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@ARTICLE{Kommaddi:257575,
      author       = {Kommaddi, Reddy Peera and Verma, Aditi and Muniz-Terrera,
                      Graciela and Tiwari, Vivek and Chithanathan, Keerthana and
                      Diwakar, Latha and Gowaikar, Ruturaj and Karunakaran, Smitha
                      and Malo, Palash Kumar and Graff-Radford, Neill R and Day,
                      Gregory S and Laske, Christoph and Vöglein, Jonathan and
                      Nübling, Georg and Ikeuchi, Takeshi and Kasuga, Kensaku and
                      Ravindranath, Vijayalakshmi},
      collaboration = {Network, Dominantly Inherited Alzheimer},
      title        = {{S}ex difference in evolution of cognitive decline: studies
                      on mouse model and the {D}ominantly {I}nherited {A}lzheimer
                      {N}etwork cohort.},
      journal      = {Translational Psychiatry},
      volume       = {13},
      number       = {1},
      issn         = {2158-3188},
      address      = {London},
      publisher    = {Nature Publishing Group},
      reportid     = {DZNE-2023-00455},
      pages        = {123},
      year         = {2023},
      abstract     = {Women carry a higher burden of Alzheimer's disease (AD)
                      compared to men, which is not accounted entirely by
                      differences in lifespan. To identify the mechanisms
                      underlying this effect, we investigated sex-specific
                      differences in the progression of familial AD in humans and
                      in APPswe/PS1ΔE9 mice. Activity dependent protein
                      translation and associative learning and memory deficits
                      were examined in APPswe/PS1ΔE9 mice and wild-type mice. As
                      a human comparator group, progression of cognitive
                      dysfunction was assessed in mutation carriers and
                      non-carriers from DIAN (Dominantly Inherited Alzheimer
                      Network) cohort. Female APPswe/PS1ΔE9 mice did not show
                      recall deficits after contextual fear conditioning until 8
                      months of age. Further, activity dependent protein
                      translation and Akt1-mTOR signaling at the synapse were
                      impaired in male but not in female mice until 8 months of
                      age. Ovariectomized APPswe/PS1ΔE9 mice displayed recall
                      deficits at 4 months of age and these were sustained until 8
                      months of age. Moreover, activity dependent protein
                      translation was also impaired in 4 months old ovariectomized
                      APPswe/PS1ΔE9 mice compared with sham female APPswe/PS1ΔE9
                      mice. Progression of memory impairment differed between men
                      and women in the DIAN cohort as analyzed using linear mixed
                      effects model, wherein men showed steeper cognitive decline
                      irrespective of the age of entry in the study, while women
                      showed significantly greater performance and slower decline
                      in immediate recall (LOGIMEM) and delayed recall (MEMUNITS)
                      than men. However, when the performance of men and women in
                      several cognitive tasks (such as Wechsler's logical memory)
                      are compared with the estimated year from expected symptom
                      onset (EYO) we found no significant differences between men
                      and women. We conclude that in familial AD patients and
                      mouse models, females are protected, and the onset of
                      disease is delayed as long as estrogen levels are intact.},
      keywords     = {Humans / Female / Male / Mice / Animals / Infant /
                      Alzheimer Disease: metabolism / Mice, Transgenic / Sex
                      Characteristics / Cognitive Dysfunction: genetics / Fear /
                      Memory Disorders / Disease Models, Animal / Amyloid
                      beta-Protein Precursor: genetics / Amyloid beta-Peptides:
                      metabolism / Amyloid beta-Protein Precursor (NLM Chemicals)
                      / Amyloid beta-Peptides (NLM Chemicals)},
      cin          = {AG Gasser 1 / AG Höglinger 1 ; AG Höglinger 1 / Clinical
                      Dementia Research München ; AG Levin},
      ddc          = {610},
      cid          = {I:(DE-2719)1210000 / I:(DE-2719)1110002 /
                      I:(DE-2719)1111016},
      pnm          = {353 - Clinical and Health Care Research (POF4-353)},
      pid          = {G:(DE-HGF)POF4-353},
      experiment   = {EXP:(DE-2719)DIAN-20090101},
      typ          = {PUB:(DE-HGF)16},
      pmc          = {pmc:PMC10097702},
      pubmed       = {pmid:37045867},
      doi          = {10.1038/s41398-023-02411-8},
      url          = {https://pub.dzne.de/record/257575},
}