in brain regions connected
                      closest to subject-specific tau epicenters and (2) that
                      higher GAP-43 strengthened the association between Aβ and
                      connectivity-associated tau spread. This suggests that
                      GAP-43-related synaptic changes are linked to faster
                      Aβ-related tau spread across connected regions and that
                      synapses could be key targets for preventing tau spreading
                      in Alzheimer's disease.},
      keywords     = {Humans / Alzheimer Disease: metabolism / GAP-43 Protein:
                      genetics / GAP-43 Protein: metabolism / tau Proteins:
                      metabolism / Amyloid beta-Peptides: metabolism / Brain:
                      metabolism / Positron-Emission Tomography / Cognitive
                      Dysfunction: metabolism / Biomarkers: metabolism / GAP-43
                      Protein (NLM Chemicals) / tau Proteins (NLM Chemicals) /
                      Amyloid beta-Peptides (NLM Chemicals) / Biomarkers (NLM
                      Chemicals)},
      cin          = {Clinical Research (Munich)},
      ddc          = {500},
      cid          = {I:(DE-2719)1111015},
      pnm          = {353 - Clinical and Health Care Research (POF4-353)},
      pid          = {G:(DE-HGF)POF4-353},
      typ          = {PUB:(DE-HGF)16},
      pmc          = {pmc:PMC10764818},
      pubmed       = {pmid:38172114},
      doi          = {10.1038/s41467-023-44374-w},
      url          = {https://pub.dzne.de/record/266772},
}