| Budget Amount *help |
¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 2001: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2000: ¥1,800,000 (Direct Cost: ¥1,800,000)
|
|---|
| Research Abstract |
It is known that occlusion of the middle cerebral artery (MCA) induces infarction and then neuronal loss and glial changes in the territory region of the MCA. α-Synuclein, a presynaptic protein, is markedly included in Lewy bodies (LB) in Parkinson's and LB diseases. We examined changes of α-synuclein after neurodegenerative insults such as MCA occlusion and KA injection, in comparison with MAP2 (a neuronal marker), CD11b (a microglial marker), GFAP (an astroglial marker) and HO-1 (a stress marker). After 2-h MCA occlusion and reperfusion, MAP2-immunoreactivity was markedly lost in the ipsilateral side of the striatum and cerebral cortex after 1 day. However, the immunoreactivities of α-synuclein did not markedly change even at 3 and 7 days after MCA occlusion, similar to after KA injection. Numerous CD11b-immunopositive microglia were observed in the regions (infarcted core) where MAP2 immunoreactivity was lost in the cerebral cortex and striatum, while GFAP-immunopositive astrocytes were activated in the border zones (perifocal regions). In addition, numerous MAP2-immunopositive glia-like cells were observed after MCA occlusion, suggesting that activated glial cells induced the phagocytosis of degenerating neurons. Thus, α-synuclein protein might not be scavenged by glial cells, although numerous neurons and dendrites are lost by neurodegenerative insults. Therefore, α-synuclein protein may readily condense in neurodegenerative regions.
|
