Copyright (c) 2020 V.Lavanya
This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.
An Overview on Parkinson Disease and Its Pharmacological Evaluation Methods
Corresponding Author(s) : V.Lavanya
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
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).
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).