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@ARTICLE{ScekicZahirovic:285456,
      author       = {Scekic-Zahirovic, Jelena and Antonucci, Stefano and
                      Wiesner, Diana and Ebner, Chiara and El Hajj, Hussein and
                      Aousji, Oumayma and Halablab, Kareen and Fan, Yiting and
                      Zelaya, Anneka and Yartas, Gizem and Baskar, Karthik and
                      Çakmak, E. Anastasia and Bayer, David and Sung, Hoon-Ki and
                      Dupuis, Luc and Park, Jeehye and Roselli, Francesco},
      title        = {{L}arge-scale mapping of the {MCH} network in {ALS} mice
                      reveals the vulnerability of dopaminergic and {GABA}ergic
                      neurons in zona incerta},
      journal      = {Acta Neuropathologica Communications},
      volume       = {14},
      number       = {1},
      issn         = {2051-5960},
      address      = {London},
      publisher    = {Biomed Central},
      reportid     = {DZNE-2026-00238},
      pages        = {46},
      year         = {2026},
      abstract     = {Weight loss and hypermetabolism are early and
                      prognostically significant features of amyotrophic lateral
                      sclerosis (ALS) and are associated with hypothalamic atrophy
                      and degeneration of melanin-concentrating hormone (MCH)
                      neurons that regulate energy balance. To investigate whether
                      MCH vulnerability arises from upstream network dysfunction,
                      we performed whole-brain retrograde rabies tracing in
                      SOD1G93A mice. We identified an early, selective loss of
                      monosynaptic inputs from the zona incerta (ZI), a
                      dopaminergic (DA)/gamma-aminobutyric acid (GABA)ergic
                      nucleus that preceded MCH neuron degeneration. Neurochemical
                      profiling confirmed the DA/GABAergic identity of these ZI
                      input neurons, and ZI/DAergic neurons later degenerated.
                      ALS-related pathology emerged early in the ZI, paralleling
                      pathology in the motor cortex, while anterograde mapping
                      revealed that motor cortical projections preferentially
                      targeted the ZI, linking vulnerable motor and metabolic
                      networks. Loss of ZI/DAergic neurons was observed in
                      conjunction with weight loss in non-SOD1 ALS models. These
                      findings identify the ZI as an early-affected node within
                      hypothalamic networks and suggest that disruption of
                      DA/GABAergic inputs to MCH neurons is associated with
                      subsequent MCH and DA neuronal vulnerability, degeneration
                      and metabolic imbalance in ALS.The online version contains
                      supplementary material available at
                      10.1186/s40478-026-02231-z.},
      keywords     = {Amyotrophic lateral sclerosis (Other) / Dopaminergic
                      neurons (Other) / Melanin-concentrating hormone neurons
                      (Other) / Monosynaptic rabies tracing (Other) / Weight loss
                      (Other) / Zona incerta (Other)},
      cin          = {AG Roselli},
      ddc          = {610},
      cid          = {I:(DE-2719)1910001},
      pnm          = {352 - Disease Mechanisms (POF4-352)},
      pid          = {G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)16},
      doi          = {10.1186/s40478-026-02231-z},
      url          = {https://pub.dzne.de/record/285456},
}