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Past Projects
Ultrashort Pulse Laser
Membrane Mechanisms
Quantum Spin Information
Organ Regeneration
Computational Brain
Nanoscale Quantum Conductor Array
Dynamic Nanomachine
Entropy Control
Calcium Oscillation
Photon Craft
Cell Mechanosensing
Quantum Entanglement
Development of HIV/AIDS vaccine for HIV-1 Subtype-E
Single Molecule Processes
Cold Trapped Ion
Mind Articulation
Ceramics Superplasticity
Quantum Transition
Subfemtomole Biorecognition
Microbial Evolution
Atom Arrangement-Design and Control for New Materials
1996.1~2000.12 NeuroGenes Project
Research Directors
Prof. Joh-E Ikeda Prof. Joh-E Ikeda
Dept. of Molecular Neurology, Integrated Medical Institute, Tokai University
Prof. Robert Korneluk   Prof. Robert Korneluk
Dept. of Health Medicine, University of Ottawa

Counterpart Organization: University of Ottawa (Canada)
Supporting National Agency: Canadian Genetic Diseases Network/Medical Research Council of Canada

Based on the molecular motion and functional analysis of isolated/identified proteins that are causes of trinucleotide repeat disorders, representing spinal muscular atrophy (SMA) and Huntington's Disease (HD), we started a cooperative research with Canada aimed to define the molecular mechanisms of selective neuronal apoptosis accompanied with aging of the brain, the motoneuron systems and diseases. Clarifing the mechanisms of molecular pathosis in neurodegeneration leads to developing the way to protect the brain and motoneuron cells against diseased degeneration, and also keep functional homeostasis.
We succeeded in isolating/identifying a candidate gene of a type-2 amyotrophic lateral sclerosis (ALS2CR6). The ALS2CR6 contributes not only to understanding the molecular pathosis and developing the healing techniques, but also finding further clues for molecular mechanisms of neuronal viability and homeostasis along with the NAIP, the genes being the cause of SMA. We could illuminate new aspects toward explicating the molecular pathosis in neurodegeneration.
Japan Science and Technology Agency
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