اخبار و اعلانات

 آمار

تعداد نشریات284
تعداد نشریات سازمان82
تعداد شماره‌ها3,037
تعداد مقالات33,984
تعداد مشاهده مقاله45,783,800
تعداد دریافت فایل اصل مقاله77,193,000
Gasmi, A, Menzel, A, Piscopo, S, Noor, S. (1400). Toxic Metals Exposure and APOE4 Gene Variant in Cognitive Decline Disorders. سامانه مدیریت نشریات علمی, 77(1), 1-10. doi: 10.22092/ari.2021.356078.1771
A Gasmi; A Menzel; S Piscopo; S Noor. "Toxic Metals Exposure and APOE4 Gene Variant in Cognitive Decline Disorders". سامانه مدیریت نشریات علمی, 77, 1, 1400, 1-10. doi: 10.22092/ari.2021.356078.1771
Gasmi, A, Menzel, A, Piscopo, S, Noor, S. (1400). 'Toxic Metals Exposure and APOE4 Gene Variant in Cognitive Decline Disorders', سامانه مدیریت نشریات علمی, 77(1), pp. 1-10. doi: 10.22092/ari.2021.356078.1771
Gasmi, A, Menzel, A, Piscopo, S, Noor, S. Toxic Metals Exposure and APOE4 Gene Variant in Cognitive Decline Disorders. سامانه مدیریت نشریات علمی, 1400; 77(1): 1-10. doi: 10.22092/ari.2021.356078.1771

Toxic Metals Exposure and APOE4 Gene Variant in Cognitive Decline Disorders

Archives of Razi Institute
مقاله 3، دوره 77، شماره 1، فروردین و اردیبهشت 2022، صفحه 1-10    اصل مقاله (400.93 K)
نوع مقاله: Review Article
شناسه دیجیتال (DOI): 10.22092/ari.2021.356078.1771
نویسندگان
A Gasmi* 1؛ A Menzel2؛ S Piscopo1، 3؛ S Noor4
1Société Francophone de Nutrithérapie et de Nutrigénétique Appliquée, Villeurbanne, France
2Laboratoires Réunis, Junglinster, Luxembourg
3Research and Development Department, Nutri-Logics SA, Weiswampach, Luxembourg
4Institute of Molecular Biology and Biotechnology, Bahauddin Zakariya University Multan, Pakistan
چکیده
Neurodegenerative disorders are those which affect cognitive functions. Misfolding of proteins especially apolipoprotein E is a key genetic factor involved in several cognitive impairments.  Increasing evidence also described the toxic effects of metals, generated by both nature and humans, on the development of neurological disorders. Understanding of interaction between toxic metals and apolipoprotein E protein in cognitive decline diosrders would provide alternative treatment options.  Google Scholar and PubMed database were used to search the articles using different search terms like ‘toxic metals’, ‘cognitive decline’, ‘Apolipoprotein E’, “neurodegenerative disorders” and “metals neurotoxicity”. Only those papers were included that discussed the metal exposure-apolipoprotein association in the development of cognitive decline disorders. Heavy metals are particularly recognized as a major source of neurotoxicity. These toxic metals can interact with genetic factors and play important role in disease etiology. Understanding the underlying mechanism of this interaction could provide tremendous benefits to treat cognitive decline disorders. In this study, the role of the apolipoprotein E4 gene in the development of cognitive disease conditions and their phenotypes has been discussed thoroughly which leads to the accumulation of amyloid-beta fibrils. This exploratory study revealed novel hypothetical findings which might contribute to the understanding of the neurotoxic effects of chronic toxic metals exposure and possibly improve our knowledge on the molecular mechanisms linking metal exposure to cognitive decline disorder risk.
کلیدواژه‌ها
Toxic Metals؛ Brain؛ Apolipoprotein E؛ Neurodegenerative disorders؛ Alzheimer’s disease
سایر فایل های مرتبط با مقاله
مراجع
  1. Voet S, Srinivasan S, Lamkanfi M, van Loo G. Inflammasomes in neuroinflammatory and neurodegenerative diseases. Molecul Med. 2019;11(6):e10248.
