% 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{North:165283,
      author       = {North, Hayley F and Weissleder, Christin and Fullerton,
                      Janice M and Webster, Maree J and Weickert, Cynthia Shannon},
      title        = {{I}ncreased immune cell and altered microglia and
                      neurogenesis transcripts in an {A}ustralian schizophrenia
                      subgroup with elevated inflammation.},
      journal      = {Schizophrenia research},
      volume       = {248},
      issn         = {0920-9964},
      address      = {Amsterdam [u.a.]},
      publisher    = {Elsevier Science},
      reportid     = {DZNE-2022-01576},
      pages        = {208 - 218},
      year         = {2022},
      abstract     = {We previously identified a subgroup of schizophrenia cases
                      (~40 $\%)$ with heightened inflammation in the neurogenic
                      subependymal zone (SEZ) (North et al., 2021b). This
                      schizophrenia subgroup had changes indicating reduced
                      microglial activity, increased peripheral immune cells,
                      increased stem cell dormancy/quiescence and reduced neuronal
                      precursor cells. The present follow-up study aimed to
                      replicate and extend those novel findings in an independent
                      post-mortem cohort of schizophrenia cases and controls from
                      Australia. RNA was extracted from SEZ tissue from 20
                      controls and 22 schizophrenia cases from the New South Wales
                      Brain Tissue Resource Centre, and gene expression analysis
                      was performed. Cluster analysis of inflammation markers
                      (IL1B, IL1R1, SERPINA3 and CXCL8) revealed a
                      high-inflammation schizophrenia subgroup comprising 52 $\%$
                      of cases, which was a significantly greater proportion than
                      the 17 $\%$ of high-inflammation controls. Consistent with
                      our previous report (North et al., 2021b), those with
                      high-inflammation and schizophrenia had unchanged mRNA
                      expression of markers for steady-state and activated
                      microglia (IBA1, HEXB, CD68), decreased expression of
                      phagocytic microglia markers (P2RY12, P2RY13), but increased
                      expression of markers for macrophages (CD163), monocytes
                      (CD14), natural killer cells (FCGR3A), and the adhesion
                      molecule ICAM1. Similarly, the high-inflammation
                      schizophrenia subgroup emulated increased quiescent stem
                      cell marker (GFAPD) and decreased neuronal progenitor
                      (DLX6-AS1) and immature neuron marker (DCX) mRNA expression;
                      but also revealed a novel increase in a marker of immature
                      astrocytes (VIM). Replicating primary results in an
                      independent cohort demonstrates that inflammatory subgroups
                      in the SEZ in schizophrenia are reliable, robust and enhance
                      understanding of neuropathological heterogeneity when
                      studying schizophrenia.},
      keywords     = {Humans / Microglia: metabolism / Schizophrenia: genetics /
                      Schizophrenia: metabolism / Follow-Up Studies / Australia /
                      Neurogenesis: physiology / Inflammation: metabolism / RNA,
                      Messenger: metabolism / RNA / Glia (Other) / Macrophages
                      (Other) / Post-mortem (Other) / Psychosis (Other) / Subtype
                      (Other) / Subventricular zone (Other)},
      cin          = {AG Deleidi},
      ddc          = {610},
      cid          = {I:(DE-2719)1210011},
      pnm          = {352 - Disease Mechanisms (POF4-352)},
      pid          = {G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:36108465},
      doi          = {10.1016/j.schres.2022.08.025},
      url          = {https://pub.dzne.de/record/165283},
}