Infertility affects between 7% and 12% of couples worldwide. The causes of male infertility include several defects of the sperm including asthenozoospermia. This is a deficiency in the motility of spermatozoa, an essential ingredient for an encounter between the sexual cells during reproduction. Asthenozoospermia, detected in more than 40% of infertile men, is often associated with low sperm production during male ejaculation and morphological anomalies (which are known as oligoasthenoteratozoospermia ).
The research group headed by Dr Aminata Touré of the Inserm team 1016 “Genomics, epigenetis and physiopathology of reproduction” of the Cochin Institute (INSERM / CNRS / Université Paris Descartes) studied the genetic component of this condition, one about which little is known despite the strong prevalence associated therewith.
In this study published in The American Journal of Human Genetics, the researchers showed that for several subjects, in an initial cohort of 146 patients presenting with asthenozoospermia, there were deleterious mutations of the SLC26A8 gene.
This gene code is for a transporter exclusively expressed in the spermatozoa. The mutations identified produce functional alterations in the transporter involved in the regulation of the interaction between spermatozoa and the external environment. A change in such interaction prevents the spermatozoa from moving correctly towards the ovule in the female genital tract. Very few genes have so far been identified that are capable of playing a decisive role in sperm mobility and its activation.
“Our work opens up the prospect of better knowledge of the genetic causes of human asthenozoospermia”, explains Aminata Touré, head of research and manager of the study. “This will eventually make it possible to offer genetic counselling for couples seeking help with infertility and wanting to have children through Medically Assisted Procreation (MAP) techniques,” she concluded.
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