An overview on parkinson disease and its pharmacological evaluation methods
Corresponding Author(s) : V.Lavanya
lavuvenkatraman@gmail.com
International Journal of Allied Medical Sciences and Clinical Research,
Vol. 2 No. 4 (2014): 2014 Volume 2- Issue -4
Abstract
Researchers have explored a diversity of clinical and laboratory tests in efforts to differentiate Parkinson’s disease patients from a healthy population multi factorial disease known to result from a variety of factors. Age is the principal risk factor; other etiological mechanisms have been identified, including gene mutations and exposure to toxins. Deregulation of energy metabolism, mostly through the loss of complex I efficiency, is involved in disease progression in both the genetic and sporadic forms of the disease. In support to data analysis, a mathematical model of the relevant metabolic pathways was developed and calibrated onto experimental data. Diagnosis of Parkinson disease (PD) and risk factors or early symptoms amenable to population-based screening, systematic review and meta-analysis of risk factors for Parkinson’s disease.
Keywords
Parkinson’s Disease
Symptoms
Animal Models
1.
V.Lavanya. An overview on parkinson disease and its pharmacological evaluation methods. Int. J. of Allied Med. Sci. and Clin. Res. [Internet]. 2020 Aug. 2 [cited 2026 Jan. 17];2(4):367-71. Available from: https://ijamscr.com/ijamscr/article/view/104
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References
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[1] Braak et al., 2003; Jankovic, (2008). Parkinson’s disease: clinical features and diagnosis. J. Neurol. Neurosurg. Psychiatry 79, 368–376
[2] Braak,H.,DelTredici,K.,Rub,U.,deVos,R.A.,JansenSteur,E.N.,andBraak, E. (2003). Neurobiol. Aging 24, 197–211.
[3] Jankovic,J.(2008). Parkinson’s disease: clinical features and diagnosis. J. Neurol. Neurosurg. Psychiatry 79, 368–376. 2007.
[4] Ward et al., 1983; Aarsland et al., 2004; Chaudhuri and Schapira, 2009
[5] Aarsland,D.,Andersen,K.,Larsen,J.P.,Perry,R.,Wentzel-Larsen,T.,Lolk,A., et al.(2004).. Arch.Neurol. 61, 1906–1911.
[6] Chaudhuri, K.R. and Schapira, A.H., (2009). Lancet Neurol. 8, 464–474.
[7] 6.Ward,C.D.,Hess,W.A.,andCalne,D.B.(1983).Olfactory impairmentin Parkinson’sdisease. Neurology 33, 943–946.
[8] Schober A. Classic toxin-induced animal models of Parkinson's disease 6-OHDA and MPTP. Cell Tissue Res. 2004;318(1):215–224.
[9] Yang JL, Chen JS, Yang YF, et al. Neuroprotection effects of retained acupuncture in neurotoxin-induced Parkinson's disease mice. Brain Behav Immun. 2011;25(7):1452–1459.
[10] Maher P. Redox control of neural function: background, mechanisms, and significance. Antioxid Redox Signal. 2006;8(11-12):1941–1970.
[11] Zhou C, Huang Y, Przedborski S. Oxidative stress in Parkinson's disease: a mechanism of pathogenic and therapeutic significance. Ann N Y Acad Sci. 2008;1147:93–104.
[12] Mounsey RB, Teismann P. Mitochondrial dysfunction in Parkinson's disease: pathogenesis and neuroprotection. Parkinsons Dis 2010. 2011 617472.
[13] Federico A, Cardaioli E, Da Pozzo P, et al. Mitochondria, oxidative stress and neurodegeneration. J Neurol Sci. 2012;322(1-2):254–262.
[14] Fabio Blandini1 and Marie-Therese Armentero1,2. Animal models of Parkinson’s disease
[15] Jankovic, J (April 2008). "Parkinson's disease: clinical features and diagnosis". Journal of Neurology, Neurosurgery, and Psychiatry 79 (4): 368–376.
