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Endocrine Abstracts (2023) 94 P371 | DOI: 10.1530/endoabs.94.P371

1Univ. Lille, Inserm, CHU Lille, Lille Neuroscience & Cognition, UMR-S 1172, FHU 1000 days for health, EGID, Lille, France. 2Univ. Lille, Inserm, CHU Lille, Lille Neuroscience & Cognition, UMR-S 1172, FHU 1000 days for health, EGID, Lille, France. 3Imperial College London, London, United Kingdom. 4CHU Lille, Department of Pathology, Centre Biologie Pathologie, Lille, France. 5CIMUS, Universidade de Santiago de Compostela, Santiago, Spain. 6Institute for Experimental and Clinical Pharmacology and Toxicology, University of Lübeck, Lübeck, Germany. 7CHU Lille, Department of Neurology, Memory Centre, Reference Centre for Early-Onset Alzheimer Disease and Related Disorders, Lille, France. 8CIC bioGUNE, Basque Research and Technology Alliance (BRTACentro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBERehd), Instituto de Salud Carlos III, Madrid, Spain. 48160 Derio, Bizkaia Technology Park, Building 801A, Bizkaia, Spain. 9Laboratory of Reproductive Neurobiology, Institute of Experimental Medicine, Budapest, Hungary. 10Univ. Lille, Inserm, CHU Lille, Service de Médecine Intensive Réanimation, U1190, EGID, F-59000, Lille, France. 11Univ. Lille, Inserm, CHU Lille, centre d’investigation clinique (CIC) 1403, F-59000, Lille, France. 12LICORNE study group, CHU Lille, Lille, France. 13Department of Experimental and Clinical Medicine, University of Florence, Florence, Italy. 14CHU Lille, Department of Neonatology, Hôpital Jeanne de Flandre, FHU 1000 days for health, F-59000, Lille, France. 15Univ. Lille, CNRS, Inserm, CHU Lille, Institut Pasteur de Lille, U1019 - UMR 9017 - CIIL - Center for Infection and Immunity of Lille, F-59000, Lille, France. 16CHU Lille, Service de Biochimie et Hormonologie, Centre de Biologie Pathologie, Lille, France. 17Univ. Lille, Inserm U1285, CHU Lille, Pôle de réanimation, CNRS, UMR 8576 - UGSF - Unite de Glycobiologie Structurale et Fonctionnelle, F-59000, Lille, France


Loss of gonadotropin-releasing hormone (GnRH) and cognitive deficits have recently been demonstrated by our group in conditions including Down syndrome and Alzhiemer’s disease. In some patients with COVID-19, olfactory and cognitive alterations persist, and persistent hypotestosteronemia in SARS-CoV-2-infected men could be a consequence of deficient GnRH. To understand whether neuroinvasion of GnRH system by SARS-CoV-2 could explain some post-COVID symptoms and thus result in accelerated or exacerbated cognitive decline, we assessed the hormonal profile of patients with COVID-19 and targets of SARS-CoV-2 infection in post-mortem brains and human fetal tissue. Our data demonstrates that persistent hypotestosteronemia in men could result from hypothalamic disruption, favouring post-COVID neurological or cognitive symptoms, and that change in body weight and testosterone levels were inversely correlated. Infection of multifunctional glia, called tanycytes, and olfactory sensory neurons, highlighted at least two viable neuroinvasion routes. Moreover, in all patient brains studied, GnRH neurons themselves were dying, resulting in reduction of GnRH expression. Human fetal GnRH neurons, as well as the fetal olfactory and vomeronasal epithelia from which GnRH neurons arise, appeared susceptible to infection. Thus, putative GnRH neuron and tanycyte dysfunction following SARS-CoV-2 neuronivasion could be responsible for resulting reproductive, metabolic and cognitive health consequences in long-COVID and could result in an increased risk of neurodevelopmental and neurodegenerative pathologies over time in all patients.

Volume 94

Society for Endocrinology BES 2023

Glasgow, UK
13 Nov 2023 - 15 Nov 2023

Society for Endocrinology 

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