Quantitative description of publications (1986-2020) related to Alzheimer disease and oxidative stress: A bibliometric study

Year 2021, Volume: 13 Issue: 1, 971 - 984, 20.09.2021

Entesar Yaseen Abdo Qaıd Idris Long Khairunnuur Fairuz Azman Asma Hayati Ahmad Zahiruddin Othman Kuttulebbai Sırajudeen Aidi Ahmi Rahimah Zakarıa

https://doi.org/10.37212/jcnos.946898

Cited By: 1

Abstract

While the pathological mechanism of Alzheimer’s Disease (AD) is unclear, oxidative stress has been proposed to be one of its related theories, which can help to uncover the disease’s pathological factors. This review aims to provide a quantitative description and data visualisation of oxidative stress and AD research from the literature obtained from the Scopus database. Based on the keywords used, which are related to oxidative stress and AD in the article title, 996 documents were retrieved for further analysis. Microsoft Excel, VOSviewer, and Harzing’s Publish or Perish were used to conduct the frequency analysis, data visualization, and citation analysis. There is a continuous growth in the number of publications on research in oxidative stress and AD, starting from 1986 and spanning 35 years. The most cited article was “Oxidative stress hypothesis in Alzheimer's disease”. The Journal of Alzheimer's Disease published the most number of publications related to oxidative stress and AD, while the United States and its institutions were the main contributors. Our findings suggest that research on aetiopathology, biomarkers, and neuroprotective agents for AD dominated this research field.
Our bibliometric analysis provides distinct trends in oxidative stress and AD research in the last 35 years. Our findings highlight current hot topics related to biomarkers for screening and diagnosis of AD as well as neuroprotective agents used as disease-modifying therapies of AD.

Keywords

Alzheimer's disease, Oxidative stress, Bibliometric, VOSviewer, Harzing Publish or Perish

