First experimental study to propose a therapy to correct memory deficit caused by disorders in the fetal alcohol spectrum

A research team of the Department of Medicine and Life Sciences (MELIS) at Pompeu Fabra University (UPF) involving the Hospital del Mar Research Institute has for the first time, in mice, identified and validated the neurobiological mechanism and therapy to correct memory deficit in individuals with fetal alcohol spectrum disorders (FASD). These results pave the way for studying whether the mechanism is the same in humans, which would enable improving the diagnosis and treatment of affected individuals.

Fetal Alcohol Spectrum Disorder (FASD) includes a number of conditions suffered by infants who have been exposed to alcohol during pregnancy. The effects of FASD range from craniofacial morphological malformations or growth problems, in the most severe cases, to hyperactivity, emotional and motivational difficulties or defects in learning and memory, in the mildest cases.

“In children of normal appearance, FASD is underdiagnosed and is often mistaken for hyperactivity or ADD”, explains Rafael de la Torre, coordinator of the Integrated Pharmacology and Systems Neuroscience Research Group at the Hospital del Mar Research Institute. “Since there is no diagnosis, there is no treatment, and symptomatic therapy is given to alleviate hyperactivity or other disorders such as anxiety”.

The results of the study published in the journal Molecular Psychiatry, have allowed the researchers to observe that “exposure to alcohol need not be chronic for FASD to occur. Sporadic consumption ending in intoxication - getting drunk- is enough to observe alterations in memory, in mice”, explains Olga Valverde, study coordinator and director of the Research Group in Behavioural Neurobiology at the MELIS-UPF.

The study shows that mice born to mothers that have consumed alcohol sporadically during pregnancy and lactation have a memory deficit that persists into adulthood. One of the reasons for this deficit is that alcohol affects the function of the endocannabinoid system, reducing the expression of the PPAR-