We developed a new strategy termed flip-excision switch (FLEX) system with unilateral spacer sequence (USS) by using AAV vector for a precise and selective control of transgene expression in target cell populations. The FLEX/USS system will enable us a detailed understanding of the structure and function of specific neural circuits.

We found that ADAMTS4, a metalloproteinase, is involved in the production pathway of APP669-711, which is comprised of a composite plasma biomarker for the detection of amyloid-beta deposition in the human brain. This may lead to refined and early diagnostic techniques for Alzheimer ‘s pathology using plasma.

Feeding and stress are deeply related, but the underlying neuronal mechanisms are not fully understood. We found that a neural pathway from the pontine lateral parabrachial nucleus (lPB) to the parasubthalamic nucleus (PSTN) in the hypothalamus plays an important role in fear-induced feeding suppression. The work has been published in Nature Communications.

We developed a novel method to identify spike signals of multiple projections among different brain areas. This method was realized by the automation and parallelization of spike collision tests with real-time processing of multi-channel recording and control of stimulations. Our result has been published in iScience.

The researchers have developed a novel multiplex fluorescent tyramide signal amplification system, namely, FT-GO (Fluorochromized Tyramide-Glucose Oxidase). FT-GO yielded 60 to 180 fold and 10 to 30 fold signal amplification compared with direct and indirect immunofluorescence detections, providing a versatile platform for histochemical analysis.

We succeeded in imaging of α-synuclein lesions, protein aggregates supposed to play a crucial role in neurodegenerative disorders, in the brains of living patients with multiple system atrophy. This technology is expected to be applicable to Parkinson's disease and Lewy body dementia, contributing to elucidating the etiological mechanism of these diseases. This work has been published in Movement Disorders.

It is believed that α-synuclein propagation in the brain causes the disease progression in Lewy body diseases, including Parkinson's disease and dementia with Lewy bodies. We have inoculated α-synuclein aggregates into the olfactory bulb of marmosets, which induced the α-synuclein propagation via olfactory pathway, and the brain dysfunction was revealed using positron emission tomography (PET) imaging.