The Levels of Amyloid β-Protein and P181 in Peripheral Blood of Patients with Alzheimer’s Disease Combined with Helicobacter pylori Infection and Their Clinical Significance

Objective. To analyze the levels of amyloid β-protein and P181 in peripheral blood of patients with Alzheimer’s disease combined with Helicobacter pylori infection and their clinical significance. Method. From January 2019 to June 2020, 59 patients were enrolled in this experiment including the AD group with 27 patients and the normal control group with 32 patients. The patients were divided into two groups: Alzheimer’s disease (AD) group ( n = 27 ) and control group ( n = 32 ), collecting the general data of patients, analyzing the diagnostic specificity and sensitivity of serum p-tau181 and Aβ42 and their influence on prognosis, and comparing the serum Aβ42 and p-tau181 concentrations for different HP infection degrees. Result. Single diagnostic sensitivity of Aβ42, p-tau181, and Aβ42 combined p-tau181 was 0.863, 0.854, and 0.972, respectively, and their specificity was 0.048, 0.206, and 0.305, respectively. Compared with the single diagnosis of serum Aβ42 and p-tau181, the combined diagnosis has higher sensitivity and specificity ( P < 0.05 ); age, years of education, serum Aβ42, and p-tau181 are factors affecting the prognosis of patients with Alzheimer’s disease combined with Helicobacter pylori infection; the concentration of Aβ42 in the control group was higher than that in the AD group, there was a statistical difference in the Aβ42 concentration between the two groups ( P < 0.05 ), and there was no statistical difference in the concentration of p-tau181 between the two groups ( P > 0.05 ); the HP positive infection rate of the AD group and the control group was 63.0% and 35.7%, respectively. The HP negative infection rate of the AD group and the control group was 37.0% and 64.3%, respectively. Compared with the control group, the positive rate of HP in the AD group was higher, and the difference was statistically significant ( P < 0.05 ); compared with HP-negative patients, HP-positive patients had a higher Aβ42 concentration, and the difference was statistically significant ( P < 0.05 ). The concentration of p-tau181 in the two groups was not statistically significant ( P > 0.05 ); Aβ42 gradually increases with increasing HP infection degree, and there are significant differences in serum Aβ42 levels between different degrees of infection. However, the level of serum p-tau181 does not change significantly with the increase of infection. Conclusion. There are significant alterations in the expression levels of Aβ42 and p-tau181 in peripheral blood of AD patients, and the levels of Aβ42 are related to HP infection; Aβ42 and p-tau181 are potential biomarkers for AD diagnosis and treatment.