| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Outline of Final Research Achievements |
We aimed to elucidate the role of Treg in neurodegenerative diseases using mouse models of Alzheimer’s disease and amyotrophic lateral sclerosis. First, we developed a mouse model using wild-type and midkine-KO mice by intraventricular injection of amyloidβ peptide (Aβ). The novel object recognition test revealed no significant improvement of cognitive deficit in Aβ-injected midkine-deficient mice, suggesting that this model represents acute Aβ-neurotoxicity and was not suitable to assess extraneuronal environment alteration. Next, we generated midkine-KO/SOD1-G93A-Tg mouse. This mouse model showed significant long survival accompanied by increases in circulating Treg. Pathological analysis demonstrated reduced motor neuron death with suppressed microglial activation in the lumbar spinal cord. This study suggested thatTreg enhancement by midkine inhibition is a potential therapeutic strategy against neurodegenerative diseases.
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