Research Lecture at Nobel Forum with Professor Nobutaka Hattori
Nobel Forum welcomes Professor Nobutaka Hattori for a Research Lecture on 19 March.
Title: Unraveling the Pathogenesis of Parkinson’s Disease: Insights from Genetic Parkinsonism and Biomarker-Driven Approaches
Speaker: Professor Nobutaka Hattori, Department of Neurology, Juntendo University School of Medicine, Neurodegenerative Disorders Collaborative Laboratory, RIKEN Center for Brain Science
Parkinson’s disease (PD) is a single disease name, but it can be considered a highly diverse group of disorders. In diagnosis, some patients exhibit resting tremor while others do not, and the progression of clinical symptoms and the presence of higher brain dysfunction vary among patients. Most cases are sporadic without a family history, but even in hereditary PD with a family history, it is known that there are at least 25 causative genes. Pathologically, many cases are characterized by the presence of Lewy bodies, which are inclusion bodies. The main component of these bodies, α-synuclein, is presumed to aggregate and propagate, and it is believed that the progression and severity of clinical symptoms are determined by this “propagation ability,” or seed activity. The pathogenic β-sheet seed conformation of α-synuclein is found in various tissues, suggesting potential as a biomarker, but few studies have been able to reliably detect these seeds in serum samples. Recently, we developed a modified assay system, immunoprecipitation-based real-time quaking-induced conversion (IP/RT-QuIC), which enables the detection of pathogenic α-synuclein seeds in the serum of individuals with synucleinopathies. Currently, PD cannot be completely cured, but symptomatic treatments have significantly improved life expectancy. However, considering the quality of life (QoL), progression is inevitable, and motor complications such as wearing-off and dyskinesia, as well as non-motor symptoms like cognitive dysfunction, hallucinations, sleep disorders, and constipation, often accompany the disease. Therefore, the necessity of disease-modifying therapies to suppress symptom progression is being advocated. As mentioned earlier, for hereditary Parkinson’s disease, it may be possible to halt progression by controlling the causative genes. For both sporadic and hereditary PD, disease-modifying therapies targeting α-synuclein are considered effective for types where α-synuclein aggregates and propagates. PD, multiple system atrophy, and dementia with Lewy bodies, where α-synuclein deposits, are collectively referred to as synucleinopathies. In this lecture, I would like to explain the current status and future of disease-modifying therapies for synucleinopathies.
Date and time: March 19th 2026, 4 pm.
Venue: Wallenbergsalen, Nobel Forum, Nobels Väg 1, Karolinska Institutet.
KI event page here.
Contact: Pernilla Witte, Nobel Office, Nobel Forum, nobelforum@nobelprizemedicine.org