  2. Davignon J, Cohn JS, Mabile L, Bernier L. Apolipoprotein E and atherosclerosis: insight from animal and human studies. Clin Chim Acta. 1999;286(1-2):115-43.
  3. Chou E. Alzheimer’s disease: current and future treatments. A review. Int J Med Stud. 2014;2(2):56-63.
  4. Risacher SL, Kim S, Shen L, Nho K, Foroud T, Green RC, et al. The role of apolipoprotein E (APOE) genotype in early mild cognitive impairment (E-MCI). Front Aging Neurosci. 2013;5:11.
  5. Nakajima C, Kulik A, Frotscher M, Herz J, Schäfer M, Bock HH, et al. Low density lipoprotein receptor-related protein 1 (LRP1) modulates N-methyl-D-aspartate (NMDA) receptor-dependent intracellular signaling and NMDA-induced regulation of postsynaptic protein complexes. J Biol Chem. 2013;288(30):21909-23.
  6. Leoni V. The effect of apolipoprotein E (ApoE) genotype on biomarkers of amyloidogenesis, tau pathology and neurodegeneration in Alzheimer's disease. Clin Chem Lab Med. 2011;49(3):375-83.
  7. Xu H, Finkelstein DI, Adlard PA. Interactions of metals and Apolipoprotein E in Alzheimer’s disease. Front Aging Neurosci. 2014;6:121.
  8. Mayeux R, Stern Y. Epidemiology of Alzheimer disease. Cold Spring Harb Perspect Med. 2012;2(8): 006239.
  9. Tchounwou PB, Yedjou CG, Patlolla AK, Sutton DJ. Heavy metal toxicity and the environment. Molecul clinic Environ Toxicol. 2012:133-64.
  10. Mason LH, Harp JP, Han DY. Pb neurotoxicity: neuropsychological effects of lead toxicity. BioMed Res Inter. 2014;2014.
  11. Branca JJV, Morucci G, Pacini A. Cadmium-induced neurotoxicity: still much ado. Neural Regen Res. 2018;13(11):1879.
  12. Huat TJ, Camats-Perna J, Newcombe EA, Valmas N, Kitazawa M, Medeiros R. Metal toxicity links to Alzheimer's disease and neuroinflammation. J Mol Biol. 2019;431(9):1843-68.
  13. Wang H, Naghavi M, Allen C, Barber RM, Bhutta ZA, Carter A, et al. Global, regional, and national life expectancy, all-cause mortality, and cause-specific mortality for 249 causes of death, 1980–2015: a systematic analysis for the Global Burden of Disease Study 2015. Lancet. 2016;388(10053):1459-544.
  14. Fleming SM. Mechanisms of gene-environment interactions in Parkinson’s disease. Curr Environ Health Rep. 2017;4(2):192-9.
  15. Sarkar S, Rokad D, Malovic E, Luo J, Harischandra DS, Jin H, et al. Manganese activates NLRP3 inflammasome signaling and propagates exosomal release of ASC in microglial cells. Sci Signal. 2019;12(563).
  16. Kawahara M, Kato-Negishi M, Tanaka K. Cross talk between neurometals and amyloidogenic proteins at the synapse and the pathogenesis of neurodegenerative diseases. Metallomics. 2017;9(6):619-33.
  17. Jenkitkasemwong S, Akinyode A, Paulus E, Weiskirchen R, Hojyo S, Fukada T, et al. SLC39A14 deficiency alters manganese homeostasis and excretion resulting in brain manganese accumulation and motor deficits in mice. Proceedings of the National Academy of Sciences. 2018;115(8):E1769-E78.
  18. Garza-Lombó C, Posadas Y, Quintanar L, Gonsebatt ME, Franco R. Neurotoxicity linked to dysfunctional metal ion homeostasis and xenobiotic metal exposure: redox signaling and oxidative stress. Antioxid Redox Signal. 2018;28(18):1669-703.
