Study On The Mechanism Of Bushen Recipe In The Treatment Of Alzheimer's Disease

Objective:Explore the role of human plasma proteins in the pathogenesis of Alzheimer's disease and its potential to become a biomarker or therapeutic target.Explore the molecular mechanism of Bushenfang intervention in Alzheimer's disease.Method:1 Three patients with AD and 3 patients with aMCI and 3 normal controls were selected as subjects.Fasting plasma was collected and the differential protein results were obtained using Label-free proteomics technique.The target protein was selected.2 40 patients with AD and 20 patients with aMCI and 20 normal controls were selected as subjects and blood was collected on a fast stomach.The concentration of the selected target protein was measured using a commercial ELIS A kit.3 Based on the modern biological information database TCMSP,this study collected the main monomer components of Bushenfang Chinese medicine,.used the IPA online database software to build a protein-protein interaction(PPI),and analyzed all its biological functions.The main 10 functions of Bushenfang's biological effects were summed up the potential mechanism of Bushenfang anti-dementia and its main signal pathways related to dementia.Result:I Three patients with AD and 3 patients with aMCI and 3 normal controls were selected as subjects.Fasting plasma was collected and the differential protein results were obtained using Label-free proteomics technique.The target protein was selected.2 Plasma TNF-?,TGF?1,and SOD1 concentrations were lower in the AD group than in the aMCI group and the NC group(P<0.01).There was no significant difference between the aMCI group and the NC group.The average concentration of plasma CRTAC1 in AD group was lower than that in aMCI group(P<0.01).There was no significant difference between aMCI group and NC group,and between AD group and NC group.3 Plasma TNF-a,TGF-?1,SOD1,and CRTAC1 concentrations were positively correlated with MMSE scores and negatively correlated with CDR scores(p<0.01).4 The sensitivity and specificity of plasma TNF-a concentration for distinguishing AD and aMCI were 80%and 80%(AUC=0.845,P<0.01),respectively;the sensitivity and specificity for distinguishing between AD and NC were 75%and 80%,respectively(AUC=0.821,P<0.01);Sensitivity and specificity to distinguish between dementia and non-dementia were 77%and 80%,respectively(AUC=0.833,P<0.01).The sensitivity and specificity of plasma TGF-?1 in distinguishing AD and aMCI were 55%and 85%,respectively(AUC=0.687,P=0.019).The sensitivity and specificity of distinguishing AD and NC were 55%and 85%respectively.AUC=0.692,P=0.017);the sensitivity and specificity for distinguishing between dementia and non-dementia were 55%and 85%,respectively(AUC=0.689,P=0.004).The sensitivity and specificity of plasma SOD1 in distinguishing AD and aMCI were 75%and 77%,respectively(AUC=0.779,P<0.01).The sensitivity and specificity of distinguishing between AD and NC were 85%and 59%,respectively(AUC= 0.740,P<0.01);the sensitivity and specificity of distinguishing between AD and non-dementia were 75%and 69%(AUC=0.760,P<0.01);the sensitivity and specificity of plasma CRTAC1 concentration to distinguish between AD and aMCI were respectively 80%,62%(AUC=0.760,P<0.01);Sensitivity and specificity for distinguishing between AD and NC were 75%and 51%(AUC=0.642,P=0.075);Sensitive to AD and non-dementia The degree and specificity were 83%and 51%,respectively(AUC=0.701,P<0.01).5 The possible action pathways of the kidney-reactive drug molecules are:neuro-inflammatory signaling pathway,eNOS signaling pathway,glucocorticoid receptor signaling,endothelin-1 signaling,and integrin-linked kinase.6 TGF-?1 may be the target of action of Bushenfang.Conclusion:1 The plasma levels of TNF-a.TGF-?1 and SOD1 in AD patients were significantly lower than those in the non-dementia group and were related to the severity of dementia.2 Plasma TNF-a,TGF-?1 and SOD1 concentrations can be used for the identification of AD and non-dementia.3 Bushenfang treatment of AD may play a role through the neural inflammation pathway,TGF-?1 is a possible target.