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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.

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

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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