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Objective: Alzheimer's disease (Alzheimer disease, AD) is a degenerative disease of the central nervous system as the main clinical manifestations of progressive cognitive dysfunction, typical pathological features relative specificity of senile plaques and nerve fibers wrapped around The knot is accompanied by the loss of neurons. AD pathological changes in the etiology remains unclear, but it may be affected by the impact of environmental and genetic factors. It is estimated that 24,000,000 people worldwide have cognitive dysfunction, most of which are considered to be the AD. Therefore, AD represents a major public health problem, which has been proven to be a cutting-edge research. Although there has been approved method of treatment that can alleviate symptoms of AD, but there is an urgent need to improve our understanding of the pathogenesis of AD, so that the more suitable for the method of treatment of the disease to develop. Continuously improve the diagnostic level at the same time, we also realize that great efforts to develop biological and neuroimaging biomarkers to better support the clinical diagnosis. Advanced glycation end products (advanced glycosylation end products, AGEs) plays an important role in the pathogenesis of AD. AGEs is under non-enzymatic conditions, the aldehyde group of the free amino groups of the protein, ammonia clump acid, lipid, or nucleic acids and other macromolecules with a reducing sugar, after condensation, rearrangement, after cleavage, oxidative modification, resulting in a group of brown, with fluorescent activity, with a high degree of cross-linking and the irreversibility of the end products. AGEs can crosslink proteins, activation of glial cells, stable neuritic plaques promote inflammation; the saccharification Ap and AGEs receptor (receptor for advanced glycation end products, RAGE) interaction of activated microglia and astrocytes cells promote oxidative stress, and secrete large amounts of inducible nitric oxide synthase (inducible nitric oxide synthase, iNOS) and proinflammatory cytokines and feedback upward AGE receptor expression; damaged neurons and oxidative stress, cytokines, promote the development of AD pathology. This study in order to explore the relationship of the older age groups of AGEs and cognitive dysfunction incidence to find a simple early diagnosis of AD, specific laboratory parameters. Methods: Select the medical staff of the Department of Neurology of our hospital outpatients and physical examination center 60 years or older, able to listen, read, write, emotionally stable, able to match the scale investigation, a total of 270 cases. Montreal Cognitive Assessment Beijing using an improved version (Montreal Cognitive Assessment, MoCA, Beijing Version) and the Montreal Cognitive Assessment Guangdong version (Montreal Cognitive Assessment, MoCA, Guangdong Version) assessment of cognitive function, and history, and to extract The fasting, 2ml of whole blood, serum was separated after centrifugation and press a certain concentration diluted molecule fluorescence analysis, the excitation wavelength (Ex) of 365nm, the emission wavelength (Em) 435nm measured the fluorescence intensity of the supernatant (int), i.e. AGEs The relative content. According to the the MoCA score results, the subjects were divided into two groups, and cognitive function in the normal group (≥ 26 points) and cognitive dysfunction group (lt; 26 points), respectively, comparison of AGEs, age, education level, gender, etc. The difference between the factors. In addition, according to the history of the separation of the diabetic group and normal control group, the analysis of the relationship between AGEs and cognitive dysfunction, as well as between the two groups of cognitive dysfunction compare the detection rate. Experimental data application SPSS17.0 statistical software analysis, The groups between MoCA scores compared using independent samples t-test or One-way analysis of variance; pairwise comparisons between the groups, such as the homogeneity of variance, LSD method; unequal variances using DunnettT3 law; cognitive function in normal and barriers between the two groups of AGEs compared using independent samples t-test: chi-square test was used to compare the detection rate of cognitive dysfunction among the groups; significant level of a = 0.05. Results: ① of 270 experimental subjects who detected cognitive dysfunction in 131 people, accounting for 48.52%, including mild cognitive impairment (Mild cognitive impairment, MCI) group of 77 people, 54 of the dementia group, detection rates were 28.52% and 20.00%, respectively. (2) in each age group and the relationship of the MoCA score. Small to large grouping by age group MoCA scores were 25.23 ± 4.12,21.68 ± 5.78,17.00 ± 6.51, among the groups there is a significant difference (F = 24.149, P = 0.000); 60-69 age group and the other two between groups, there are significant differences (P = 0.000, P = 0.000) ,70-79 age group ≥ 80-year-old group also exist between the significant difference (P = 0.040). Cognitive dysfunction detection rates were 35.17%, 61.47%, 81.25%, among the groups there are significant differences (x2 = 24.520, P = 0.000). (3) the relationship between education level grouping with MoCA score. MoCA score there was a significant difference (F = 59.352, P = 0.000) between the groups of different cultural levels. MoCA score mean of illiteracy and primary group were: 13.50 ± 4.11 and 21.62 ± 4.76, significant difference (P = 0.000), junior high school, high school and university students, MoCA score mean their respectively were: 24.86 ± 4.38,26.24 ± 3.17 and 26.35 ± 2.97, while the junior high school, high school and college groups no significant difference (P = 0.322, P = 0.343, P = 1.000). With the educational level incremental, MoCA score gradually increased the detection rate of cognitive dysfunction decreased significantly among the groups there is a significant difference (x2 = 84.936, P = 0.000). The ④ gender grouping and MoCA score. MoCA score comparison: Male: 24.45 ± 4.65, female: 22.63 ± 5.86, significant differences exist between the two (t = -2.806, P = 0.005). Male and female cognitive dysfunction detection rates were 42.57% and 52.07%, respectively, in women than men, but there was no significant difference (x2 = 2.283, P = 0.131). ⑤ AGEs and MoCA score. The AGEs content: normal cognitive function group: 55.14 ± 15.15, cognitive dysfunction group: 57.95 ± 16.01, between the two groups no significant difference (t = -1.479, P = 0.140). ⑥ the diabetic group and healthy control group the AGEs and cognitive dysfunction detection rate comparison. AGEs content: diabetic group: 65.54 ± 21.05, healthy control group: 49.81 ± 9.30, both the existence of significant differences (t = -5.487, P = 0.000). AGES content in the diabetic group: normal cognitive function group: 67.66 ± 23.90, cognitive dysfunction Group: 63.98 ± 18.89, there was no significant difference (t = 0.688, P = 0.494). The detection rate of cognitive dysfunction: diabetes group: 57.81% of the healthy control group: 34.33% diabetic group than in the normal control group, there was a significant difference (x2 = 7.272, P = 0.007), prompted diabetic patients compared to healthy subjects prone to cognitive dysfunction. Conclusion: This study population data analysis that: cognitive dysfunction is proportional to the age, inversely proportional to the level of education, women with a high incidence in men, which coincide with most of the results of epidemiological studies. In addition, the present study, the diabetic group cognitive dysfunction detection rate was significantly higher than the non-diabetic group, which is also consistent with many articles results. Cognitive dysfunction group and the group of normal cognitive function AGEs no significant sex difference, including diabetes, cognitive dysfunction also no significant difference in the group and the normal group of AGEs, AGEs can not be used as early diagnosis of Alzheimer's disease the laboratory parameters. For early diagnosis of AD, the whole society to its understanding of the need to strengthen early treatment, early intervention.
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