Date: 01 Apr 2010

Key role of nuclear medicine in seeking biomarkers of Huntington’s disease

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Huntington’s disease (HD) is a progressive and severely disabling degenerative disease caused by a dominant CAG expansion mutation in huntingtin (htt), a large protein ubiquitously expressed in all body tissues [1]. The disease primarily affects the nervous system (i.e. brain cortex and striatum) determining widely varying neuropsychiatric signs and symptoms including movement disorders, behavioural changes and cognitive decline evolving more severely in patients homozygous for HD mutation [2] and with juvenile age at onset before 20 years [3]. All these polymorphic symptoms start in an unpredictable fashion, evolve on average over about 14 years and progressively worsen as the disease stage advances. The disease progresses through the various stages in a nonlinear manner [4]. Progression rates are worst during the early disease stages, thus reflecting progressive neuropathology as longitudinally assessed by volumetric imaging studies on brain structure [5]. Because the disease starts