CSF microRNA in patients with Huntington disease
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Huntington disease (HD) is a neurodegenerative disorder characterized by an expanded polyglutamine (CAG) huntingtin gene, with dominant inheritance. Patients with greater than 39 repeats are fully penetrant, and there exist unique clinical research opportunities to assess interventions that would delay onset, slow symptom progression, or interrupt the pathogenic process, especially in presymptomatic patients. Necessary for the evaluation of these interventions are quantitative biomarkers that can accurately characterize and track disease progression. Given the relationship of longer CAG length with younger age at clinical onset, the CAG–Age Product (CAP) score is most frequently used to quantitate exposure to mutant huntingtin in an individual patient, where in premanifest patients, a higher CAP score reflects greater likelihood of impending motor diagnosis.1 In this issue of Neurology®, Reed et al.2 characterize cross-sectional CSF microRNA (miRNA) levels in prodromal and symptomatic participants with HD. Participants were recruited from the larger cohort of the observational PREDICT-HD study, a study that followed the clinical progression of participants with premanifest HD over time. Using this CAP score, participants were categorized as a low (n = 10), medium (n = 8), or high (n = 10) risk of converting to a clinical diagnosis (n = 14) of HD. An additional 14 control samples were also collected.
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MicroRNAs in CSF as prodromal biomarkers for Huntington disease in the PREDICT-HD study 157
- Copyright © 2017 American Academy of Neurology
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