Huntingtin protein and cephalization: a dialectic

The 3/7/15  Economist has an interesting article entitled ‘A Faustian bargain’ about some research into Huntington’s disease and a protein implicated in its pathogenesis, huntingtin.  A fair amount of hard science has been done here to find that the gene that produces huntingtin includes a string where an amino acid, glutamate, is repeated several times.  The number of repetitions in humans varies widely.  If glutamate repeats 35 times or less, the person will not suffer from Huntington’s, is at risk with repetitions from 36 to 40, and greater than 40, they will develop this disease.  Some other findings are interesting.  First, the protein huntingtin has been found to increase the number of neurons in the embryological development of the brain; children tend to have more repeats than their parents (remembering that if it goes too far, they will suffer the disease).

More huntingtin protein than its parents and so more neurons, but too much and the child is at risk for Huntington's disease.

More huntingtin protein than its parents and so more neurons, but too much and the child is at risk for Huntington’s disease.

Cross species research has shown that the larger the CNS is, the more repeats.  Sea urchins with a vary simple nervous system have 2 repeats, zebrafish 4, mice 7, dogs 10, and rhesus monkeys around 15.  These results have led some researchers to speculate about a ‘Faustian bargain’.  The more repeats up to a point, the bigger the brain, but go too far and Huntington’s disease comes on to damage your ability to control your movements, mind and continue your life.  Another example where balance is quite important.

The protein huntingtin would also seem to be implicated in cephalization, the process whereby the central nervous system expands into a brain in the head with the further implication that more that can be organized into ‘higher’ functions.  This can be seen in our embryological development as the brain adds the hindbrain and midbrain and then the forebrain.  Huntington’s disease starts in midbrain structures.

The layering of growth in the embryonic brain

The layering of growth in the embryonic brain. 

An important protein, this huntingtin, for many reasons. Now in previous posts I have talked Susanne Langer’s notion of one dialectic governing the advance of our mental faculties, the balance between the soma and our symbolic capacity. If imbalanced towards the soma, our intellect suffers, and if imbalanced towards our symbolic capacity, out intellect loses its grounding in somatic reality with predictable results. The huntingtin gene would seem something of a pivot point. A low amount and the brain is smaller in structure and organization, thus function, and a higher amount leads to greater capacity but at the risk of debilitating the soma. Evolution has progressed by limiting the survival of those who brains ‘grew’ larger too fast to maintain the somatic-mental balance yet still pushing forward to larger brains. That, I think, illustrates beautifully what Dr. Langer had in mind when she articulated this dialectic.

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