% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@ARTICLE{Biel:276777,
      author       = {Biel, Davina and Suarez-Calvet, Marc and Dewenter, Anna and
                      Steward, Anna and Roemer, Sebastian N and Dehsarvi, Amir and
                      Zhu, Zeyu and Pescoller, Julia and Frontzkowski, Lukas and
                      Kreuzer, Annika and Haass, Christian and Schöll, Michael
                      and Brendel, Matthias and Franzmeier, Nicolai},
      title        = {{F}emale sex is linked to a stronger association between
                      s{TREM}2 and {CSF} p-tau in {A}lzheimer's disease.},
      journal      = {EMBO molecular medicine},
      volume       = {17},
      number       = {2},
      issn         = {1757-4676},
      address      = {[London]},
      publisher    = {Nature Publishing Group UK},
      reportid     = {DZNE-2025-00316},
      pages        = {235 - 248},
      year         = {2025},
      abstract     = {In Alzheimer's disease (AD), Aβ triggers p-tau secretion,
                      which drives tau aggregation. Therefore, it is critical to
                      characterize modulators of Aβ-related p-tau increases which
                      may alter AD trajectories. Here, we assessed whether factors
                      known to alter tau levels in AD modulate the association
                      between fibrillar Aβ and secreted p-tau181 determined in
                      the cerebrospinal fluid (CSF). To assess potentially
                      modulating effects of female sex, younger age, and ApoE4, we
                      included 322 ADNI participants with
                      cross-sectional/longitudinal p-tau181. To determine effects
                      of microglial activation on p-tau181, we included 454
                      subjects with cross-sectional CSF sTREM2. Running ANCOVAs
                      for nominal and linear regressions for metric variables, we
                      found that women had higher Aβ-related p-tau181 levels.
                      Higher sTREM2 was associated with elevated p-tau181, with
                      stronger associations in women. Similarly, ApoE4 was related
                      to higher p-tau181 levels and faster p-tau181 increases,
                      with stronger effects in female ApoE4 carriers. Our results
                      show that sex alone modulates the Aβ to p-tau axis, where
                      women show higher Aβ-dependent p-tau secretion, potentially
                      driven by elevated sTREM2-related microglial activation and
                      stronger effects of ApoE4 carriership in women.},
      keywords     = {Humans / Alzheimer Disease: cerebrospinal fluid / Female /
                      tau Proteins: cerebrospinal fluid / tau Proteins: metabolism
                      / Membrane Glycoproteins: cerebrospinal fluid / Membrane
                      Glycoproteins: metabolism / Receptors, Immunologic:
                      metabolism / Aged / Male / Sex Factors / Cross-Sectional
                      Studies / Amyloid beta-Peptides: cerebrospinal fluid /
                      Amyloid beta-Peptides: metabolism / Aged, 80 and over /
                      Apolipoprotein E4: genetics / Middle Aged / Alzheimer’s
                      Disease (Other) / Microglia (Other) / Sex Differences
                      (Other) / p-tau (Other) / sTREM2 (Other) / tau Proteins (NLM
                      Chemicals) / TREM2 protein, human (NLM Chemicals) / Membrane
                      Glycoproteins (NLM Chemicals) / Receptors, Immunologic (NLM
                      Chemicals) / Amyloid beta-Peptides (NLM Chemicals) /
                      Apolipoprotein E4 (NLM Chemicals) / MAPT protein, human (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)16},
      pubmed       = {pmid:39794447},
      pmc          = {pmc:PMC11822105},
      doi          = {10.1038/s44321-024-00190-3},
      url          = {https://pub.dzne.de/record/276777},
}