% 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{Hoenig:285017,
      author       = {Hoenig, Merle C and Dzialas, Verena and Doering, Elena and
                      Bischof, Gérard N and Eimeren, Thilo and Drzezga,
                      Alexander},
      collaboration = {Initiative, Alzheimer’s Disease Neuroimaging},
      title        = {{M}odifiable {F}actors {A}ssociated with the {L}ongitudinal
                      {I}ncrease and {S}patial {E}xtent of {T}au {P}athology in
                      {A}lzheimer {D}isease.},
      journal      = {Journal of nuclear medicine},
      volume       = {67},
      number       = {2},
      issn         = {0097-9058},
      address      = {New York, NY},
      publisher    = {Soc.},
      reportid     = {DZNE-2026-00143},
      pages        = {291-296},
      year         = {2026},
      abstract     = {There are 14 modifiable factors that are associated with a
                      significantly lower risk of dementia. We tested the
                      interactive effect of modifiable factors, genetic
                      determinants, and initial pathologic burden on the spatial
                      progression and local amplification of tau pathology.
                      Methods: In total, 162 amyloid-positive individuals were
                      included, for whom longitudinal [18F]AV-1451 PET scans,
                      baseline information on global amyloid burden, ApoE4 status,
                      body mass index (BMI), hypertension, education,
                      neuropsychiatric symptom severity, and demographic
                      information were available in the Alzheimer Disease
                      Neuroimaging Initiative. All [18F]AV-1451 scans were
                      intensity-standardized (reference: inferior cerebellum),
                      z-transformed (control sample: 147 amyloid-negative
                      subjects), thresholded (z score, >1.96), and converted to
                      volume maps. Longitudinal tau changes were then assessed in
                      terms of tau spatial extent (i.e., newly affected volume at
                      follow-up) and tau level rise (i.e., tau increase in
                      previously affected volume). These 2 measures were entered
                      as dependent variables in linear mixed-effects models,
                      including baseline modifiable risk factors (BMI, education,
                      hypertension, neuropsychiatric symptom severity), global
                      amyloid, tau volume or tau burden, ApoE4 status, clinical
                      stage, sex, and age as predictors. Next, we tested the
                      interactive effects between baseline amyloid or tau burden
                      with the 4 modifiable factors on tau extent or tau level
                      rise, respectively. Results: Greater tau extent was linked
                      to higher BMI (β = 0.002; $95\%$ CI, 0.0003-0.003), ApoE4
                      status (β = 0.024; $95\%$ CI, 0.001-0.046), and baseline
                      tau volume (β = 0.207; $95\%$ CI, 0.107-0.308) across
                      groups. In terms of tau level rise, we observed that absence
                      of hypertension (β = 0.295; $95\%$ CI, -0.477 to -0.114),
                      dementia group (β = 0.305; $95\%$ CI, 0.088-0.522), and BMI
                      (β = 0.011; $95\%$ CI, 0.00004-0.022) were linked to
                      increased tau burden. A load-dependent effect of baseline
                      amyloid and tau volume/burden was found for both tau extent
                      (β = -0.005; $95\%$ CI, -0.008 to -0.002) and tau level
                      rise (β = -0.003; $95\%$ CI, -0.005 to -0.001). Higher
                      amyloid and BMI (β = 0.001; $95\%$ CI, 0.0004-0.001) and
                      lower education and higher tau burden (β = -0.035; $95\%$
                      CI, -0.064 to -0.006) were linked to greater tau level rise.
                      Conclusion: Education, BMI, and hypertension differentially
                      influence tau's spatial extent and increase by its
                      interaction with initial pathologic burden. Timely
                      modification of these factors may overall slow tau
                      progression.},
      keywords     = {Humans / tau Proteins: metabolism / Male / Alzheimer
                      Disease: diagnostic imaging / Alzheimer Disease: metabolism
                      / Alzheimer Disease: pathology / Female / Aged /
                      Longitudinal Studies / Positron-Emission Tomography /
                      Carbolines / Aged, 80 and over / Middle Aged / Body Mass
                      Index / Risk Factors / (non-)modifiable risk factors (Other)
                      / spatial extent (Other) / tau pathology (Other) / tau
                      Proteins (NLM Chemicals) /
                      7-(6-fluoropyridin-3-yl)-5H-pyrido(4,3-b)indole (NLM
                      Chemicals) / Carbolines (NLM Chemicals)},
      cin          = {AG Boecker},
      ddc          = {610},
      cid          = {I:(DE-2719)1011202},
      pnm          = {353 - Clinical and Health Care Research (POF4-353)},
      pid          = {G:(DE-HGF)POF4-353},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:41266256},
      pmc          = {pmc:PMC12866421},
      doi          = {10.2967/jnumed.125.270593},
      url          = {https://pub.dzne.de/record/285017},
}