Seeking brain biomarkers for preventive therapy in Huntington disease.

摘要: Huntington disease (HD) is a severe incurable nervous system that generally has an onset age of around 35–50, and caused by dominantly transmitted expansion mutation. A genetic test allows persons at risk, i.e., offspring or siblings affected individuals, to discover their status. Unaffected mutation-positive subjects will manifest HD sometime during life. Despite major advances in research on pathogenic mechanisms, no studies have yet fully validated preventive therapy biomarkers for use before the symptoms become clinically manifest. Seeking brain peripheral requisite develop cure HD. Changes can be observed vivo using methods such as structural magnetic resonance imaging (MRI), diffusion tensor (DTI), functional MRI (fMRI), positron emission tomography (PET), detecting volumetric changes, microstructural connectivity alterations, abnormalities activity response specific tasks, metabolism receptor distribution. Although all these techniques detect early markers asymptomatic gene carriers premanifest screening pharmacological responses therapeutic interventions single modality provided optimal marker probably because this task requires integrative multimodal approach. In article, we review findings from procedures attempt identify potential markers, so-called dry biomarkers, possible application further, unavailable, neuroprotective therapies manifestations.