% 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”.

@INPROCEEDINGS{Teipel:283087,
      author       = {Teipel, Stefan J. and Baena, Ana Y and He, Bing and
                      Martinez, Lusiana and Niño, David Fernando Aguillón and
                      Quiroz, Yakeel T. and Grazia, Alice},
      title        = {{T}halamus but not basal forebrain and hippocampus atrophy
                      in prodromal carriers of the {C}olumbian mutation for
                      autosomal dominant {A}lzheimer’s disease – a {B}ayesian
                      confirmatory analysis},
      journal      = {Alzheimer's and dementia},
      volume       = {21},
      number       = {S7},
      issn         = {1552-5260},
      reportid     = {DZNE-2025-01494},
      pages        = {e108535},
      year         = {2025},
      abstract     = {Background:In sporadic Alzheimer's Disease (AD), the
                      cholinergic basal forebrain degenerates early, but seems to
                      be preserved in the Colombian PSEN1-E280A genetic mutation
                      for familial AD. In two cross-sectional studies analyzing
                      basal forebrain volume and connectivity from the API
                      Colombia cohort, we found no reduction in basal forebrain
                      volume or connectivity in carriers, but observed reduced
                      thalamic volume. Confirming these findings in other groups
                      with the same genetic mutation, such as those in the
                      Colombia-Boston (COLBOS) biomarker study, will help
                      determine whether the new hypothesis about basal forebrain
                      preservation in familial AD holds true.Method:We used
                      multi-modal imaging (MRI, amyloid and tau-PET) data of 57
                      cognitively unimpaired individuals from the COLBOS study
                      comprising PSEN1-E280A carriers (n = 27) and non-carriers (n
                      =30). Staging of functional impairment was done using the
                      Functional Assessment Staging Tool (FAST). Volumetry
                      analyses were performed using basal forebrain, hippocampus
                      and thalamus as regions of interest. We used Bayesian
                      multiple regression with both flat and informed priors to
                      test the hypothesis of preservation. As a secondary
                      analysis, we investigated the associations of amyloid and
                      tau pathology with brain volumes.Result:We found evidence
                      for no effect of mutation carrier status on basal forebrain
                      volume (BF₁₀: flat = 0.076; inf =0.54) and hippocampal
                      volume (BF₁₀: flat =0.16; inf =1.05). In contrast, we
                      observed moderate evidence for an effect of mutation carrier
                      status on thalamus volume, with smaller volumes in mutation
                      carriers (BF₁₀: flat =5.42; inf =8.74) (Figure 1).
                      Lastly, we found strong evidence against an effect of
                      amyloid status on basal forebrain and hippocampus, but
                      moderate evidence for an effect on thalamic volume (Figure
                      2A). Similarly, tau pathology was not associated with basal
                      forebrain, but showed associations with thalamus and
                      hippocampus. (Figure 2B).Conclusion:Our findings show that
                      in the PSEN1-E280A cohort, the cholinergic basal forebrain
                      and hippocampus are not affected early in the disease,
                      whereas the thalamus is, pointing to important
                      considerations for treatment target selection in this group.
                      These results should be further explored in other autosomal
                      dominant AD mutations.},
      month         = {Jul},
      date          = {2025-07-27},
      organization  = {Alzheimer’s Association
                       International Conference, Toronto
                       (Canada), 27 Jul 2025 - 31 Jul 2025},
      cin          = {AG Teipel},
      ddc          = {610},
      cid          = {I:(DE-2719)1510100},
      pnm          = {353 - Clinical and Health Care Research (POF4-353)},
      pid          = {G:(DE-HGF)POF4-353},
      typ          = {PUB:(DE-HGF)1 / PUB:(DE-HGF)16},
      doi          = {10.1002/alz70861_108535},
      url          = {https://pub.dzne.de/record/283087},
}