Davie CA (2008). "A review of Parkinson's disease". Br. Med. Bull. 86 (1): 109–27.
[16] Nuytemans, J; Theuns; Cruts, M; Van Broeckhoven, C (July 2010) "Genetic etiology of Parkinson disease associated with mutations in the SNCA, PARK2, PINK1, PARK7, and LRRK2 genes: a mutation update". Human Mutatation 31 (7): 763–780.
[17] Galpern, WR; Lang, AE (March 2006) [February 2006]. "Interface between tauopathies and synucleinopathies: a tale of two proteins". Annals of Neurology 59 (3): 449–458.
[18] Samii, A; Nutt, JG; Ransom, BR (May 2004). "Parkinson's disease". Lancet 363 (9423): 1783–1193.
[19] Fung, VS; Thompson, PD (2007). "Rigidity and spasticity". In Tolosa, E. Parkinson's disease and movement disorders. Hagerstown, MD: Lippincott Williams & Wilkins.
[20] Yao, S.C.; Hart, A.D.; Terzella, M.J. (May 2013). "An evidence-based osteopathic approach to Parkinson disease". Osteopathic Family Physician 5 (3): 96–101.
[21] de Lau LM, Breteler MM (June 2006). "Epidemiology of Parkinson's disease". Lancet Neurol. 5 (6): 525–35.
[22] IOM (Institute of Medicine), ed. (2009). "Neurologic disorders". Veterans and Agent Orange: Update 2008. Washington D.C.: The National Academies press. pp. 510–45. ISBN 0-309-13884-1.
[23] Freire C, Koifman S (October2012). "Pesticide exposure and Parkinson's disease: epidemiological evidence of association". Neurotoxicology 33 (5): 947–71.
[24] Tanner CM, Kamel F, Ross GW, et al. (January 2011). "Rotenone, Paraquat and Parkinson's Disease". Environ Health Perspect 119 (6): 866–72.
[25] Fabio Blandini1 and Marie-Therese Armentero “Animal models of Parkinson’s disease”1,2(the febs journal mini review)
[26] J. Mo, H. Zhang, L.-P. Yu, P.-H. Sun, G.-Z. Jin, and X. Zhen,“L-Stepholidine reduced L-DOPA-induced dyskinesia in 6- OHDA-lesioned rat model of Parkinson’s disease,” Neurobiology of Aging, vol. 31, no. 6, pp. 926–936, 2010.)
[27] Zhao X, Zhai S, An M-S, Wang Y-H, Yang Y-F, et al. (2013) Neuroprotective Effects of Protocatechuic Aldehyde against Neurotoxin-Induced Cellular and Animal Models of Parkinson’s Disease . PLoS ONE 8(10): e78220.
[28] Poliquin PO, Chen J, Cloutier M, Trudeau L-E´ , Jolicoeur M (2013) Metabolomics and In-Silico Analysis Reveal Critical Energy Deregulations in Animal Models of Parkinson’s Disease.
[29] O. Rascol, C. Goetz, W. Koller, W. Poewe, and C. Sampaio. Treatment interventions for parkinson’s disease: an evidence based assessment. Lancet. 359:1589–1598 (2002).
[30] J. A. Obeso, C. W. Olanow, and J. G. Nutt. Levodopa motor complications in Parkinson’s disease. Trends Neurosci. 23:S2–S7 (2000).
[31] J. A. Obeso, F. Grandas, M. T. Herrero, and R. Horowski. The role of pulsatile versus continuous dopamine receptor stimulation for functional recovery in Parkinson's disease. Eur. J.
[32] Neurosci. 6:889–897 (1994).
References
[1] Braak et al., 2003; Jankovic, (2008). Parkinson’s disease: clinical features and diagnosis. J. Neurol. Neurosurg. Psychiatry 79, 368–376
[2] Braak,H.,DelTredici,K.,Rub,U.,deVos,R.A.,JansenSteur,E.N.,andBraak, E. (2003). Neurobiol. Aging 24, 197–211.