References

• Ahmed T, Gilani AH. (2014). Therapeutic potential of turmeric in Alzheimer's disease: curcumin or curcuminoids? Phytother Res. 28(4):517-525.
• Akbar H, Duan X, Saleem S, Davis AK, Zheng Y. (2016). RhoA and Rac1 GTPases differentially regulate agonist-receptor mediated reactive oxygen species generation in platelets. PLOS One. 11:e0163227.
• Alzheimer's disease facts and figures. (2021). Alzheimers Dement. 17(3):327-406.
• Atack JR, Perry EK, Bonham JR, Candy JM, Perry RH. (1987). Molecular forms of butyrylcholinesterase in the human neocortex during development and degeneration of the cortical cholinergic system. J Neurochem. 48:1687-1692.
• Avramopoulos D. (2009). Genetics of Alzheimer's disease: recent advances. Genome Med. 1(3):34.
• Blennow K, Zetterberg H. (2018). Biomarkers for Alzheimer's disease: current status and prospects for the future. J Intern Med. 284(6):643-663.
• Burns A, Iliffe S. (2009). Alzheimer's disease. BMJ. 338:b158.
• Burns A, Jacoby R, Levy R. (1990). Psychiatric phenomena in Alzheimer's disease. IV: disorders of behaviour. Br J Psychiatry. 157:86-94.
• Butterfield DA. (2002). Amyloid beta-peptide (1-42)-induced oxidative stress and neurotoxicity: implications for neurodegeneration in Alzheimer's disease brain. A review. Free Radic Res. 36(12):1307-1313.
• Butterfield DA, Castegna A, Lauderback CM, Drake J. (2002). Evidence that amyloid beta-peptide-induced lipid peroxidation and its sequelae in Alzheimer's disease brain contribute to neuronal death. Neurobiol Aging. 23(5):655-664.
• Butterfield DA, Lauderback CM. (2002), Lipid peroxidation and protein oxidation in Alzheimer's disease brain: potential causes and consequences involving amyloid beta-peptide-associated free radical oxidative stress. Free Radic Biol Med. 32(11):1050-1060.
• Butterfield DA, Poon HF, Clair DS, Keller JN, Pierce WM, Klein JB, Markesbery WR. (2006). Redox proteomics identification of oxidatively modified hippocampal proteins in mild cognitive impairment: Insights into the development of Alzheimer’s disease. Neurobiol Dis. 22:223-232.
• Cheignon C, Tomas M, Bonnefont-Rousselot D, Faller P, Hureau C, Collin F. (2018). Oxidative stress and the amyloid beta peptide in Alzheimer's disease. Redox Biol. 14:450-464.
• Chen H, Wan Y, Jiang S, Cheng Y. (2014). Alzheimer’s disease research in the future: bibliometric analysis of cholinesterase inhibitors from 1993 to 2012. Scientometrics. 98:1865-1877.
• Christen Y. (2000). Oxidative stress and Alzheimer disease. Am J Clin Nutr. 71(2):621S-629S.
• Cioffi F, Adam RHI, Broersen K. (2019). Molecular mechanisms and genetics of oxidative stress in Alzheimer’s disease. J Alzheimer’s Dis. 72(4):981-1017.
• Cummings J, Aisen PS, DuBois B, Frölich L, Jack CRJr, Jones RW, Morris JC, Raskin J, Dowsett SA, Scheltens P. (2016). Drug development in Alzheimer’s disease: the path to 2025. Alzheimer’s Res Ther. 8:39.
• Cutler RG, Kelly J, Storie K, Pedersen WA, Tammara A, Hatanpaa K, Troncoso JC, Mattson MP. (2004). Involvement of oxidative stress-induced abnormalities in ceramide and cholesterol metabolism in brain aging and Alzheimer's disease. PNAS USA. 101(7):2070-2075.
• De Felice FG, Velasco PT, Lambert MP, Viola K, Fernandez SJ, Ferreira ST, Klein WL. (2007). A beta oligomers induce neuronal oxidative stress through an N-methyl-D-aspartate receptor-dependent mechanism that is blocked by the Alzheimer drug memantine. J Biol Chem. 282(15):11590-11601.
• Dong R, Wang H, Ye J, Wang M, Bi Y. (2019). Publication trends for Alzheimer’s disease worldwide and in China: a 30-year bibliometric analysis. Front Hum Neurosci. 13:259.
• Hensley K, Carney JM, Mattson MP, Aksenova M, Harris M, Wu JF, Floyd RA, Butterfield DA. (1994). A model for beta-amyloid aggregation and neurotoxicity based on free radical generation by the peptide: relevance to Alzheimer disease. PNAS USA. 91(8):3270-3274.
• Jiang T, Sun Q, Chen S. (2016). Oxidative Stress: A major pathogenesis and potential therapeutics target of antioxidative agents in Parkinson’s disease and Alzheimer disease. Prog Neurobiol. 147:1-19.
• Kamat PK. (2015). Streptozotocin induced Alzheimer's disease like changes and the underlying neural degeneration and regeneration mechanism. Neural Regen Res. 10(7):1050-1052.
• Kamat PK, Rai S, Nath C. (2013). Okadaic acid induced neurotoxicity: an emerging tool to study Alzheimer's disease pathology. Neurotoxicology. 37:163-172.
• Kumar A, Seghal N, Naidu PS, Padi SS, Goyal R. (2007). Colchicines-induced neurotoxicity as an animal model of sporadic dementia of Alzheimer's type. Pharmacol Rep. 59(3):274-283.
• Lahiri DK, Farlow MR, Greig NH, Sambamurti K. (2002). Current drug targets for Alzheimer's disease treatment. Drug Dev Res. 56:267-281.
• Manczak M, Anekonda TS, Henson E, Park BS, Quinn J, Reddy PH. (2006). Mitochondria are a direct site of A beta accumulation in Alzheimer's disease neurons: implications for free radical generation and oxidative damage in disease progression. Hum Mol Genet. 15(9):1437-1449.
