Significance

It is clear that Huntingtin protein and its diseased state counterpart has a role in intracellular trafficking.  Disruption of this process in cells and neurons most likely play a part in degenerating neurons.  Further research into how mutant Huntingtin mediates disruptions in microtubule organization and transport can inspire new treatment therapies that can reduce the impact that Huntingtin protein has on neurodegeneration.  Personalized medicine can be a better way of treating this disease because of its genetic and quantitative basis, both of which varies from patient to patient.  Early genetic screening is important in assessing severity of each patient which is related to how expanded exon1 of Huntingtin gene has become.  Drug dosages could vary between patients as a result which would require personalized treatment and hence personalized medicine.