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@ARTICLE{GmezPascual:285354,
      author       = {Gómez-Pascual, Alicia and Glikman, Dow M and Ng, Hui Xin
                      and Tomkins, James E and Lu, Lu and Xu, Ying and Ashbrook,
                      David G and Kaczorowski, Catherine and Kempermann, Gerd and
                      Killmar, John and Mozhui, Khyobeni and Ohlenschläger,
                      Oliver and Aebersold, Rudolf and Ingram, Donald K and
                      Williams, Evan G and Jucker, Mathias and Overall, Rupert W
                      and Williams, Robert W and de Bakker, Dennis E M},
      title        = {{T}he {S}marcal1-{U}sp37 locus modulates glycogen
                      aggregation in astrocytes of the aged hippocampus.},
      journal      = {Cell systems},
      volume       = {17},
      number       = {2},
      issn         = {2405-4712},
      address      = {Maryland Heights, MO},
      publisher    = {Elsevier},
      reportid     = {DZNE-2026-00220},
      pages        = {101488},
      year         = {2026},
      abstract     = {In aged humans and mice, hypobranched glycogen aggregates,
                      known as polyglucosan bodies (PGBs), accumulate in
                      hippocampal astrocytes. While PGBs are linked to cognitive
                      decline in neurological diseases, they remain largely
                      unstudied in the context of typical aging. We show that PGBs
                      arise in autophagy-dysregulated astrocytes in the aged
                      hippocampus, with substantial variation among 32 inbred BXD
                      mouse strains. Genetic mapping through quantitative trait
                      locus analysis identified a major locus (Pgb1) that
                      modulates hippocampal PGB burden. Extensive transcriptomic
                      and proteomic datasets were produced for the aged
                      hippocampus of the BXD family to investigate the mechanism
                      by which the Pgb1 locus modulates PGB burden. We identified
                      that Pgb1 contains allelic Smarcal1 and Usp37 variants and
                      influences PGB burden through trans-regulation of mRNA and
                      protein expression levels, including abundance of
                      glycogen-mobilizing factor PYGB. Furthermore, comprehensive
                      phenome-wide association scans, transcriptomic analyses, and
                      direct behavioral testing demonstrated that cognition
                      remains intact despite age-related PGB burden. A record of
                      this paper's transparent peer review process is included in
                      the supplemental information.},
      keywords     = {Animals / Hippocampus: metabolism / Glycogen: metabolism /
                      Mice / Astrocytes: metabolism / Aging: genetics / Aging:
                      metabolism / Male / Quantitative Trait Loci: genetics /
                      Mice, Inbred C57BL / Humans / Glucans / astrocytes (Other) /
                      brain aging (Other) / glycogen metabolism (Other) /
                      hippocampus (Other) / polyglucosan bodies (Other) /
                      quantitative trait locus analysis (Other) / system genetics
                      (Other) / Glycogen (NLM Chemicals) / polyglucosan (NLM
                      Chemicals) / Glucans (NLM Chemicals)},
      cin          = {AG Jucker / AG Kempermann},
      ddc          = {570},
      cid          = {I:(DE-2719)1210001 / I:(DE-2719)1710001},
      pnm          = {352 - Disease Mechanisms (POF4-352)},
      pid          = {G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:41633365},
      doi          = {10.1016/j.cels.2025.101488},
      url          = {https://pub.dzne.de/record/285354},
}