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Erschienen in: Drugs & Aging 11/2001

01.11.2001 | Leading Article

Current Evidence for Neuroprotective Effects of Nicotine and Caffeine Against Parkinson’s Disease

verfasst von: G. Webster Ross, Helen Petrovitch

Erschienen in: Drugs & Aging | Ausgabe 11/2001

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Abstract

Parkinson’s disease (PD) is the second most common neurodegenerative disorder affecting 1 to 3% of individuals over the age of 65 years. While effective therapy exists for treating the bradykinesia, rigidity and tremor associated with the disease, the cause is unknown. There is no treatment available to prevent or slow the progressive neuronal loss in the substantia nigra and associated decreased levels of dopamine in the striatum that underlie the cardinal features of the disease.
Both retrospective and prospective epidemiological studies have consistently demonstrated an inverse association between cigarette smoking and PD, leading to theories that smoking in general and nicotine in particular might be neuroprotective. Nicotine has been shown in animals to stimulate the release of dopamine in the striatum, and to preserve nigral neurons and striatal dopamine levels in laboratory animals with lesioned nigrostriatal pathways.
Coffee and caffeine consumption have also been shown in epidemiological studies to be inversely related to PD risk. Caffeine is an adenosine A2A receptor antagonist that enhances locomotor activity in animal models of parkinsonism. Theophylline, a related compound that has A2A receptor blocking properties, has been shown in one small trial to improve motor function in patients with PD.
Recently, potent and highly selective A2A receptor antagonists have been developed that have demonstrated improvement in motor function in animal models of parkinsonism. Exciting findings are emerging that demonstrate attenuation of dopaminergic neurotoxicity with caffeine and other adenosine receptor antagonists in mice given the neurotoxin l-methyl-4-phenyl-l,2,3,6-tetrahydropyridine (MPTP), suggesting that these compounds may be neuroprotective.
Evidence for the neuroprotective potential of nicotine and caffeine is compelling, but further work is needed before testing these and related compounds in clinical trials for both individuals at high risk of developing PD and those with early, untreated disease.
Literatur
1.
Zurück zum Zitat Lang AE, Lozano AM. Parkinson’s disease. First of two parts. N Engl J Med 1998; 339(15): 1044–53PubMedCrossRef Lang AE, Lozano AM. Parkinson’s disease. First of two parts. N Engl J Med 1998; 339(15): 1044–53PubMedCrossRef
2.
Zurück zum Zitat Langston JW, Widner H, Goetz CG, et al. Core assessment program for intracerebral transplantations (CAPIT). Mov Disord 1992; 7(1): 2–13PubMedCrossRef Langston JW, Widner H, Goetz CG, et al. Core assessment program for intracerebral transplantations (CAPIT). Mov Disord 1992; 7(1): 2–13PubMedCrossRef
3.
Zurück zum Zitat Whetten-Goldstein K, Sloan F, Kulas E, et al. The burden of Parkinson’s disease on society, family, and the individual. J Am Geriatr Soc 1997; 45(7): 844–9PubMed Whetten-Goldstein K, Sloan F, Kulas E, et al. The burden of Parkinson’s disease on society, family, and the individual. J Am Geriatr Soc 1997; 45(7): 844–9PubMed
4.
Zurück zum Zitat Siderowf AD, Holloway RG, Stern MB. Cost-effectiveness analysis in Parkinson’s disease: determining the value of interventions. Mov Disord 2000; 15(3): 439–45PubMedCrossRef Siderowf AD, Holloway RG, Stern MB. Cost-effectiveness analysis in Parkinson’s disease: determining the value of interventions. Mov Disord 2000; 15(3): 439–45PubMedCrossRef
5.
Zurück zum Zitat Langsten JW, Tanner CM. Selegiline and Parkinson’s disease: it’s deja vu-again. Neurology 2000; 55(12): 1770–1CrossRef Langsten JW, Tanner CM. Selegiline and Parkinson’s disease: it’s deja vu-again. Neurology 2000; 55(12): 1770–1CrossRef
6.
Zurück zum Zitat The Parkinson Study Group. Effect of deprenyl on the progression of disability in early Parkinson’s disease. N Engl J Med 1989; 321(20): 1364–71CrossRef The Parkinson Study Group. Effect of deprenyl on the progression of disability in early Parkinson’s disease. N Engl J Med 1989; 321(20): 1364–71CrossRef
7.
Zurück zum Zitat Dorn HF. Tobacco consumption and mortality from cancer and other diseases. Public Health Rep 1959; 74: 581–93PubMedCrossRef Dorn HF. Tobacco consumption and mortality from cancer and other diseases. Public Health Rep 1959; 74: 581–93PubMedCrossRef
8.
Zurück zum Zitat Baumann RJ, Jameson HD, McKean HE, et al. Cigarette smoking and Parkinson disease: 1. Comparison of cases with matched neighbors. Neurology 1980; 30(8): 839–43PubMedCrossRef Baumann RJ, Jameson HD, McKean HE, et al. Cigarette smoking and Parkinson disease: 1. Comparison of cases with matched neighbors. Neurology 1980; 30(8): 839–43PubMedCrossRef
9.
Zurück zum Zitat Nefzger MD, Quadfasel FA, Karl VC. A retrospective study of smoking in Parkinson’s disease. Am J Epidemiol 1968; 88(2): 149–58PubMed Nefzger MD, Quadfasel FA, Karl VC. A retrospective study of smoking in Parkinson’s disease. Am J Epidemiol 1968; 88(2): 149–58PubMed
10.
Zurück zum Zitat Baron JA. Beneficial effects of nicotine and cigarette smoking: the real, the possible and the spurious. Br Med Bull 1996; 52(1): 58–73PubMedCrossRef Baron JA. Beneficial effects of nicotine and cigarette smoking: the real, the possible and the spurious. Br Med Bull 1996; 52(1): 58–73PubMedCrossRef
11.
Zurück zum Zitat Morens DM, Grandinetti A, