Researchers from Korea University Ansan Hospital and collaborators report that patients with restless legs syndrome (RLS) face a higher risk of developing Parkinson’s disease (PD). In a nationwide cohort of nearly 20,000 people, untreated RLS patients showed approximately double the PD incidence, while dopamine agonist treatment appeared to have a protective effect. The findings highlight the importance of early screening and effective RLS management to support long-term brain health.

Aggregation of α-synuclein leads to fibril formation and finally the formation of Lewy bodies, the hallmark of Parkinson’s disease pathogenesis. The exact molecular mechanism of this aggregation process is elusive. A group of researchers from Juntendo University recently found that ubiquilin-2 liquid droplets influence and catalyze this process. Their study also suggests that SO286, a small compound, inhibits the interaction between these proteins, hindering the aggregation process.

For decades, scientists have known that mitochondria, which produce energy inside our cells, malfunction in Parkinson’s disease. But a critical question remained: do the failing mitochondria cause Parkinson’s, or do they become damaged when brain cells die during the course of disease? Many studies have sought to answer this question over the years. Yet, progress has been slow—in large part due to the limitations of animal models used to research this highly complex disease. Now, a team of scientists from Gladstone Institutes has achieved a new level of clarity through discoveries demonstrating that dysfunctional mitochondria can initiate the onset of Parkinson’s.

The study, which appears in Science Advances, centers on a unique mouse model that exhibits symptoms of a rare, inherited form of Parkinson’s that is otherwise indistinguishable from the most common form, which develops later in life and accounts for about 90 percent of cases.