Brain metabolic patterns correlate with symptom onset in preclinical HD
Original article
Feigin A et al. (2007) Thalamic metabolism and symptom onset in preclinical Huntington's disease. Brain 130: 2858–2867 PubMed
Neurodegeneration occurs before disease symptoms in patients who carry the Huntington's disease (HD) mutation, but current tests cannot predict the onset of clinical disease. Feigin et al. have described a unique pattern of brain metabolism that reflects the HD neurodegenerative process in preclinical HD-gene carrying (p-HD) individuals.
At baseline 18F-fluorodeoxyglucose PET, p-HD individuals (n = 12; mean age 46.8 
11.0 years) could be distinguished from controls (n = 12; mean age 40.8 14.7 years) on the basis of the expression of an HD-related metabolic covariance pattern (HDRP; P <0.01), which comprised reduced striatal and anterior cingulate activity, and increased activity in the thalamus, cerebellar vermis and the motor and visual regions of the cerebral cortex. Expression of this pattern in p-HD individuals increased during the first 18 months of follow-up (P <0.003) and decreased at 44 months (P <0.04 compared with 18 months). The depressed striatal metabolic activity in the p-HD group declined by a greater amount in p-HD individuals who progressed to HD than in p-HD individuals who did not, and the elevated thalamic activity progressively declined in p-HD patients, to values below those of the controls in individuals who progressed to HD. By use of 11C-raclopride PET imaging, the authors showed that striatal D2-receptor binding declined from baseline in the HD group (P <0.005) and did not correlate with expression of the HDRP.
The authors conclude that the presence of the HDRP in p-HD individuals characterizes the preclinical period and that declines in thalamic metabolism might predict progression to symptomatic HD. In addition, reductions in D2-receptor binding continue throughout the presymptomatic phase of HD.
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Subject areas under which this article appears: Neurodegenerative disease