What do disease-associated molecules normally do inside a cell, and where does aging become disease? Evolutionary origins and a fundamental view of pathology guide the work, from cells to fish, mice and the human brain. We combine evolutionary methods, the BRI brain bank, and experiments that AI will not replace in the next twenty to fifty years.
Make the next discovery your own.
Neurological disease can look complex and uniquely human. Other animals develop similar brain disease in the ordinary course of life and during aging. In our laboratory, the African turquoise killifish develops pathology closely resembling Parkinson’s disease as it ages, and that finding has opened routes into human brain disease. Alpha-synuclein, a protein implicated in Parkinson’s disease, first appeared in fish. Proteins related to amyloid precursor protein (APP), which is implicated in Alzheimer’s disease, are also found in fish and insects.
Question What physiological roles do the molecules implicated in brain disease play inside the cell?
What we want to ask next How do molecules such as APP, APOE and α-synuclein (SNCA) take part in the mechanisms that protect cells? How do changes or failures in those functions lead to disease?
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 brain development and behavioural traits?
What we want to ask next How does the brain contribute to social behaviour and sensory processing? How can that understanding be connected to environments and support that fit each person?
Question What are the evolutionary origins of brain disease, developmental disorders, or aging?
What we want to ask next Why have molecules that are also involved in disease been passed down for hundreds of millions of years? How have the diversity of brain function and its vulnerabilities to disease and disability arisen through evolution?
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.
This finding recasts APP as a molecule that protects the cell, not only as the precursor of amyloid-β.
In models of Parkinson’s disease, mitochondrial DNA that leaks into the cytosol drives inflammation and cell death.
Reducing accumulation of this DNA improved motor impairment and neurodegeneration in the model fish.
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 show reduced social approach in an unfamiliar, anxiety-provoking environment, but improved social behaviour in a familiar environment.
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.
We study age-related disease in the turquoise killifish and explore the normal functions of α-synuclein and APP from an evolutionary perspective.
We study brain functions involved in autism and ADHD through cerebellar circuits and through how genes and the environment change behaviour.
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 work toward preventing and treating disease, and toward a society in which a person can live as themselves with disability or aging.
Carry an idea through to a paper. Solve diseases thought incurable. Rewrite the textbook.
