Advances in the Relationship between Tau Protein and Morphine De-pendence in Cognitive Dysfunction
Keywords:
Tau Protein, Morphine Dependence, Cognitive Impairment, Correlation
Abstract
Morphine is an opioid drug. Long-term use can cause morphine dependence or addiction, and there are cognitive dysfunction such as abnormal mental behavior, decline in learning and memory, and decline in executive ability. The occurrence of this disease is related to many factors, such as oxidative stress, hippocampal neuronal injury, mitochondrial function injury, etc. Tau protein is a microtubule-associated protein involved in nervous system development. Studies have found that hyperphosphorylation of tau proteins can cause apoptosis of hippocampal neurons[1], and tau proteins can cause oxidative stress[2]. Therefore, tau proteins play an important role in the pathogenesis of cognitive disorders. The relationship between morphine dependence and cognitive dysfunction is now reviewed.References
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[2] Puvenna V, Engeler M, Banjara M, et al. Is phos-phorylated Tau unique to chronic traumatic encephalopathy? Phosphorylated Tau in epileptic brain and chronic traumatic encephalopathy. Brain Research 2016; 1630: 225–40.
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[6] Small GW, Siddarth P, Li Z, et al. Memory and brain amyloid and Tau effects of a bioavailable form of curcumin in non-demented adults: A double-blind, placebo-controlled 18-month trial. The American Journal of Geriatric Psychiatry 2018; 26(3): 266–277.
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[9] Ma D. P1-099: CIG suppresses tau pathology in a mouse model of tauopathy through regulating the activity of PP2A. The Journal of the Alzheimer’s Association 2019; 15(7S): 272–273.
[10] Cao M, Liu F, Ji F, et al. Effect of c-Jun N-terminal kinase (JNK)/p38 mitogen-activated protein kinase (p38 MAPK) in morphine-induced tau protein hy-perphosphorylation. Behavioural Brain Research 2013; 237: 249–255.
[11] Wang X, Zhao Y. The effect of AnshenDingzhi Fang on tau protein phosphorylation and BDNF/TrkB signaling pathway in Alzheimer’s disease rats. Journal of Hainan Medical University 2019; 25(21): 1612–1616.
[12] Frederiksen KS, Nielsen TR, Appollonio I, et al. Biomarker counselling, disclosure of diagnosis and follow-up in patients with mild cognitive impair-ment: A European Alzheimer’ disease consortium survey. International Journal of Geriatric Psychiatry 2021; 36(2): 324–333.
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[15] Armentero MT, Sinforiani E, Ghezzi C, et al. Pe-ripheral expression of key regulatory kinases in Alzheimer’s disease and Parkinson’s disease. Neu-robiology of Aging 2011; 32(12): 2142–51.
[16] Winston CN, Goetzl EJ, Schwartz JB, et al. Com-plement protein levels in plasma astrocyte-derived exosomes are abnormal in conversion from mild cognitive impairment to Alzheimer’s disease de-mentia. Alzheimer’s & Dementia: Diagnosis, As-sessment & Disease Monitoring 2019; 11(1): 61–66.
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[18] Tang SC, Yang KC, Chen CH, et al. Plasma h-Yueh,Chiu Ming-Japroteins in patients with vas-cular cognitive impairment. Neuromolecular Medi-cine 2018; 20(4): 498–503.
[19] Viisanen H, Lilius TO, Sagalajev B, et al. Neuro-physiological response properties of medullary pain-control neurons following chronic treatment with morphine or oxycodone: Modulation by acute ketamine. Journal of Neurophysiology 2020; 124(3): 790–801.
[20] Yang S. Study on the role and mechanism of Tau and MAP-2 in CCK-8 mitigation of mor-phine-induced spatial memory damage (in Chinese) [PhD thesis]. Shijiazhuang: Hebei Medical Univer-sity; 2013.
[21] Ding K. Effect of the change of ghrelin and its re-ceptor on accelerating diabetic encephalopathy by blood glucose fluctuation in GK rats. China Medical Abstracts (Internal Medicine) 2017; (1).
[22] Xiao X, Sun J, Li S, et al. Acrylamide induced apoptosis in VSC4.1 cells through endoplasmic re-ticulum stress. Journal of Environmental & Occu-pational Medicine 2017; 34(12): 1087–1092.
[23] Cao X, Qi X, Wang S. Protective effects of astaxanthin on hippocampal neurons damage in-duced by hydrogen peroxide. Chinese Journal of Marine Drugs 2012; 31(6): 45–49.
[24] Szabo L, Eckert A, Grimm A. Insights into disease-associated tau impact on mitochondria. Inter-national Journal of Molecular Sciences 2020; 21(17): 6344.
[25] Abisambra J, Jinwal U, Blair L, et al. O2lues, Mathew Cockman, Amirthaa Suntharalingham, Pengfei Li, Ying Jin, Christopher Atkins, Chad Dickeymemo-associated degradation. The Journal of the Alzheimer’s Association 2013; 9(4S): 329–330.
[2] Puvenna V, Engeler M, Banjara M, et al. Is phos-phorylated Tau unique to chronic traumatic encephalopathy? Phosphorylated Tau in epileptic brain and chronic traumatic encephalopathy. Brain Research 2016; 1630: 225–40.
[3] Aribisala BS, Hernandez MCV, Royle NA, et al. Brain atrophy associations with white matter lesions in the ageing brain: The lothian birth cohort 1936. European Radiology 2013; 23(4): 1084–92.
