1994 Fiscal Year Final Research Report Summary
Circulating suppressing factor for muscarinic acetylcholine receptor in patients with senile dementia
| Project/Area Number |
05670809
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Psychiatric science
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| Research Institution | Osaka University |
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Principal Investigator |
MORIMOTO Shigeto Osaka University, Medical School Department of Geriatric Medicine Assistant professor, 医学部, 講師 (20150336)
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| Co-Investigator(Kenkyū-buntansha) |
FUKUO Keisuke Osaka University, Medical School Department of Geriatric Medicine Lecturer, 医学部, 助手 (40156758)
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| Project Period (FY) |
1993 – 1994
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| Keywords | Senile dementia of Alzheimer type / Lysophosphatidylcholine / Albumin |
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| Research Abstract |
We evaluated the nature of circulating suppressing factors for muscarinic acetylcholine receptor (SFAMR) in patients with senile dementia of Alzheimer type (SDAT). SFAMR was evaluated in 48 patients with SDAT,in 17 patients with vascular type dementia (VD), in 5 patients with familial Alzheimer disease (FAD), 11 normal elderly controls (EC), and in 10 normal young controls (YC). SFAMR in YC was significantly lower then those in the other groups. SFAMR in SDAT was significantly greater than that in the EC,and that in FAD was much greater. SFAMR in VD was similar to that in EC.These observations suggest that SFAMR was increased in the senile groups and further increased in SDAT and FAD.After purification by CN column and HSG15S column, two peaks of SFAMR were detected with molecular weight of about 600 and 800. The former was coeluted with lysophosphatidylcholine. In vitro addition of lysophosphatidylcholine significantly suppressed the binding of [^3H] QNB to synaptosomal membranes, although lysophosphatidyl ethanolamine or lysophosphatidyl serine did not. Further addition of albumin almost completely blocked the suppressing effect of lysophosphatidylcholine. Moreover, serum levels of albumin was significantly lower in SDAT patients and FAD patients than those in other groups. These results indicate that lysophosphatidylcholine is one of factors causing SDAT through its suppressing effect on muscarinic acetylcholine receptor.
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