The Mechanisms Of Ietm In Alzheimer’s Disease

The pathogenesis of AD is not clear yet. The chronic inflammatory response in brain causedby Aβactivating microglia is the center event in the development of AD, along with the wholeprocess of AD pathogenesis. Early animal experiments confirmed the AD rats were accompaniedwith intestinal endotoxemia (IETM). While, whether AD patients are also accompanied IETM?How does it work then? If we confirm this argument, it will provide new ideas and theoreticalbasis for AD prevention and treatment.ObjectiveTo observe the AD patients whether accompanied IETM, and further explore thepathogenesis in the course of AD. This will provide new thinking and theoretical basis forelucidating the pathogenesis of AD.Methods(1) Screen subject: Based on the inclusion and exclusion criteria, 80 elderly subje cts arecome from hospitals, communities and nursing homes in shanxi province between January 2011and January 2012. The topics have been approved by the Medical Ethics Committee of ShanxiMedical University, all selected samples signed informed consent by family members orguardians, and willing to participate in this research work, otherwise the sample is not to hire.(2) Collect general information: including gender, age, race, marital status, education level,family history, medical history, vital signs and imaging data.(3) Neuropsychological tests: including the Mini Mental State Examination (MMSE) andAlzheimer’s Disease Assessment Scale cognitive subscale (ADAS-cog).(4) Blood collecting: venous blood 5ml in the morning and subjects on an empty stomach,then centrifuge within 2 hours（3500r/min，15min，4°C）, and remove supernatant (plasma) understerile conditions, then -80°C frozen spare.(5) Detect indicators:①LPS level was detected by Chromogenic End-point TachypleusAmebocyte Lysate (CE TAL);②TNF-αlevel was detected by ELISA;③Aβ1-42level wasdetected by ELISA;④Tau protein level was detected by ELISA.(6) Analysis the molecular mechanism of Alzheimer disease from multi- level andsystematic: use biological view, methods and combine with neuropathological features, clinicalsymptoms, neuroimaging, neuropsychological tests and molecular biological data levels describethe pathogenesis of Alzheimer’s disease in systematic. Results(1) Gender (χ~2=0.202，P=0.653)、age (t=1.266，P=0.209) and educational level (t=0.444，P=0.658) were no statistically significant between two groups.(2) MMSE scores in the AD group was significantly lower than the control group(t=16.473，P＜0.001); ADAS-Cog scores in the AD group was significantly higher than thecontrol group (t=18.067，P＜0.001).(3) LPS, TNF-alpha , Aβ1-42and Tau protein levels in AD group were significantly higherthan the control group (t=5.317、5.014、10.694、17.393，P＜0.001).ConclusionIn this study, we observed AD patients were complained with cognitive dysfunction,specificity of markers in the AD-Aβand Tauprotein phosphorylation levels were significantlyincreased, further confirmed the accuracy of clinical diagnosis. At the same time, confirmed ADpatients existed intestinal endotoxemia (IETM), and compared with age of non-AD patients thedifference was significant. It prompted endotoxin may cause inflammation, and played animportant role in AD pathogenesis.