  19. Mold M, Linhart C, Gómez-Ramírez J, Villegas-Lanau A, Exley C. Aluminum and amyloid-β in familial Alzheimer’s disease. J Alzheimer's Dis. 2020;73(4):1627-35.
  20. Mezzaroba L, Alfieri DF, Simão ANC, Reiche EMV. The role of zinc, copper, manganese and iron in neurodegenerative diseases. Neurotoxicology. 2019;74:230-41.
  21. Karri V, Ramos D, Martinez JB, Odena A, Oliveira E, Coort SL, et al. Differential protein expression of hippocampal cells associated with heavy metals (Pb, As, and MeHg) neurotoxicity: Deepening into the molecular mechanism of neurodegenerative diseases. J Proteomics. 2018;187:106-25.
  22. Karri V, Kumar V. A systems toxicology approach to compare the heavy metal mixtures (Pb, As, MeHg) impact in neurodegenerative diseases. Food Chem Toxicol. 2020;139:111257.
  23. Xu X, Rao X, Wang T-Y, Jiang SY, Ying Z, Liu C, et al. Effect of co-exposure to nickel and particulate matter on insulin resistance and mitochondrial dysfunction in a mouse model. Part Fibre Toxicol. 2012;9(1):40.
  24. Huang X, Atwood CS, Hartshorn MA, Multhaup G, Goldstein LE, Scarpa RC, et al. The Aβ peptide of Alzheimer's disease directly produces hydrogen peroxide through metal ion reduction. Biochemistry. 1999;38(24):7609-16.
  25. Richter P, Faroon O, Pappas RS. Cadmium and cadmium/zinc ratios and tobacco-related morbidities. Int J Environ Res. 2017;14(10):1154.
  26. Wang H, Zhang L, Abel GM, Storm DR, Xia Z. Cadmium exposure impairs cognition and olfactory memory in male C57BL/6 mice. Toxicol Sci. 2018;161(1):87-102.
  27. Yuan Y, Zhang Y, Zhao S, Chen J, Yang J, Wang T, et al. Cadmium-induced apoptosis in neuronal cells is mediated by Fas/FasL-mediated mitochondrial apoptotic signaling pathway. Sci Rep. 2018;8(1):1-11.
  28. Maodaa SN, Allam AA, Ajarem J, Abdel-Maksoud MA, Al-Basher GI, Wang ZY. Effect of parsley (Petroselinum crispum, Apiaceae) juice against cadmium neurotoxicity in albino mice (Mus musculus). Behav Brain Funct. 2016;12(1):1-16.
  29. Ciesielski T, Bellinger DC, Schwartz J, Hauser R, Wright RO. Associations between cadmium exposure and neurocognitive test scores in a cross-sectional study of US adults. J Environ Health. 2013;12(1):1-11.
  30. Zhang L, Wang H, Abel GM, Storm DR, Xia Z. The effects of gene-environment interactions between cadmium exposure and apolipoprotein E4 on memory in a mouse model of Alzheimer’s disease. Toxicol Sci. 2020;173(1):189-201.
  31. Bijoor AR, Sudha S, Venkatesh T. Neurochemical and neurobehavioral effects of low lead exposure on the developing brain. Indian J Clin Biochem. 2012;27(2):147-51.
  32. Gu H, Robison G, Hong L, Barrea R, Wei X, Farlow MR, et al. Increased β-amyloid deposition in Tg-SWDI transgenic mouse brain following in vivo lead exposure. Toxicol Lett. 2012;213(2):211-9.
  1. Huang H, Bihaqi SW, Cui L, Zawia NH. In vitro Pb exposure disturbs the balance between Aβ production and elimination: the role of AβPP and neprilysin. Neurotoxicology. 2011;32(3):300-6.
  2. Basha MR, Wei W, Bakheet SA, Benitez N, Siddiqi HK, Ge Y-W, et al. The fetal basis of amyloidogenesis: exposure to lead and latent overexpression of amyloid precursor protein and β-amyloid in the aging brain. J Neurosci. 2005;25(4):823-9.
