Evolutionary origins, and a fundamental view of pathology grounded in what disease molecules normally do. We combine cells, fishes and mice, evolutionary methods, the BRI brain bank, and research techniques that AI will not replace in the next twenty to fifty years, to take on brain disease and aging.
Make the next discovery your research.
While neurological diseases may seem complex and unique to humans, various animals also naturally develop similar brain diseases during aging. For example, our laboratory has discovered that the African killifish exhibits symptoms very similar to Parkinson’s disease during aging. This has provided us with many new insights into the pathophysiology of human brain diseases. Dementia in various animals is also occasionally reported in news and scientific papers. Furthermore, alpha-synuclein, the molecule responsible for Parkinson’s disease, first appeared in fish, and amyloid precursor protein, the molecule responsible for Alzheimer’s disease, exists in fish and insects through evolution.
Question What physiological roles do the molecules implicated in brain disease play inside the cell?
What we want to ask next The molecules behind brain disease are there to protect cells in the first place. So why do they stop protecting?
Question Where does aging end and disease begin?
What we want to ask next Can we stop disease without stopping aging? And why do we age at all?
Question How do genes and environment shape neuropsychiatric developmental disorders?
What we want to ask next Long seen as a motor centre, how does the cerebellum take part in sociability and the mind? And what makes a better society?
Question What are the evolutionary origins of brain disease, developmental disorders, or aging?
What we want to ask next Why has life kept disease-causing molecules for hundreds of millions of years? And why have disabilities persisted to this day?
Discuss research opportunities
Projects develop through discussion, starting from the lab’s research strengths and your interests and experience. We value researchers who learn from their results, refine the question and help shape the direction of their work.
APP sends nuclear waste out of the cell by lysosomal exocytosis. Familial Alzheimer's variants do this poorly.
APP is not only an amyloid-β precursor; it may protect neurons from nuclear stress.
In Parkinson's models, mtDNA leaks to the cytosol and, via IFI16, causes cell death and neuronal loss.
Cytosolic leakage of mitochondrial DNA may be an important cause of neurodegeneration in Parkinson’s disease.
The turquoise killifish shows dopaminergic degeneration and α-synuclein accumulation with age. T64 phosphorylation is toxic.
Age-dependent, mostly sporadic-like disease in a short-lived vertebrate.
From ube3a mutant zebrafish
ube3a mutant zebrafish lose social approach in a novel anxious tank and recover in a familiar one.
ASD-like social change exists in fish and is shaped by sensation and context.
Early-career faculty | Joined as Assistant Professor in 2022; Associate Professor from 2026
The question How does the environment change sociability? And what does APP normally do in neurons?
What they did He showed that sociability in ube3a mutant zebrafish changes with the environment. He was also first author of the laboratory’s paper showing that APP protects cells by discharging nuclear-derived waste.
What followed He was promoted to Associate Professor in September 2026.
First-author papers: Mol. Psychiatry 2025 · PNAS 2026
Graduate student (PhD program)
The question How do intracellular trafficking and quality control relate to neurodegeneration?
What they did When his first project did not go well, he designed a different project himself. He showed that phosphorylation of optineurin by TBK1 drives Golgi fragmentation, and made this his doctoral thesis.
What followed He completed his Ph.D. in September 2026 and is starting a postdoc at Johns Hopkins University (Dr. Sawa).
First-author papers: Biochem. Biophys. Res. Commun. 2025
Research experience or a finished research plan is not required. What we ask is the ability to understand the purpose of what you are taught, to examine results critically, and to work out for yourself what to investigate next. Lab visits are welcome.
Nuclear-derived waste and mtDNA leakage. APP, α-synuclein, lysosomes. We study neurodegenerative diseases including Alzheimer’s disease, Parkinson’s disease and ALS.
Age-related disease in the turquoise killifish. Alpha-synuclein first appeared in fish; amyloid precursor protein exists in fish and insects.
Autism, ADHD and related neurodevelopmental conditions. UBE3A, environment-dependent sociability, and cerebellar maps.
By elucidating the essence of neurological diseases, research outcomes will be developed into industry-academia collaboration, drug discovery, and preventive medicine, contributing to treatment and healthy longevity.
We actively propose ways to coexist with disabilities and aging that we must live with.
Carry an idea through to a paper. Solve diseases thought incurable. Rewrite the textbook.
