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@ARTICLE{Villacampa:278791,
      author       = {Villacampa, Nàdia and Sarlus, Heela and Martorell, Paula
                      and Bhalla, Khushbu and Gomez-Castro, Sergio and
                      Vieira-Saecker, Ana and Slutzkin, Ilya and Händler,
                      Kristian and Venegas, Carmen and McManus, Róisín and Ulas,
                      Thomas and Beyer, Marc and Segal, Eran and Heneka, Michael},
      title        = {{P}roliferating {M}icroglia {E}xhibit {U}nique
                      {T}ranscriptional and {F}unctional {A}lterations in
                      {A}lzheimer's {D}isease.},
      journal      = {ASN NEURO},
      volume       = {17},
      number       = {1},
      issn         = {1759-0914},
      address      = {London},
      publisher    = {Sage Publishing},
      reportid     = {DZNE-2025-00627},
      pages        = {2506406},
      year         = {2025},
      abstract     = {Proliferation of microglia represents a physiological
                      process, which is accelerated in several neurodegenerative
                      disorders including Alzheimer disease (AD). The effect of
                      such neurodegeneration-associated microglial proliferation
                      on function and disease progression remains unclear. Here,
                      we show that proliferation results in profound alterations
                      of cellular function by providing evidence that newly
                      proliferated microglia show impaired beta-amyloid clearance
                      in vivo. Through sorting of proliferating microglia of
                      APP/PS1 mice and subsequent transcriptome analysis, we
                      define unique proliferation-associated transcriptomic
                      signatures that change with age and beta-amyloid
                      accumulation and are characterized by enrichment of immune
                      system-related pathways. Of note, we identify the DEAD-Box
                      Helicase 3 X-Linked (DDX3X) as a key molecule to modulate
                      microglia activation and cytokine secretion and it is
                      expressed in the AD brain. Together, these results argue for
                      a novel concept by which phenotypic and functional
                      microglial changes occur longitudinally as a response to
                      accelerated proliferation in a neurodegenerative
                      environment.},
      keywords     = {Animals / Microglia: metabolism / Microglia: pathology /
                      Microglia: physiology / Alzheimer Disease: pathology /
                      Alzheimer Disease: genetics / Alzheimer Disease: metabolism
                      / Cell Proliferation: physiology / Mice, Transgenic /
                      Amyloid beta-Protein Precursor: genetics / Amyloid
                      beta-Protein Precursor: metabolism / Mice / Presenilin-1:
                      genetics / Presenilin-1: metabolism / Disease Models, Animal
                      / Brain: pathology / Brain: metabolism / Amyloid
                      beta-Peptides: metabolism / DEAD-box RNA Helicases:
                      metabolism / DEAD-box RNA Helicases: genetics / Mice, Inbred
                      C57BL / Humans / Male / Alzheimer’s disease (Other) /
                      inflammasome (Other) / microglia (Other) / proliferation
                      (Other) / transcriptome (Other) / Amyloid beta-Protein
                      Precursor (NLM Chemicals) / Presenilin-1 (NLM Chemicals) /
                      Amyloid beta-Peptides (NLM Chemicals) / DEAD-box RNA
                      Helicases (NLM Chemicals)},
      cin          = {AG Heneka / Tech Transfer / AG Schultze / AG McManus / AG
                      Beyer},
      ddc          = {610},
      cid          = {I:(DE-2719)1011303 / I:(DE-2719)1030028 /
                      I:(DE-2719)1013038 / I:(DE-2719)1013042 /
                      I:(DE-2719)1013035},
      pnm          = {353 - Clinical and Health Care Research (POF4-353) / 354 -
                      Disease Prevention and Healthy Aging (POF4-354) / 352 -
                      Disease Mechanisms (POF4-352) / 351 - Brain Function
                      (POF4-351)},
      pid          = {G:(DE-HGF)POF4-353 / G:(DE-HGF)POF4-354 /
                      G:(DE-HGF)POF4-352 / G:(DE-HGF)POF4-351},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:40387894},
      doi          = {10.1080/17590914.2025.2506406},
      url          = {https://pub.dzne.de/record/278791},
}