【摘 要】
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Objective Generation and deposition of amyloid beta peptides (Aβ) and neurofibrillary tangle formation are key mechanisms involved in Alzheimers disease (AD) pathogenesis.There is evidence supporting
【机 构】
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Department of Physiology, Shandong Provincial Key Laboratory of Pathogenesis and Prevention of Neuro
【出 处】
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中国神经科学学会第九届全国学术会议暨第五届会员代表大会
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Objective Generation and deposition of amyloid beta peptides (Aβ) and neurofibrillary tangle formation are key mechanisms involved in Alzheimers disease (AD) pathogenesis.There is evidence supporting that tumor necrosis factor-α (TNF-α) receptors (TNFRs)-mediated signal pathway might contribute to production of Aβ and the subsequent cytotoxicity in the brain.However, the levels of soluble form of TNFRs (sTNFRs) and TNF-α converting enzyme (TACE/ADAM-17) was not determined in AD patients.Methods In the present study, we analyzed sTNFRs levels and TACE activity in plasma at baseline in 76 patients of AD and 40 age-and sex-matched controls.Results The AD patients had higher levels of both sTNFRs and TACE activity in plasma at baseline when compared with age-and sex-matched controls.In the subjects of AD, the sTNFR1 levels correlated significantly to TACE activity (rs =0.385, P < 0.01) and there were also positive and strong correlations between the sTNFR1 and sTNFR2 in AD (rs =0.526, P < 0.001).Conclusion These results suggest that sTNFRs and TACE might be involved in the neuropathogenesis of AD.
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