Plasma Oligomeric Beta Amyloid in Alzheimer’s Disease with History of Agent Orange Exposure
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Background and Purpose: During the Vietnam War, many Korean soldiers were exposed to Agent Orange. Until now, there existed only limited evidence of association between exposure to Agent Orange and Alzheimer's disease (AD). The main pathological feature of AD is brain amyloidosis. To explore the pathophysiological characteristic of AD with Agent Orange exposure, we compared newly developed amyloid beta (Aβ) oligomer levels in plasma between AD with Agent Orange exposure and without exposure. Methods: We recruited 48 AD patients with Agent Orange exposure and 66 AD patients without Agent Orange. Using the Multimer Detection System technique, which was based on an enzyme-linked immunosorbent assay, we measured Aβ oligomers in the plasma of study subjects. Results: Compared to normal control patients, plasma Aβ oligomer levels were higher in AD patients regardless of history of Agent Orange exposure. However, AD patients with Agent Orange exposure showed higher plasma Aβ oligomer levels than AD patients without Agent Orange. Discussion: This study showed higher plasma Aβ oligomer levels in AD patients with Agent Orange exposure compared to AD patients without Agent Orange. This finding suggests the possibility of a different pathophysiology of AD patients with Agent Orange exposure from AD patients without Agent Orange.
Abstract
Background and Purpose: During the Vietnam War, many Korean soldiers were exposed to Agent Orange. Until now, there existed only limited evidence of association between exposure to Agent Orange and Alzheimer's disease (AD). The main pathological feature of AD is brain amyloidosis. To explore the pathophysiological characteristic of AD with Agent Orange exposure, we compared newly developed amyloid beta (Aβ) oligomer levels in plasma between AD with Agent Orange exposure and without exposure. Methods: We recruited 48 AD patients with Agent Orange exposure and 66 AD patients without Agent Orange. Using the Multimer Detection System technique, which was based on an enzyme-linked immunosorbent assay, we measured Aβ oligomers in the plasma of study subjects. Results: Compared to normal control patients, plasma Aβ oligomer levels were higher in AD patients regardless of history of Agent Orange exposure. However, AD patients with Agent Orange exposure showed higher plasma Aβ oligomer levels than AD patients without Agent Orange. Discussion: This study showed higher plasma Aβ oligomer levels in AD patients with Agent Orange exposure compared to AD patients without Agent Orange. This finding suggests the possibility of a different pathophysiology of AD patients with Agent Orange exposure from AD patients without Agent Orange.
참고문헌 (26)
- Yi SW, "Agent Orange exposure and disease prevalence in Korean Vietnam veterans: the Korean veterans health study", Environ Res, 133, pp.56~65 (2014)[DOI]
- 양영순, "Is Parkinson’s Disease with History of Agent Orange Exposure Different from Idiopathic Parkinson’s Disease?", Dementia and Neurocognitive Disorders(대한치매학회지), 15(3), pp.75~81 (2016), 대한치매학회[DOI]
- Zober A, "Morbidity follow up study of BASF employees exposed to 2,3,7, 8-tetrachlorodibenzo-p-dioxin (TCDD) after a 1953 chemical reactor incident", Occup Environ Med, 51, pp.479~486 (1994)[DOI]
- McKhann GM, "The diagnosis of dementia due to Alzheimer's disease: recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease", Alzheimers Dement, 7, pp.263~269 (2011)[DOI]
- Gong Y, "Alzheimer's disease-affected brain: presence of oligomeric A <TEX>${\beta}$<", TEX> ligands (ADDLs) suggests a molecular basis for reversible memory loss, 2003, pp.100, 10417~10422
- Lesne SE, "Brain amyloid-<TEX>${\beta}$<", TEX> oligomers in ageing and Alzheimer's disease, 2013, pp.136, 1383~1398
- Larson ME, "Soluble <TEX>$A{\beta}$<", TEX> oligomer production and toxicity, 2012, pp.120(Suppl 1), 125~139
- Sakono M, "Amyloid oligomers: formation and toxicity of Abeta oligomers", FEBS J, 277, pp.1348~1358 (2010)[DOI]
- Terry RD, "Physical basis of cognitive alterations in Alzheimer's disease: synapse loss is the major correlate of cognitive impairment", Ann Neurol, 30, pp.572~580 (1991)[DOI]
- Apostolova LG, "Brain amyloidosis ascertainment from cognitive, imaging, and peripheral blood protein measures", Neurology, 84, pp.729~737 (2015)[DOI]
- Snyder HM, "Developing novel blood-based biomarkers for Alzheimer's disease", Alzheimers Dement, 10, pp.109~114 (2014)[DOI]
- Doecke JD, "Blood-based protein biomarkers for diagnosis of Alzheimer disease", Arch Neurol, 69, pp.1318~1325 (2012)[DOI]
- An SS, "Differentiating blood samples from scrapie infected and non-infected hamsters by detecting disease-associated prion proteins using Multimer Detection System", Biochem Biophys Res Commun, 392, pp.505~509 (2010)[DOI]
- Lim K, "Magnetic microparticle-based multimer detection system for the detection of prion oligomers in sheep", Int J Nanomedicine, 10, pp.241~250 (2015)[DOI]
- Decoufle P, "Self-reported health status of Vietnam veterans in relation to perceived exposure to herbicides and combat", Am J Epidemiol, 135, pp.312~323 (1992)[DOI]
- Gauthier E, "Environmental pesticide exposure as a risk factor for Alzheimer's disease: a case-control study", Environ Res, 86, pp.37~45 (2001)[DOI]
- Baldi I, "Neurodegenerative diseases and exposure to pesticides in the elderly", Am J Epidemiol, 157, pp.409~414 (2003)[DOI]
- Konjuh C, "Neonatal hypomyelination by the herbicide 2,4-dichlorophenoxyacetic acid. Chemical and ultrastructural studies in rats", Toxicol Sci, 104, pp.332~340 (2008)[DOI]
- Urban P, "Neurological and neurophysiological examinations on workers with chronic poisoning by 2,3,7,8-TCDD: follow-up 35 years after exposure", Eur J Neurol, 14, pp.213~218 (2007)[DOI]
- Peper M, "Neuropsychological effects of chronic exposure to environmental dioxins and furans", Environ Res, 60, pp.124~135 (1993)[DOI]
- Byers JP, "Association between the levels of biogenic amines and superoxide anion production in brain regions of rats after subchronic exposure to TCDD", Toxicology, 228, pp.291~298 (2006)[DOI]
- Wan C, "2, 3, 7, 8-Tetrachlorodibenzo-P-dioxin (TCDD) induces premature senescence in human and rodent neuronal cells via ROS-dependent mechanisms", PLoS One, 9, pp.e89811~ (2014)[DOI]
- Veloso AJ, "Electrochemical immunosensors for effective evaluation of amyloid-beta modulators on oligomeric and fibrillar aggregation processes", Anal Chem, 86, pp.4901~4909 (2014)[DOI]
- Lambert MP, "Monoclonal antibodies that target pathological assemblies of Abeta", J Neurochem, 100, pp.23~35 (2007)[DOI]
- Shanthi KB, "A systematic review and meta-analysis of plasma amyloid 1-42 and tau as biomarkers for Alzheimer's disease", SAGE Open Med, 3 (2015)
- Kim SY, "Measurement of <TEX>$A{\beta}$<", TEX> oligomer in plasma and a significant correspondence to diagnosis of CSF biomarkers and PIB-PET, 2015, ~[DOI]