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HOW YOUR DONATION WILL HELP

Your donation will be used for research projects to better understand PFS mechanism and find a cure

OUR COMMITMENTS TO YOU

We are committed to responsible and transparent communication with our donors. In our various publications we actively inform them about our principles, our role, our tasks, our intervention methods and the use of their donations. We strive to inform them of the reasons for our decisions, the results of our actions and the challenges associated with our work as a medical-humanitarian organization.

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Ongoing project

Targeting androgen signalling for mitochondria protection in PFS

George Barreto, University of Limerick, Ireland

Status: active fundraising

George Barreto is a neuroscientist at the University of Limerick, Ireland. His research focus is the investigation of how sexual hormone deprivation affects the brain – especially the mitochondria.  
After completing his Ph.D. in neuroscience George Barreto spent his post-doc training at the  Stanford University School of Medicine. He is a lecturer in Cell Biology/Immunology and serves as editor of several impactful scientific journals. George Barreto is involved in drug development and has co-authored publications together with the PFS lead researchers Roberto Melcangi. 

Description of the project:

The androgen receptor (AR) has a mitochondrial localization sequence that, once bound to androgen, is internalised to this organelle, and regulates a great variety of functions ranging from cellular metabolism to oxidative phosphorylation by promoting the transcription of mitochondrial proteins related to respiratory complexes. Any interference on the way androgens effect mitochondria may provoke devastating consequences on how this organelle processes energy substrates for ATP production. Considering these non-genomic actions of AR over mitochondria and the fact that PFS is characterized by an alteration of androgen metabolism, this likely affects mitochondria causing their dysfunction which may lead to apoptosis, dampened fatty acid metabolism and oxidative phosphorylation, augmented reactive oxidative stress (ROS), and, ultimately, promoting a pro-inflammatory environment that may endanger brain cells.