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REPRODAMH SIGNED

Extra-gonadal roles of Anti-Müllerian Hormone in the aetiology of polycystic ovary syndrome: the domino effect to reproductive neuroendocrine dysfunctions

Total Cost €

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EC-Contrib. €

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Partnership

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 REPRODAMH project word cloud

Explore the words cloud of the REPRODAMH project. It provides you a very rough idea of what is the project "REPRODAMH" about.

infertility    anti    acts    phenotype    functional    elevated    elusive    gonadal    excess    hypothesis    morbidities    frequent    diagnosis    disturbances    androgen    models    pathology    goals    levels    rescues    mullerian    lh    nervous    leads    polycystic    animal    alterations    hyperactivation    amh    showed    neuroendocrine    syndrome    dependent    reprodamh    secreting    oligo    ovarian    neuronal    human    modifications    central    women    integrative    dysfunctions    neurons    female    pathophysiology    metabolic    abnormal    biosynthesis    reproductive    intriguing    gnrh    developmental    vivo    postnatal    release    reproduction    releasing    gonadotropin    plasticity    interactions    patients    mouse    anovulation    inferred    neuropeptide    endocrine    combined    clinical    deficient    pulse    mainly    fertility    disorders    hypothalamic    final    regulation    secretion    frequency    form    indicating    relevance    regulations    10    luteinizing    mammals    inhibition    pcos    mechanistic    structural    prevalence    hormone    strategies    preclinical    investigations    therapeutic    ovary    humans    accelerated   

Project "REPRODAMH" data sheet

The following table provides information about the project.

Coordinator
INSTITUT NATIONAL DE LA SANTE ET DE LA RECHERCHE MEDICALE 

Organization address
address: RUE DE TOLBIAC 101
city: PARIS
postcode: 75654
website: www.inserm.fr

contact info
title: n.a.
name: n.a.
surname: n.a.
function: n.a.
email: n.a.
telephone: n.a.
fax: n.a.

 Coordinator Country France [FR]
 Total cost 1˙999˙740 €
 EC max contribution 1˙999˙740 € (100%)
 Programme 1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
 Code Call ERC-2016-COG
 Funding Scheme ERC-COG
 Starting year 2017
 Duration (year-month-day) from 2017-05-01   to  2022-04-30

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    INSTITUT NATIONAL DE LA SANTE ET DE LA RECHERCHE MEDICALE FR (PARIS) coordinator 1˙999˙740.00

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 Project objective

Reproduction in mammals is dependent on specific neurons secreting the Gonadotropin Hormone-Releasing Hormone (GnRH). Many reproductive disorders in humans are associated with abnormal or deficient GnRH secretion. Among reproductive dysfunctions, polycystic ovary syndrome (PCOS) is the most common form of female infertility with a prevalence of up to 10%, characterized by increased ovarian androgen biosynthesis, oligo-anovulation and frequent metabolic morbidities. Because women with PCOS have increased luteinizing hormone (LH) pulse frequency, it has been inferred that the pulse frequency of GnRH must be accelerated as well. However, so far PCOS has been considered mainly as a gonadal pathology and possible regulations from the central nervous system or interactions with it remain elusive. In patients with PCOS, ovarian levels of Anti-Mullerian Hormone (AMH) are also elevated, indicating the potential relevance of AMH for PCOS diagnosis and management. Recently, we showed that AMH acts directly on GnRH neurons to increase neuropeptide secretion, raising the intriguing hypothesis that AMH-dependent regulation of GnRH release could be involved in the neuroendocrine control of fertility and pathophysiology of PCOS. By providing integrative, functional and mechanistic in vivo strategies, combined with clinical human investigations, REPRODAMH will represent a major step forward into the understanding of PCOS with the final goal of developing new therapeutic strategies. To achieve these goals we will: 1: Determine whether developmental or postnatal AMH excess leads to PCOS endocrine disturbances by hyperactivation of GnRH neurons. 2: Study whether inhibition of GnRH neuronal activity rescues the neuroendocrine reproductive phenotype in PCOS-mouse models. 3: Study whether modifications of the hypothalamic structural plasticity occur in PCOS and contribute to alterations of GnRH release. 4: Design and test new preclinical therapeutic strategies in PCOS animal models.

 Publications

year authors and title journal last update
List of publications.
2019 Samuel Andrew Malone, Georgios E Papadakis, Andrea Messina, Nour El Houda Mimouni, Sara Trova, Monica Imbernon, Cecile Allet, Irene Cimino, James Acierno, Daniele Cassatella, Cheng Xu, Richard Quinton, Gabor Szinnai, Pascal Pigny, Lur Alonso-Cotchico, Laura Masgrau, Jean-Didier Maréchal, Vincent Prevot, Nelly Pitteloud, Paolo Giacobini
Defective AMH signaling disrupts GnRH neuron development and function and contributes to hypogonadotropic hypogonadism
published pages: , ISSN: 2050-084X, DOI: 10.7554/elife.47198
eLife 8 2019-11-13
2018 Vincent Prevot, Bénédicte Dehouck, Ariane Sharif, Philippe Ciofi, Paolo Giacobini, Jerome Clasadonte
The Versatile Tanycyte: A Hypothalamic Integrator of Reproduction and Energy Metabolism
published pages: 333-368, ISSN: 0163-769X, DOI: 10.1210/er.2017-00235
Endocrine Reviews 39/3 2019-11-13
2019 Anne-Laure Barbotin, Maëliss Peigné, Samuel Andrew Malone, Paolo Giacobini
Emerging Roles of Anti-Müllerian Hormone in Hypothalamic-Pituitary Function
published pages: 218-229, ISSN: 0028-3835, DOI: 10.1159/000500689
Neuroendocrinology 109/3 2019-11-13
2018 Brooke Tata, Nour El Houda Mimouni, Anne-Laure Barbotin, Samuel A. Malone, Anne Loyens, Pascal Pigny, Didier Dewailly, Sophie Catteau-Jonard, Inger Sundström-Poromaa, Terhi T. Piltonen, Federica Dal Bello, Claudio Medana, Vincent Prevot, Jerome Clasadonte, Paolo Giacobini
Elevated prenatal anti-Müllerian hormone reprograms the fetus and induces polycystic ovary syndrome in adulthood
published pages: 834-846, ISSN: 1078-8956, DOI: 10.1038/s41591-018-0035-5
Nature Medicine 24/6 2019-05-29

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