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@ARTICLE{Grazia:276276,
      author       = {Grazia, Alice and Dyrba, Martin and Pomara, Nunzio and
                      Temp, Anna G and Grothe, Michel J and Teipel, Stefan J},
      collaboration = {Initiative, Alzheimer's Prevention},
      title        = {{B}asal forebrain global functional connectivity is
                      preserved in asymptomatic presenilin-1 {E}280{A} mutation
                      carriers: {R}esults from the {C}olombia cohort.},
      journal      = {The journal of prevention of Alzheimer's disease},
      volume       = {12},
      number       = {2},
      issn         = {2274-5807},
      address      = {Cham},
      publisher    = {Springer International Publishing},
      reportid     = {DZNE-2025-00255},
      pages        = {100030},
      year         = {2025},
      abstract     = {Imaging studies showed early atrophy of the cholinergic
                      basal forebrain in prodromal sporadic Alzheimer's disease
                      and reduced posterior basal forebrain functional
                      connectivity in amyloid positive individuals with subjective
                      cognitive decline. Similar investigations in familial cases
                      of Alzheimer's disease are still lacking.To test whether
                      presenilin-1 E280A mutation carriers have reduced basal
                      forebrain functional connectivity and whether this is linked
                      to amyloid pathology.This is a cross-sectional study that
                      analyzes baseline functional imaging data.We obtained data
                      from the Colombia cohort Alzheimer's Prevention Initiative
                      Autosomal-Dominant Alzheimer's Disease Trial.We analyzed
                      data from 215 asymptomatic subjects carrying the
                      presenilin-1 E280A mutation $[64\%$ female; 147 carriers (M
                      = 35 years), 68 noncarriers (M = 40 years)].We extracted
                      functional magnetic resonance imaging data using seed-based
                      connectivity analysis to examine the anterior and posterior
                      subdivisions of the basal forebrain. Subsequently, we
                      performed a Bayesian Analysis of Covariance to assess the
                      impact of carrier status on functional connectivity in
                      relation to amyloid positivity. For comparison, we also
                      investigated hippocampus connectivity.We found no effect of
                      carrier status on anterior (Bayesian Factor10 = 1.167) and
                      posterior basal forebrain connectivity (Bayesian Factor10 =
                      0.033). In carriers, we found no association of amyloid
                      positivity with basal forebrain connectivity.We falsified
                      the hypothesis of basal forebrain connectivity reduction in
                      preclinical mutation carriers with amyloid pathology. If
                      replicated, these findings may not only confirm a
                      discrepancy between familial and sporadic Alzheimer's
                      disease, but also suggest new potential targets for future
                      treatments.},
      keywords     = {Humans / Presenilin-1: genetics / Female / Colombia / Male
                      / Cross-Sectional Studies / Adult / Magnetic Resonance
                      Imaging / Mutation / Basal Forebrain: diagnostic imaging /
                      Alzheimer Disease: genetics / Alzheimer Disease: diagnostic
                      imaging / Alzheimer Disease: physiopathology / Heterozygote
                      / Cohort Studies / Middle Aged / Basal forebrain (Other) /
                      Bayesian analysis (Other) / Colombia cohort (Other) / PSEN1
                      E280A (Other) / Resting-state fMRI (Other) / Presenilin-1
                      (NLM Chemicals) / PSEN1 protein, human (NLM Chemicals)},
      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)16},
      pubmed       = {pmid:39863323},
      doi          = {10.1016/j.tjpad.2024.100030},
      url          = {https://pub.dzne.de/record/276276},
}