Hippocampal Myo-inositol and Cognitive Ability in Adults With Down Syndrome

Arch Gen Psych brings us some hope-inspiring news about Down Syndrome.  They report on a finding of a correlation between myo-inositol levels in the brain, and the severity of cognitive impairment in patients with DS.  There appears to be a strong correlation: the higher the level of myo-inositol, the worse the impairment.  There is a understandable interpretation of the study in a BBC News story here.  There is a somewhat understandable explainer about myo-inositol at the PDR Health website, here.  

Of course, the usual caveats apply: this is a basic science study that is a long way from clinical application.  However, it is a finding that occurs in the context of a large body of knowledge about myo-inositol, the role of myo-inositol in the brain, and various ways of influencing the amount of the substance floating around up there.  For example, it is known that brain cells clear out proteins that are prone to aggregation, via a process known as autophagy.  This process is regulated, in part, by an enzyme that controls the metabolism of myo-inositol.  Note that there are reasons to believe that excessive aggregation of certain proteins is known to be a factor in several neurodegenerative diseases, such as Alzheimer disease.  We know that some of the changes in the brains of persons with DS are similar to those seen in AD.  So finding out that there is a link between the regulation of the level of myo-inositol and the degree of cognitive impairment in DS is entirely consistent with what already was known about the neurobiology of DS.  It helps provide some direction for further research into treatment for the disorder.  The challenge is going to be this: since the degenerative changes occur over a very long time scale, it is going to take a long time to demonstrate the effectiveness of any intervention intended to halt the progression.  Also, since persons with DS develop impairment early in life, it will be a challenge to figure out what interventions to begin and when in life they should be started.  

If I were asked to anticipate the potential clinical significance of this, I would say the benefits could be important, albeit modest.  If we can find an effective way to slow the neurodegenerative changes of DS, it will result in greater quality of life for patients and caregivers, and probably will prolong life.  Unfortunately, it is only a microscopic step toward an eventual cure.