Study of the correlation between biomarkers of Alzheimer's disease in aqueous humor and age in normal people

doi:10.3969/j.issn.1006-7795.2017.03.025

Abstract

Abstract: Objective To evaluate the correlation between biomarkers of Alzheimer's disease in aqueous humor and age in normal people. Biomarkers of Alzheimer's disease including amyloid β(Aβ), Tau protein, amyloid precursor protein(APP).Methods Aqueous humor was obtained from 116 patients undergoing routine cataract surgery and was divided into 4 groups as follows:A group (age<60 years old,n=25),B group (age from 60 to 69 years old, n=30),C group (age from 70 to 79 years old, n=32), D group (age ≥ 80 years old, n=29).Quantitative analysis of Aβ40,Aβ42,Tau protein, APP in the aqueous humor was evaluated via Elisa method.Results There was no significant difference in the expression levels of Aβ40,Aβ42, Tau, APP among the 4 groups(P>0.05).Conclusion The content of Aβ40,Aβ42, Tau, APP in aqueous humor had no association with age in normal people.

Key words: normal people, aqueous humor, β-amyloid protein, Tau protein, amyloid precursor protein

CLC Number:

R331.5⁺6

Lu Yan, Li Zhen, Wu Yue, Zhang Jian, Jiang Huizhong, Wang Ningli. Study of the correlation between biomarkers of Alzheimer's disease in aqueous humor and age in normal people[J]. Journal of Capital Medical University, 2017, 38(3): 461-464.

0
/ / Recommend

Add to citation manager EndNote|Reference Manager|ProCite|BibTeX|RefWorks

URL: https://journal03.magtech.org.cn/Jweb_sdykdxxb/EN/10.3969/j.issn.1006-7795.2017.03.025

https://journal03.magtech.org.cn/Jweb_sdykdxxb/EN/Y2017/V38/I3/461

References

[1] 葛夏, 徐晓云. 2型糖尿病与老年痴呆病人认知损害的相关生物学标记物研究进展[J]. 国际神经病学神经外科学杂志, 2012, 39(3):274-278.
[2] 戎志斌, 吴正治. 阿尔茨海默病的病因病理和治疗的研究进展[J]. 贵阳中医学院学报, 2012, 34(5):208-212.
[3] Hinton D R, Sadun A A, Blanks J C, et al. Optic nerve degeneration in Alzheimer's disease[J]. N Engl J Med, 1986, 315(8):485-487.
[4] Sadun A A, Bassi C J. Optic nerve damage in Alzheimer's disease[J]. Ophthalmology, 1990, 97(1):9-17.
[5] Kesler A, Vakhapova V, Korczyn A D, et al. Retinal thickness in patients with mild cognitive impairment and Alzheimer's disease[J]. Clin Neurol Neurosurg, 2011, 113(7):523-526.
[6] Lu Y, Li Z, Zhang X, et al. Retinal nerve fiber layer structure abnormalities in early Alzheimer's disease:evidence in optical coherence tomography[J]. Neurosci Lett, 2010, 480(1):69-72.
[7] Shimazawa M, Inokuchi Y, Okuno T, et al. Reduced retinal function in amyloid precursor protein-over-expressing transgenic mice via attenuating glutamate-N-methyl-d-aspartate receptor signaling[J]. J Neurochem,2008,107(1):279-290.
[8] Ning A, Cui J, To E, et al. Amyloid-β deposits lead to retinal degeneration in a mouse model of Alzheimer disease[J]. Invest Ophthalmol Vis Sci, 2008, 49(11):5136-5143.
[9] Dutescu R M, Li Q X, Crowston J, et al. Amyloid precursor protein processing and retinal pathology in mouse models of Alzheimer's disease[J]. Graefes Arch Clin Exp Ophthalmol, 2009, 247(9):1213-1221.
[10] 卢艳, 唐娜, 王蓉. APP/PS1双转基因阿尔茨海默病模型小鼠视网膜神经节细胞丢失的初步观察[J]. 中华眼科杂志, 2012,48(9):836-841.
[11] Koronyo-Hamaoui M, Koronyo Y, Ljubimov A V, et al. Identification of amyloid plaques in retinas from Alzheimer's patients and noninvasive in vivo optical imaging of retinal plaques in a mouse model[J]. Neuroimage, 2011, 54(Suppl 1):S204-217.
[12] Koronyo Y, Salumbides B C, Black K L, et al. Alzheimer's disease in the retina:imaging retinal Aβ plaques for early diagnosis and therapy assessment[J]. Neurodegener Dis, 2012, 10(1-4):285-293.
[13] 卢艳, 董海莲, 张丽娜, 等. 淀粉样前体蛋白转基因痴呆模型小鼠视网膜和视神经纤维层病理改变[J]. 眼科新进展, 2012, 32(9):810-813.
[14] Prakasam A, Muthuswamy A, Ablonczy Z, et al. Differential accumulation of secreted Abeta PP metabolites in ocular fluids[J]. J Alzheimers Dis, 2010, 20(4):1243-1253.
[15] Glenner G G, Wong C W. Alzheimer's disease and Down's syndrome:sharing of a unique cerebrovascular amyloid fibril protein[J]. Biochem Biophys Res Commun, 1984, 122(3):1131-1135.
[16] Tamura H, Kawakami H, Kanamoto T, et al. High frequency of open-angle glaucoma in Japanese patients with Alzheimer's disease[J]. J Neurol Sci, 2006,246 (1-2):79-83.
[17] Ferri C P, Prince M, Brayne C, et al. Global prevalence of dementia:a Delphi consensus study[J]. Lancet, 2005, 366(9503):2112-2117.
[18] 吴越, 卢艳. 阿尔茨海默病眼底改变研究进展[J]. 中华眼底病杂志, 2015, 31(6):610-613.
[19] Wostyn P, De Groot V, Van Dam D, et al. Senescent changes in cerebrospinal fluid circulatory physiology and their role in the pathogenesis of normal-tension glaucoma[J]. Am J Ophthalmol, 2013, 156(1):5-14.e2.
[20] Ito Y, Shimazawa M, Tsuruma K, et al. Induction of amyloid-β(1-42) in the retina and optic nerve head of chronic ocular hypertensive monkeys[J]. Mol Vis, 2012,18:2647-2657.
[21] 罗轮杰, 罗本燕.视网膜微血管异常与认知功能障碍关系的临床研究现状[J].中国脑血管病杂志,2014,11(2):100-104.
[22] 周金子, 鲁建华, 张文芳. 青光眼病人房水中β淀粉样蛋白的检测[J]. 临床眼科杂志, 2005, 13(3):202-204.