Theme of Research
Neurocognitive disorders, particularly Alzheimer’s disease, are urgent social problems that must be overcome as soon as possible. However, the molecular mechanisms underlying pathogenesis of the diseases are still elusive. Until now, we have succeeded to generate next-generation mouse models of Alzheimer’s disease, and are now using these animal models to conduct research focusing on the neuro-glial and brain-peripheral interactions. Our final goals are to find drug targets and biomarkers to overcome Alzheimer’s disease, and to develop preventive, therapeutic and early diagnostic ways for other neurodegenerative diseases.
Specific responses of glial cells such as microglia (red) and astrocytes (green) to the amyloid pathology (blue) characteristic of Alzheimer’s disease.（Saito et al., Nat Neurosci. 2014）
Member
Professor
Takashi SAITO, Ph.D
Junior Associate Professor
Kaori ASAMITSU, Ph.D
Assistant Professor
Masanori HIJIOKA, Ph.D
Assistant Professor
Tatsuya MANABE, Ph.D
Technical Manager
Natsuki DOHI, Ph.D
Major research achievements
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Inflammasome signaling is dispensable for ß-amyloid-induced neuropathology in preclinical models of Alzheimer's disease.
Nature Communications 15, 1323409 (2024) -
Tau binding protein CAPON induces tau aggregation and neurodegeneration.
Nature Communications 10, 2394 (2019) -
Humanization of the entire murine Mapt gene provides a murine model of pathological human tau propagation.
Journal of Biological Chemistry 294, 12754-12765 (2019) -
Calpain activation in Alzheimer's model mice is an artifact of APP and presenilin overexpression.
Journal of Neuroscience 36, 9933-9936 (2016) -
Single APP knockin mouse models of Alzheimer’ s disease.
Nature Neuroscience 17, 661-663 (2014) -
Potent amyloidogenicity and pathogenicity of Aβ43.
Nature Neuroscience 14, 1023-1032 (2011) -
Link to the original HP