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Does Dopamine Transporter Deficit Identify Prodromal Parkinson’s Disease in Patients With REM Sleep Behavior Disorder?


 

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SAN DIEGO—Dopamine transporter (DAT) scans may identify prodromal Parkinson’s disease in patients with REM sleep behavior disorder (RBD), according to research presented at the 19th International Congress of Parkinson’s Disease and Movement Disorders. Among a cohort of patients with RBD, about half had DAT deficits. Follow-up of this cohort may help researchers understand prodromal Parkinson’s disease biomarkers for subjects with RBD.

Previous studies have shown that people with nonmotor symptoms of Parkinson’s disease, such as olfactory impairment, and DAT deficit have a high risk of the disease. Studies also have shown that RBD is a risk factor for synucleinopathies, including Parkinson’s disease and multiple system atrophy. The Parkinson’s Progression Markers Initiative (PPMI) RBD Investigators in New Haven, Connecticut, worked with sleep centers to recruit patients with polysomnograms from recent sleep studies who had evidence of RBD. A central reading laboratory assessed those patients for RBD as determined by REM sleep without atonia using the Montplaisir 2010 or Frauscher 2012 criteria. The PPMI imaging core laboratory assessed patients for DAT deficit, compared with healthy subjects, using standardized visual and quantitative outcomes.

Researchers recruited 108 subjects with evidence of RBD. Ninety of the subjects (83%) met evidence of RBD as assessed by the central reading laboratory. DaTscan imaging was completed on 70 subjects (65%). Thirty-six of those participants (51%) had DAT deficit.

“Long-term studies have now definitively shown that most patients with idiopathic RBD are in fact in early (prodromal) stages of neurodegenerative disease,” said Ron Postuma, MD, Associate Professor at Montreal General Hospital. “This study shows that this prodromal status can be demonstrated with DAT scanning. It will be extremely interesting to watch how these patients evolve over time, both to see how the DAT deficit progresses, and how strongly it can predict when a patient with prodromal disease converts to full clinical disease.”

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