[3] Jankovic,J.(2008). Parkinson’s disease: clinical features and diagnosis. J. Neurol. Neurosurg. Psychiatry 79, 368–376. 2007.
[4] Ward et al., 1983; Aarsland et al., 2004; Chaudhuri and Schapira, 2009
[5] Aarsland,D.,Andersen,K.,Larsen,J.P.,Perry,R.,Wentzel-Larsen,T.,Lolk,A., et al.(2004).. Arch.Neurol. 61, 1906–1911.
[6] Chaudhuri, K.R. and Schapira, A.H., (2009). Lancet Neurol. 8, 464–474.
[7] 6.Ward,C.D.,Hess,W.A.,andCalne,D.B.(1983).Olfactory impairmentin Parkinson’sdisease. Neurology 33, 943–946.
[8] Schober A. Classic toxin-induced animal models of Parkinson's disease 6-OHDA and MPTP. Cell Tissue Res. 2004;318(1):215–224.
[9] Yang JL, Chen JS, Yang YF, et al. Neuroprotection effects of retained acupuncture in neurotoxin-induced Parkinson's disease mice. Brain Behav Immun. 2011;25(7):1452–1459.
[10] Maher P. Redox control of neural function: background, mechanisms, and significance. Antioxid Redox Signal. 2006;8(11-12):1941–1970.
[11] Zhou C, Huang Y, Przedborski S. Oxidative stress in Parkinson's disease: a mechanism of pathogenic and therapeutic significance. Ann N Y Acad Sci. 2008;1147:93–104.
[12] Mounsey RB, Teismann P. Mitochondrial dysfunction in Parkinson's disease: pathogenesis and neuroprotection. Parkinsons Dis 2010. 2011 617472.
[13] Federico A, Cardaioli E, Da Pozzo P, et al. Mitochondria, oxidative stress and neurodegeneration. J Neurol Sci. 2012;322(1-2):254–262.
[14] Fabio Blandini1 and Marie-Therese Armentero1,2. Animal models of Parkinson’s disease
[15] Jankovic, J (April 2008). "Parkinson's disease: clinical features and diagnosis". Journal of Neurology, Neurosurgery, and Psychiatry 79 (4): 368–376.
Davie CA (2008). "A review of Parkinson's disease". Br. Med. Bull. 86 (1): 109–27.
[16] Nuytemans, J; Theuns; Cruts, M; Van Broeckhoven, C (July 2010) "Genetic etiology of Parkinson disease associated with mutations in the SNCA, PARK2, PINK1, PARK7, and LRRK2 genes: a mutation update". Human Mutatation 31 (7): 763–780.
[17] Galpern, WR; Lang, AE (March 2006) [February 2006]. "Interface between tauopathies and synucleinopathies: a tale of two proteins". Annals of Neurology 59 (3): 449–458.
[18] Samii, A; Nutt, JG; Ransom, BR (May 2004). "Parkinson's disease". Lancet 363 (9423): 1783–1193.
[19] Fung, VS; Thompson, PD (2007). "Rigidity and spasticity". In Tolosa, E. Parkinson's disease and movement disorders. Hagerstown, MD: Lippincott Williams & Wilkins.
[20] Yao, S.C.; Hart, A.D.; Terzella, M.J. (May 2013). "An evidence-based osteopathic approach to Parkinson disease". Osteopathic Family Physician 5 (3): 96–101.
[21] de Lau LM, Breteler MM (June 2006). "Epidemiology of Parkinson's disease". Lancet Neurol. 5 (6): 525–35.
[22] IOM (Institute of Medicine), ed. (2009). "Neurologic disorders". Veterans and Agent Orange: Update 2008. Washington D.C.: The National Academies press. pp. 510–45. ISBN 0-309-13884-1.
[23] Freire C, Koifman S (October2012). "Pesticide exposure and Parkinson's disease: epidemiological evidence of association". Neurotoxicology 33 (5): 947–71.