  3. Niklowitz WJ, Mandybur TI. Neurofibrillary changes following childhood lead encephalopathy: case report. J Neuropathol Exp Neurol. 1975;34(5):445-55.
  4. Mazumdar M, Xia W, Hofmann O, Gregas M, Sui SH, Hide W, et al. Prenatal lead levels, plasma amyloid β levels, and gene expression in young adulthood. Environ Health Perspect. 2012;120(5):702-7.
  5. Sobel E, Davanipour Z. Electromagnetic field exposure may cause increased production of amyloid beta and eventually lead to Alzheimer's disease. Neurology. 1996;47(6):1594-600.
  6. Mutter J, Naumann J, Sadaghiani C, Schneider R, Walach H. Alzheimer disease: mercury as pathogenetic factor and apolipoprotein E as a moderator. Neuro Endocrinol Lett. 2004;25(5):331-9.
  7. Prada D, Colicino E, Power MC, Weisskopf MG, Zhong J, Hou L, et al. APOE ε4 allele modifies the association of lead exposure with age-related cognitive decline in older individuals. Environ Res. 2016;151:101-5.
  8. Rossi E. Low level environmental lead exposure–a continuing challenge. Clin Biochem Rev. 2008;29(2):63.
  9. Factor-Litvak P, Wasserman G, Kline JK, Graziano J. The Yugoslavia Prospective Study of environmental lead exposure. Environ Health Perspect. 1999;107(1):9-15.
  10. Shih R, Glass T, Bandeen-Roche K, Carlson MC, Bolla KI, Todd A, et al. Environmental lead exposure and cognitive function in community-dwelling older adults. Neurology. 2006;67(9):1556-62.
  1. Clark C, Bornschein R, Succop P, Hee SQ, Hammond P, Peace B. Condition and type of housing as an indicator of potential environmental lead exposure and pediatric blood lead levels. Environ Res. 1985;38(1):46-53.
  2. Taylor MP, Camenzuli D, Kristensen LJ, Forbes M, Zahran S. Environmental lead exposure risks associated with children's outdoor playgrounds. Environ Pollut. 2013;178:447-54.
  3. Appenzeller BM, Tsatsakis AM. Hair analysis for biomonitoring of environmental and occupational exposure to organic pollutants: state of the art, critical review and future needs. Toxicol Lett. 2012;210(2):119-40.
  4. Hu H, Rabinowitz M, Smith D. Bone lead as a biological marker in epidemiologic studies of chronic toxicity: conceptual paradigms. Environ Health Perspect. 1998;106(1):1-8.
  5. Franzblau A, Lilis R. Acute arsenic intoxication from environmental arsenic exposure. Arch Environ Health. 1989;44(6):385-90.
  6. Hwang Y-H, Bornschein RL, Grote J, Menrath W, Roda S. Environmental arsenic exposure of children around a former copper smelter site. Environ Res. 1997;72(1):72-81.
  7. Wong O, Whorton MD, Foliart DE, Lowengart R. An ecologic study of skin cancer and environmental arsenic exposure. Int Arch Occup Environ Health. 1992;64(4):235-41.
  8. Hossain MB, Vahter M, Concha G, Broberg K. Environmental arsenic exposure and DNA methylation of the tumor suppressor gene p16 and the DNA repair gene MLH1: effect of arsenic metabolism and genotype. Metallomics. 2012;4(11):1167-75.
51.          Park SK, Elmarsafawy S, Mukherjee B, Spiro III A, Vokonas PS, Nie H, et al. Cumulative lead exposure and age-related hearing loss: the VA Normative Aging Study. Hear Res. 2010;269(1-2):48-55. 

آمار
تعداد مشاهده مقاله: 2,232
تعداد دریافت فایل اصل مقاله: 2,944


counter
سامانه مدیریت نشریات علمی. طراحی و پیاده سازی از سیناوب