| Project/Area Number |
10670821
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Radiation science
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| Research Institution | Yamagata University |
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Principal Investigator |
KOMATANI Akio School of Medicine, Radiology, Yamagata University Assistant Professor, 医学部, 講師 (10107188)
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| Project Period (FY) |
1998 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2000: ¥200,000 (Direct Cost: ¥200,000)
Fiscal Year 1999: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1998: ¥500,000 (Direct Cost: ¥500,000)
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| Keywords | Xe-133 / Tc-99m-HMPAO / Tc-99m-ECD / Alzheimer7s disease / Regional cerebral blood flow / Rsgional cerebral blood flow / SPECT / Alzheimer's disease, |
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| Research Abstract |
The discrepancy between Tc-99m hexamethylpropyleneamine oxime (HMPAO) and TC-99m ethyl cysteinate dimer (ECD) in Alzheimer disease (AD) was investigated and compared with in cerebral ischemic disease (CID).
In the CID group, both of HMPAO and ECD SPECT could hardly detect the mildly reduced rCBF lesion on Xe-133 SPECT but normal on X-CT.In the case of AD group, the rCBF-reduced lesion on Xe-133 SPECT could be detected well by ECD SPECT, but the HMPAO hardly detected the reduced lesion.
This discrepancy between HMPAO and ECD may be due to the difference of the retention mechanism. In the case of AD, the injury of esterase ctivity that participates with the ECD retention may be more notable than that of glutathione activity for the HMPAO retention.
These results suggest that the reduction of ECD or HMPAO density depend directly on the insufficiency of retention mechanism rather than the rCBF reduction. And the insufficiency of this retention mechanism depend on also type of the disease i.e. AD or CID.
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