[24] Tanner CM, Kamel F, Ross GW, et al. (January 2011). "Rotenone, Paraquat and Parkinson's Disease". Environ Health Perspect 119 (6): 866–72.
[25] Fabio Blandini1 and Marie-Therese Armentero “Animal models of Parkinson’s disease”1,2(the febs journal mini review)
[26] J. Mo, H. Zhang, L.-P. Yu, P.-H. Sun, G.-Z. Jin, and X. Zhen,“L-Stepholidine reduced L-DOPA-induced dyskinesia in 6- OHDA-lesioned rat model of Parkinson’s disease,” Neurobiology of Aging, vol. 31, no. 6, pp. 926–936, 2010.)
[27] Zhao X, Zhai S, An M-S, Wang Y-H, Yang Y-F, et al. (2013) Neuroprotective Effects of Protocatechuic Aldehyde against Neurotoxin-Induced Cellular and Animal Models of Parkinson’s Disease . PLoS ONE 8(10): e78220.
[28] Poliquin PO, Chen J, Cloutier M, Trudeau L-E´ , Jolicoeur M (2013) Metabolomics and In-Silico Analysis Reveal Critical Energy Deregulations in Animal Models of Parkinson’s Disease.
[29] O. Rascol, C. Goetz, W. Koller, W. Poewe, and C. Sampaio. Treatment interventions for parkinson’s disease: an evidence based assessment. Lancet. 359:1589–1598 (2002).
[30] J. A. Obeso, C. W. Olanow, and J. G. Nutt. Levodopa motor complications in Parkinson’s disease. Trends Neurosci. 23:S2–S7 (2000).
[31] J. A. Obeso, F. Grandas, M. T. Herrero, and R. Horowski. The role of pulsatile versus continuous dopamine receptor stimulation for functional recovery in Parkinson's disease. Eur. J.
[32] Neurosci. 6:889–897 (1994).
[2] Braak,H.,DelTredici,K.,Rub,U.,deVos,R.A.,JansenSteur,E.N.,andBraak, E. (2003). Neurobiol. Aging 24, 197–211.
[3] Jankovic,J.(2008). Parkinson’s disease: clinical features and diagnosis. J. Neurol. Neurosurg. Psychiatry 79, 368–376. 2007.
[4] Ward et al., 1983; Aarsland et al., 2004; Chaudhuri and Schapira, 2009
[5] Aarsland,D.,Andersen,K.,Larsen,J.P.,Perry,R.,Wentzel-Larsen,T.,Lolk,A., et al.(2004).. Arch.Neurol. 61, 1906–1911.
[6] Chaudhuri, K.R. and Schapira, A.H., (2009). Lancet Neurol. 8, 464–474.
[7] 6.Ward,C.D.,Hess,W.A.,andCalne,D.B.(1983).Olfactory impairmentin Parkinson’sdisease. Neurology 33, 943–946.
[8] Schober A. Classic toxin-induced animal models of Parkinson's disease 6-OHDA and MPTP. Cell Tissue Res. 2004;318(1):215–224.
[9] Yang JL, Chen JS, Yang YF, et al. Neuroprotection effects of retained acupuncture in neurotoxin-induced Parkinson's disease mice. Brain Behav Immun. 2011;25(7):1452–1459.
[10] Maher P. Redox control of neural function: background, mechanisms, and significance. Antioxid Redox Signal. 2006;8(11-12):1941–1970.
[11] Zhou C, Huang Y, Przedborski S. Oxidative stress in Parkinson's disease: a mechanism of pathogenic and therapeutic significance. Ann N Y Acad Sci. 2008;1147:93–104.
[12] Mounsey RB, Teismann P. Mitochondrial dysfunction in Parkinson's disease: pathogenesis and neuroprotection. Parkinsons Dis 2010. 2011 617472.
[13] Federico A, Cardaioli E, Da Pozzo P, et al. Mitochondria, oxidative stress and neurodegeneration. J Neurol Sci. 2012;322(1-2):254–262.
