2000 Fiscal Year Final Research Report Summary
The relationship between disease and retention mechanism of the accumulation type tracer for the cerebral blood flow.
| 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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| Keywords | Xe-133 / Tc-99m-HMPAO / Tc-99m-ECD / Alzheimer7s disease / Regional cerebral blood flow |
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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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