• Mangialasche F, Polidori MC, Monastero R, Ercolani S, Camarda C, Cecchetti R, Mecocci P. (2009). Biomarkers of oxidative and nitrosative damage in Alzheimer’s disease and mild cognitive impairment. Ageing Res Rev. 8:285-305.
• Mariani E, Polidori MC, Cherubini A, Mecocci P. (2005). Oxidative stress in brain aging, neurodegenerative and vascular diseases: An overview. J Chromatogr B. 827:65-75.
• Markesbery WR. (1997). Oxidative stress hypothesis in Alzheimer's disease. Free Radic Biol Med. 23(1):134-147.
• Markesbery WR, Lovell MA. (1998). Four-hydroxynonenal, a product of lipid peroxidation, is increased in the brain in Alzheimer's disease. Neurobiol Aging. 19(1):33-36.
• Matsuoka Y, Picciano M, La Francois J, Duff K. (2001). Fibrillar β-amyloid evokes oxidative damage in a transgenic mouse model of Alzheimer’s disease. Neuroscience. 104:609-613.
• Mattson MP. (2004). Pathways towards and away from Alzheimer’s disease. Nature. 430:631-639.
• Mecocci P, Polidori MC. (2012). Antioxidant clinical trials in mild cognitive impairment and Alzheimer’s disease. Biochim Biophys Acta. 1822:631-638.
• Melo JB, Agostinho P, Oliveira CR. (2003). Involvement of oxidative stress in the enhancement of acetylcholinesterase activity induced by amyloid beta-peptide. Neurosci Res. 45(1):117-127.
• Moreira PI, Carvalho C, Zhu X, Smith MA, Perry G. (2010). Mitochondrial dysfunction is a trigger of Alzheimer’s disease pathophysiology. Biochim Biophys Acta. 1802:2-10.
• Persson T, Popescu BO, Cedazo-Minguez A. (2014). Oxidative stress in Alzheimer’s disease: Why did antioxidant therapy fail? Oxid Med Cell Longev. 2014:427318.
• Praticò D, Uryu K, Leight S, Trojanoswki JQ, Lee VM (2001) Increased lipid peroxidation precedes amyloid plaque formation in an animal model of Alzheimer amyloidosis. J Neurosci. 21(12):4183-4187.
• Ramassamy C, Averill D, Beffert U, Bastianetto S, Theroux L, Lussier-Cacan S, Cohn JS, Christen Y, Davignon J, Quirion R, Poirier J. (1999). Oxidative damage and protection by antioxidants in the frontal cortex of Alzheimer’s disease is related to the apolipoprotein E genotype. Free Radic Biol Med. 27:544-553.
• Sayre LM, Zelasko DA, Harris PL, Perry G, Salomon RG, Smith MA. (1997). 4-hydroxynonenal-derived advanced lipid peroxidation end products are increased in Alzheimer's disease. J Neurochem. 68(5):2092-2097.
• Schilder IPA, Veening-Griffioen DH, Ferreira GS, Van Meer PJK, Wied CCG-d, Schellekens H, Boon WPC, Moors EHM. (2020). Pathways in the drug development for Alzheimer’s disease (1906-2016): a bibliometric study. J Scientometric Res. 9:277-292.
• Serrano-Pozo A, Aldridge GM, Zhang Q. (2017). Four decades of research in Alzheimer’s disease (1975-2014): a bibliometric and scientometric analysis. J Alzheimer’s Dis. 59(2):763-783.
• Simpson DSA, Oliver PL. (2020). ROS Generation in microglia: understanding oxidative stress and inflammation in neurodegenerative disease. Antioxidants (Basel). 9(8):743.
• Singh A, Kukreti R, Saso L, Kukreti S. (2019). Oxidative Stress: A Key Modulator in Neurodegenerative Diseases. Molecules. 24(8):1583.
• Smith MA, Harris PL, Sayre LM, Perry G. (1997). Iron accumulation in Alzheimer disease is a source of redox-generated free radicals. PNAS USA. 94(18):9866-9868.
• Smith MA, Rottkamp CA, Nunomura A, Raina AK, Perry G. (2000). Oxidative stress in Alzheimer's disease. Biochim Biophys Acta. 1502(1):139-144.
• Song M, Heo GE, Lee D. (2015). Identifying the landscape of Alzheimer’s disease research with network and content analysis. Scientometrics. 102:905-927.
• Sorensen AA. (2009). Alzheimer’s disease research: scientific productivity and impact of the top 100 investigators in the field. J Alzheimer’s Dis. 16(3):451-465.
• Sorensen AA, Seary A, Riopelle K. (2010). Alzheimer’s disease research: A COIN study using coauthorship network analytics. Procedia Soc Behav Sci. 2(4):6582-6586.
• Teixeira JP, de Castro AA, Soares FV, da Cunha EFF, Ramalho TC. (2019). Future therapeutic perspectives into the Alzheimer’s disease targeting the oxidative stress hypothesis. Molecules. 24(23):4410.
• Tobore TO. (2019). On the central role of mitochondria dysfunction and oxidative stress in Alzheimer's disease. Neurol Sci. 40(8):1527-1540.
• Varadarajan S, Yatin S, Aksenova M, Butterfield DA. (2000). Review: Alzheimer's amyloid beta-peptide-associated free radical oxidative stress and neurotoxicity. J Struct Biol. 130(2-3):184-208.
• Wang X, Wang W, Li L, Perry G, Lee HG, Zhu X. (2014). Oxidative stress and mitochondrial dysfunction in Alzheimer's disease. Biochim Biophys Acta. 1842(8):1240-1247.
• Weintraub MK, Kranjac D, Eimerbrink MJ, Pearson SJ, Vinson BT, Patel J, Summers WM, Parnell TB, Boehm GW, Chumley MJ. (2014). Peripheral administration of poly I:C leads to increased hippocampal amyloid-beta and cognitive deficits in a non-transgenic mouse. Behav Brain Res. 266:183-187.
• Zakaria R, Wan Yaacob WM, Othman Z, Long I, Ahmad AH, Al-Rahbi B. (2017). Lipopolysaccharide-induced memory impairment in rats: a model of Alzheimer's disease. Physiol Res. 66(4):553-565.