Research Theme

1. Development of therapeutic agents for Lewy body disease targeting fatty acid-binding proteins

So far, we have succeeded in creating a number of lead compounds targeting fatty acid-binding protein (FABP), and succeeded in preventing the intracellular aggregation of α-synuclein, which is the causative protein of Lewy body disease. There are many types of FABP, which are expressed in various cells such as glial cells and oligodendrocytes in addition to nerve cells. We have created these cell-specific ligands and are developing radical preventive and therapeutic agents.

FABP3 ligand

2. Development of therapeutic drug for Alzheimer's disease targeting proteasome

Recently, we have succeeded in activating the proteasome, promoting the degradation of amyloid β, the causative protein of Alzheimer's disease, and preventing intracellular accumulation. The results of this research are expected to be applied to Parkinson's disease and Lewy body dementias.

FABP3 ligand

FABP3 ligand

3. Development of ultra-early diagnosis technology for Lewy body dementias and Parkinson's disease

Recently, we have succeeded in developing a unique biomarker for Lewy body disease (patent application 2021-012620). With this technology, it is possible to accurately distinguish Alzheimer's disease, including Lewy body dementias and Parkinson's disease, and it is expected to be applied to the diagnosis of cognitive and motor diseases before the onset.

Press Release: New Prediction and Differentiation Technology for Brain Diseases - Expectations for Ultra-Early Diagnosis of Dementia
https://www.tohoku.ac.jp/japanese/2023/09/press20230925-03-ad.html
http://www.pharm.tohoku.ac.jp/file/information/20230925.pdf

FABP3 ligand

4. Elucidation of the onset mechanism of Lewy body disease and the transmission mechanism of α-synuclein

Alpha-synuclein, the causative protein of Lewy body disease, is thought to be the cause of the disease when it propagates through the body and accumulates in the brain. We have elucidated a new mechanism by which this α-synuclein interacts with the fatty acid-binding protein FABP3 and receptors on various cell membrane surfaces and is taken up into cells. We also found that this phenomenon leads to the disappearance of tyrosine hydroxylase, which is important for dopamine biosynthesis. We are also developing a therapeutic drug that can prevent Lewy body disease by fundamentally suppressing the transmission of α-synuclein itself (patent application 202-127958).

FABP3 ligand

5. Analysis of causative genes of hereditary neurological diseases and childhood diseases and elucidation of the onset mechanism

We are conducting genetic analysis to deepen our understanding of pediatric neurology, focusing on hereditary degenerative diseases, especially dopa-responsive dystonia (Segawa disease), which is a pediatric hereditary disease.

sequencer