[14] Fabio Blandini1 and Marie-Therese Armentero1,2. Animal models of Parkinson’s disease
[15] Jankovic, J (April 2008). "Parkinson's disease: clinical features and diagnosis". Journal of Neurology, Neurosurgery, and Psychiatry 79 (4): 368–376.
Davie CA (2008). "A review of Parkinson's disease". Br. Med. Bull. 86 (1): 109–27.
[16] Nuytemans, J; Theuns; Cruts, M; Van Broeckhoven, C (July 2010) "Genetic etiology of Parkinson disease associated with mutations in the SNCA, PARK2, PINK1, PARK7, and LRRK2 genes: a mutation update". Human Mutatation 31 (7): 763–780.
[17] Galpern, WR; Lang, AE (March 2006) [February 2006]. "Interface between tauopathies and synucleinopathies: a tale of two proteins". Annals of Neurology 59 (3): 449–458.
[18] Samii, A; Nutt, JG; Ransom, BR (May 2004). "Parkinson's disease". Lancet 363 (9423): 1783–1193.
[19] Fung, VS; Thompson, PD (2007). "Rigidity and spasticity". In Tolosa, E. Parkinson's disease and movement disorders. Hagerstown, MD: Lippincott Williams & Wilkins.
[20] Yao, S.C.; Hart, A.D.; Terzella, M.J. (May 2013). "An evidence-based osteopathic approach to Parkinson disease". Osteopathic Family Physician 5 (3): 96–101.
[21] de Lau LM, Breteler MM (June 2006). "Epidemiology of Parkinson's disease". Lancet Neurol. 5 (6): 525–35.
[22] IOM (Institute of Medicine), ed. (2009). "Neurologic disorders". Veterans and Agent Orange: Update 2008. Washington D.C.: The National Academies press. pp. 510–45. ISBN 0-309-13884-1.
[23] Freire C, Koifman S (October2012). "Pesticide exposure and Parkinson's disease: epidemiological evidence of association". Neurotoxicology 33 (5): 947–71.
[24] Tanner CM, Kamel F, Ross GW, et al. (January 2011). "Rotenone, Paraquat and Parkinson's Disease". Environ Health Perspect 119 (6): 866–72.
[25] Fabio Blandini1 and Marie-Therese Armentero “Animal models of Parkinson’s disease”1,2(the febs journal mini review)
[26] J. Mo, H. Zhang, L.-P. Yu, P.-H. Sun, G.-Z. Jin, and X. Zhen,“L-Stepholidine reduced L-DOPA-induced dyskinesia in 6- OHDA-lesioned rat model of Parkinson’s disease,” Neurobiology of Aging, vol. 31, no. 6, pp. 926–936, 2010.)
[27] Zhao X, Zhai S, An M-S, Wang Y-H, Yang Y-F, et al. (2013) Neuroprotective Effects of Protocatechuic Aldehyde against Neurotoxin-Induced Cellular and Animal Models of Parkinson’s Disease . PLoS ONE 8(10): e78220.
[28] Poliquin PO, Chen J, Cloutier M, Trudeau L-E´ , Jolicoeur M (2013) Metabolomics and In-Silico Analysis Reveal Critical Energy Deregulations in Animal Models of Parkinson’s Disease.
[29] O. Rascol, C. Goetz, W. Koller, W. Poewe, and C. Sampaio. Treatment interventions for parkinson’s disease: an evidence based assessment. Lancet. 359:1589–1598 (2002).
[30] J. A. Obeso, C. W. Olanow, and J. G. Nutt. Levodopa motor complications in Parkinson’s disease. Trends Neurosci. 23:S2–S7 (2000).
[31] J. A. Obeso, F. Grandas, M. T. Herrero, and R. Horowski. The role of pulsatile versus continuous dopamine receptor stimulation for functional recovery in Parkinson's disease. Eur. J.
[32] Neurosci. 6:889–897 (1994).