% 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{Guillot:276320,
      author       = {Guillot, Simon J and Lang, Christina and Simonot, Marie and
                      Beckett, Daniel and Lulé, Dorothée and Balz, Luisa T and
                      Knehr, Antje and Stuart-Lopez, Geoffrey and Vercruysse,
                      Pauline and Dieterlé, Stéphane and Weydt, Patrick and
                      Dorst, Johannes and Kandler, Katharina and Kassubek, Jan and
                      Wassermann, Laura and Rouaux, Caroline and Arthaud,
                      Sébastien and Da Cruz, Sandrine and Luppi, Pierre-Hervé
                      and Roselli, Francesco and Ludolph, Albert C and Dupuis, Luc
                      and Bolborea, Matei},
      title        = {{E}arly-onset sleep alterations found in patients with
                      amyotrophic lateral sclerosis are ameliorated by orexin
                      antagonist in mouse models.},
      journal      = {Science translational medicine},
      volume       = {17},
      number       = {783},
      issn         = {1946-6234},
      address      = {Washington, DC},
      publisher    = {AAAS},
      reportid     = {DZNE-2025-00283},
      pages        = {eadm7580},
      year         = {2025},
      abstract     = {Sleep alterations have been described in several
                      neurodegenerative diseases yet are currently poorly
                      characterized in amyotrophic lateral sclerosis (ALS). This
                      study investigates sleep macroarchitecture and related
                      hypothalamic signaling disruptions in ALS. Using
                      polysomnography, we found that both patients with ALS as
                      well as asymptomatic C9ORF72 and SOD1 mutation carriers
                      exhibited increased wakefulness and reduced non-rapid eye
                      movement sleep. Increased wakefulness correlated with
                      diminished cognitive performance in both clinical cohorts.
                      Similar changes in sleep macroarchitecture were observed in
                      three ALS mouse models (Sod1G86R, FusΔNLS/+, and
                      TDP43Q331K). A single oral administration of a dual-orexin
                      receptor antagonist or intracerebroventricular delivery of
                      melanin-concentrating hormone (MCH) through an osmotic pump
                      over 15 days partially normalized sleep patterns in mouse
                      models. MCH treatment did not extend the survival of
                      Sod1G86R mice but did decrease the loss of lumbar motor
                      neurons. These findings suggest MCH and orexin signaling as
                      potential targets to treat sleep alterations that arise in
                      early stages of the disease.},
      keywords     = {Animals / Amyotrophic Lateral Sclerosis: drug therapy /
                      Amyotrophic Lateral Sclerosis: pathology / Amyotrophic
                      Lateral Sclerosis: metabolism / Orexins: metabolism /
                      Disease Models, Animal / Humans / Sleep: drug effects / Male
                      / Melanins: metabolism / Mice / Wakefulness: drug effects /
                      Female / Motor Neurons: drug effects / Motor Neurons:
                      pathology / Motor Neurons: metabolism / Hypothalamic
                      Hormones: metabolism / Pituitary Hormones: metabolism /
                      Orexin Receptors: metabolism / Superoxide Dismutase-1:
                      metabolism / Superoxide Dismutase-1: genetics / Mice,
                      Transgenic / Orexins (NLM Chemicals) / Melanins (NLM
                      Chemicals) / melanin-concentrating hormone (NLM Chemicals) /
                      Hypothalamic Hormones (NLM Chemicals) / Pituitary Hormones
                      (NLM Chemicals) / Orexin Receptors (NLM Chemicals) /
                      Superoxide Dismutase-1 (NLM Chemicals)},
      cin          = {Clinical Study Center (Ulm) / AG Roselli},
      ddc          = {500},
      cid          = {I:(DE-2719)5000077 / I:(DE-2719)1910001},
      pnm          = {353 - Clinical and Health Care Research (POF4-353) / 352 -
                      Disease Mechanisms (POF4-352)},
      pid          = {G:(DE-HGF)POF4-353 / G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:39879320},
      doi          = {10.1126/scitranslmed.adm7580},
      url          = {https://pub.dzne.de/record/276320},
}