Unraveling the mystery of cognitive inflexibility in Fragile X Syndromes
The latest finding in understanding how mice with genetic defects perceive information has led to a path-breaking discovery into the mysterious cognitive inflexibility among individuals. The genetically defective mice with induced Fragile X Syndromes (FXS) were seen to learn and remember normally.
However, when it comes to perceiving something new that contradicted their earlier learning, the mice were unable to do so.
This study was led by a research team including a group of renowned neuroscientists. Fragile X syndrome is commonly a cause of autism and intellectual disability.
Andre Fenton, professor and senior author of the citation says, “The findings suggest that neurological circuits, although fundamentally intact, could be improperly tuned which in turn results in inflexible learning’s.”
The professor further comments, “With tireless studies and subsequent findings, we are now in a better position to understand the cognitive deficits that result in the inability to correctly process the gained insights.”
Dino Dvorak, a post-doctorate, has also been honored with co-authoring the study. Dvorak has a particular focus on the hippocampus, a part of the brain that is critical to memory and requires encoding and remembering processed information.
Since the same neurons are involved in remembering and encoding, it is unknown what underlying neurological events control the hippocampus neurons which are crucial in accurate recollection of information from the individual’s memory. The team highlights this information being crucial in understanding the dynamics of FXS which is seen to impair effective memory in multiple ways.
To gain deeper insights, the team first uncovered electrophysiological signatures of recollections in the hippocampus region. This mapping was important in pinpointing whether the present neurons are encoding the memory or recollecting information already present in the memory.
The result highlighted two critical points, particularly that the recollection and encoding behind the memory being observed was a tug of war between two rhythmic activities engulfing the hippocampus. Further, the encoding was seen to occur when fast rhythmic activities overwhelmed slower rhythmic activity while recollection was seen to occur when slower rhythms engulfed the medium rhythms.
The team emphasizes that FXS hippocampus neurons can be normal and mice induced with fragile x syndromes can remember as well as learn in similar ways to their other peers. Due to the excessive dominance observed in the slower rhythm mice, these mice were seen to lag in learning and grasping new information when it contradicted their initial learnings. In other words, neutrality in the tug of war was seen to take dominance and more often than not, was won by slower rhythms, preventing the adaptive functionality of the cognitive function.
Fenton concludes, “These cognitive behavioral inflexibilities are an underlying characteristic of autism and FXS and can be explained by the recollection of excessive information that could be previously correct but is presently incorrect information that is stored in the hippocampus region.”