Amyloid Precursor Protein (APP) is a physiological neuroprotective and neurodevelopmental protein—it supports synapse formation, neurite outgrowth, and activity-dependent signaling—but when its processing is shifted (by mutations, aging, stress, or inflammation) toward amyloidogenic pathways, it is renown to generate Aβ and toxic fragments that drive synaptic failure and Alzheimer’s disease. This duality makes APP a powerful bridge between neurodevelopmental disorders and neurodegeneration, where disrupted trafficking/signaling early in life can prime circuits for later vulnerability.

Can we extend this logic to other “double-edge” regulators (e.g., mTOR/autophagy–lysosome, mitochondrial pathways, and inflammatory glial signaling) to understand how neuron–glia interactions and neurotransmitter imbalance shape brain health across the lifespan?

Neurodevelopmental risk genes for autism and ADHD (e.g., UBE3A, FMR1, SHANK3, CNTNAP2, SCN2A, DRD4/DAT1 pathways) are essential for wiring synapses and stabilizing excitation–inhibition balance, yet their disruption can also prime long-term circuit fragility and stress sensitivity. Investigating the cross-talk between neurons and glia is important to uncover how synaptic dysfunction, cilia signaling, and neurotransmitter imbalance evolve from early-life genetic risk into lifelong vulnerability. By integrating zebrafish, mouse, and cell models, we will identify convergent mechanisms shared across neurodevelopment and Alzheimer’s-related pathology, opening routes for cross-disorder therapeutics, and translation to human. 

2026/02/08
I gave a talk at the 15th NIPS-BRI-EHUB Joint Symposium. Inuyama-city, Japan (5-6 February 2026) and at the 2026 IYNA-Alzheimer's Association Ideathon (8 February 2026).

2026/01/15
Selected for a new research grant from the Kobayashi Foundation (公益財団法人 小林財団).

2026/01/10
I was at the 48th Annual Meeting of the Molecular Biology Society of Japan (December 3-5, Pacifico Yokohama).

2025/12/01
New Manuscript in Translational Neurodegeneration!!!
Lipofuscin accumulation in aging and neurodegeneration: a potential “timebomb” overlooked in Alzheimer’s disease . Translational Neurodegeneration.


2025/11/16
New Manuscript was published in Translational Psychiatry!!!
Behavioral and molecular insights into anxiety in ube3a and fmr1 zebrafish models of autism spectrum disorders. Translational Psychiatry.


2025/08/30
New Manuscript was published in Molecular Psychiatry!!!
Environmental context modulates sociability in ube3a zebrafish mutants via alterations in sensory pathways. Molecular Psychiatry. A tiny fish might provide clue on autism.

University HP https://www.bri.niigata-u.ac.jp/research/result/002346.html 

X https://x.com/niigata_nouken/status/1963837182575259870

English version

University HP https://www.bri.niigata-u.ac.jp/en/research/result/002347.html 

X  https://x.com/ngt_nouken_eng/status/1963837252318175342 

https://www.eurekalert.org/news-releases/1097002 

Assistant Professor at the Brain Research Institute, Niigata University (Department of Neuroscience of Disease, Matsui Lab).

I study molecular mechanisms linking brain development and degeneration, using mouse and zebrafish models to understand pathways relevant to ADHD, autism, Alzheimer’s disease, and Parkinson’s disease. 

I received my PhD (2022) from Kyoto University (Graduate School of Pharmaceutical Sciences, Department of Pharmacognosy), where I studied the neuropsychopharmacological actions of bioactive plant-derived volatile compounds. Building on this foundation, my current work integrates behavioral neuroscience, molecular profiling, and advanced imaging to identify mechanistic targets and biomarkers that can bridge model systems and human disease. 

Please feel free to reach out for scientific discussion and potential collaborations. 

French, English, Japanse, Fon