This is one of the main and most surprising conclusions to be drawn from a study led by Dr Miquel Bosch, researcher from the Department of Basic Sciences and lecturer on the Bachelor’s Degree in Biomedical Sciences, which he carried out when working at the Picower Institute for Learning and Memory at MIT
It has been revealed that learning, memory and behavioural disorders may occur if the connection between neurons (known as synapsis) does not suitably change in response to a given situation. Until now, studies have demonstrated that functional and structural changes to neuronal connections were closely associated. However, Dr Bosch and his team, including Dr Bear from MIT, have discovered that synapses could weaken their electrical connection without altering their shape. This happens during a process called synaptic plasticity, which is closely related to neurodevelopmental disorders such as autism. This new finding has biomedical implications and will help scientists better understand the molecular mechanisms behind these types of brain disorders.
As stated by Dr Miquel Bosch, one of the project’s principal investigators and lecturer on the Bachelor’s Degree in Biomedical Sciences, “the majority of the results obtained in this study were really surprising. Our initial hypotheses were contradicted by the results of our experiments, therefore calling into question some of the dogmas accepted by the scientific community thus far. We believe they could open up new avenues of research for treating diseases and disorders such as the autism spectrum”.
The study, which was published recently in the journal
Molecular Psychiatry, also reveals how the plasticity mechanisms linked to another type of receptor is completely different from what is was previously believed to be. “We have been able to prove this by comparing normal mice with transgenic mice that develop fragile X syndrome, the most common hereditary form of autism”, Bosch explained. “In these latter mice, the mechanism of synaptic weakening undergoes an alteration that was unknown until now. These are unexpected results that, when combined with up-to-date knowledge on the subject, allows us to develop a broad model that could explain many neuronal alterations observed in autism spectrum disorders, and therefore optimise the search for pharmacological treatment".