[4] Nikseresht S, Etebary S, Roodsari HRS, et al. The role of nitrergic system in antidepressant effects of acute administration of zinc, magnesium and thia-mine on progesterone induced postpartum depres-sion in mice. Tehran University Medical Journal 2010; 68(5): 261–267.
[5] Miloi MM. The DsTau experiment: A study for Tau-neutrino production. Particles 2020; 3(1): 164–168.
[6] Small GW, Siddarth P, Li Z, et al. Memory and brain amyloid and Tau effects of a bioavailable form of curcumin in non-demented adults: A double-blind, placebo-controlled 18-month trial. The American Journal of Geriatric Psychiatry 2018; 26(3): 266–277.
[7] Ameri M, Shabaninejad Z, Movahedpour A, et al. Biosensors for detection of Tau protein as an Alz-heimer’s disease marker. International Journal of Biological Macromolecules 2020; 162: 1100–1108.
[8] Horie K, Barthelemy NR, Mallipeddi N, et al. Re-gional correlation of biochemical measures of am-yloid and tau phosphorylation in the brain. Acta Neuropathologica Communications 2020.
[9] Ma D. P1-099: CIG suppresses tau pathology in a mouse model of tauopathy through regulating the activity of PP2A. The Journal of the Alzheimer’s Association 2019; 15(7S): 272–273.
[10] Cao M, Liu F, Ji F, et al. Effect of c-Jun N-terminal kinase (JNK)/p38 mitogen-activated protein kinase (p38 MAPK) in morphine-induced tau protein hy-perphosphorylation. Behavioural Brain Research 2013; 237: 249–255.
[11] Wang X, Zhao Y. The effect of AnshenDingzhi Fang on tau protein phosphorylation and BDNF/TrkB signaling pathway in Alzheimer’s disease rats. Journal of Hainan Medical University 2019; 25(21): 1612–1616.
[12] Frederiksen KS, Nielsen TR, Appollonio I, et al. Biomarker counselling, disclosure of diagnosis and follow-up in patients with mild cognitive impair-ment: A European Alzheimer’ disease consortium survey. International Journal of Geriatric Psychiatry 2021; 36(2): 324–333.
[13] Nicolia V, Ciraci V, Cavallaro RA, et al. GSK3 Fer-flanking DNA methylation and expression in Alzheimer’s disease patients. Current Alzheimer Research 2017; 14(7): 753–759.
[14] Huin V, Deramecourt V, Caparros-Lefebvre D, et al. The MAPT gene is differentially methylated in the progressive supranuclear palsy brain. Movement Disorders 2016; 31(12): 1883–1890.
[15] Armentero MT, Sinforiani E, Ghezzi C, et al. Pe-ripheral expression of key regulatory kinases in Alzheimer’s disease and Parkinson’s disease. Neu-robiology of Aging 2011; 32(12): 2142–51.
[16] Winston CN, Goetzl EJ, Schwartz JB, et al. Com-plement protein levels in plasma astrocyte-derived exosomes are abnormal in conversion from mild cognitive impairment to Alzheimer’s disease de-mentia. Alzheimer’s & Dementia: Diagnosis, As-sessment & Disease Monitoring 2019; 11(1): 61–66.
[17] Chen X, Jiang H. Tau as a potential therapeutic target for ischemic stroke. Aging 2019; 11(24): 12827–12843.
[18] Tang SC, Yang KC, Chen CH, et al. Plasma h-Yueh,Chiu Ming-Japroteins in patients with vas-cular cognitive impairment. Neuromolecular Medi-cine 2018; 20(4): 498–503.
[19] Viisanen H, Lilius TO, Sagalajev B, et al. Neuro-physiological response properties of medullary pain-control neurons following chronic treatment with morphine or oxycodone: Modulation by acute ketamine. Journal of Neurophysiology 2020; 124(3): 790–801.
[20] Yang S. Study on the role and mechanism of Tau and MAP-2 in CCK-8 mitigation of mor-phine-induced spatial memory damage (in Chinese) [PhD thesis]. Shijiazhuang: Hebei Medical Univer-sity; 2013.
[21] Ding K. Effect of the change of ghrelin and its re-ceptor on accelerating diabetic encephalopathy by blood glucose fluctuation in GK rats. China Medical Abstracts (Internal Medicine) 2017; (1).
[22] Xiao X, Sun J, Li S, et al. Acrylamide induced apoptosis in VSC4.1 cells through endoplasmic re-ticulum stress. Journal of Environmental & Occu-pational Medicine 2017; 34(12): 1087–1092.
[23] Cao X, Qi X, Wang S. Protective effects of astaxanthin on hippocampal neurons damage in-duced by hydrogen peroxide. Chinese Journal of Marine Drugs 2012; 31(6): 45–49.
[24] Szabo L, Eckert A, Grimm A. Insights into disease-associated tau impact on mitochondria. Inter-national Journal of Molecular Sciences 2020; 21(17): 6344.
[25] Abisambra J, Jinwal U, Blair L, et al. O2lues, Mathew Cockman, Amirthaa Suntharalingham, Pengfei Li, Ying Jin, Christopher Atkins, Chad Dickeymemo-associated degradation. The Journal of the Alzheimer’s Association 2013; 9(4S): 329–330.
Published
2021-02-02
Issue
Section
Original Research Article
Copyright (c) 2021 Qing Ji, Xin Li
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