| Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2013: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2012: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Outline of Final Research Achievements |
In the present study, we analyzed the change of neuroimmune system (e.g. microglia) as the reaction to the neurodegeneration to elucidate the neuroprotective effect of that and apply the result to new therapeutic strategy. We observed accumulation of CD68 (which is phagocytic marker) positive activated microglia at Aβ deposition sites in the brain of an intra-hippocampal Aβ-injected mouse model of AD. Those phagocytosed Aβ deposition early after Aβ injection. By contrast, we observed the gradual increase of activated microglia accumulation at Aβ deposition sites in the brain of AD transgenic model mice (APdE9 mice). In the early stage of AD-like pathology, alpha 7 nicotinic acetylcholine receptor (α7nAChR) in microglia was upregulated. On the other hand, CD68 was significantly increased in the late stage of AD-like pathology.
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