The immune system hypothesis for synesthesia

[This post is also cross-posted at our Psychology Today blog]

Synesthesia is a condition in which attributes, such as color, shape, sound, smell and taste, bind together in unusual ways, giving rise to atypical experiences, mental images or thoughts. For example, a synesthete may experience numbers and letters printed in black as having their own unique colors or spoken words as having specific tastes normally only associated with food and drinks. People who have the condition usually have had since early childhood, though there are also cases in which people acquire it after brain injury or disease later in life.

One hypothesis about how synesthesia develops in early childhood suggests that somtimes the brain fails to get rid of structural connections between neural regions that do not normally project to each other. In early childhood the brain develops many more neural connections than it ends up using. During development, pruning processes eliminate a large number of these structural connections. We don't know much about the principles underlying neural pruning, though some of the connections that the brain prunes away appear to be pathways that are not needed. So, one possibility is that the pruning processes in synesthetes are less effective compared to those in non-synesthetes, and that some pathways that are pruned away in most people remain active in synesthetes.

If this hypothesis is correct for at least some forms of synesthesia, then the question arises what causes the deviations in pruning processes in some individuals. In an interesting new paper recently published in Frontiers in Neuroscience neuropsychologists Duncan A Carmichael and Julia Simner from University of Edinburgh suggest that developmental synesthesia may be linked to abnormalities in genes coding for proteins crucial to the immune system.

In support of this hypothesis they list evidence showing that many genes have a dual function, expressing proteins involved in forming structural connections in the brain and maintaining the body's immune system. While we used to think that the immune system was functionally isolated from the central nervous system, it has later become clear that immune-system processes play an important role in brain development, particularly in early childhood where the greatest number of neurons and new neural pathways are formed and during adolescence where the most extensive pruning of the brain takes place.

Though there is only a limited number of genetic studies of synesthesia, the studies completed so far provide some evidence for the immune hypothesis. Two studies of families with synesthesia have located regions on the genome that appear to implicated in synesthesia (here and here). These regions also contain genes that code for proteins crucial to immune function.

Further evidence for a possible connection between synesthesia and the immune system comes from the co-morbidity of synesthesia and immune system defects. The authors report on some preliminary data suggesting that there may be a higher incidence of synesthesia among people with autoimmune diseases, such as multiple sclerosis. Several researchers have also suggested that there may be a higher incidence of synesthesia among individuals with autism, a condition that has been linked to both immune system defects and atypical structural brain connectivity.

Finally, the authors point out that there could be a connection between the immune system and synesthesia acquired after brain injury and disease, as injuries to the brain lead to cell death and heightened immune responses.

Synesthesia has on many occasions been linked to improved memory and enhanced cognitive and creative function. So, one lesson of this exciting new hypothesis is that the very same processes that can lead to disadvantageous deficits in bodily function may have numerous advantages in terms of cognitive function.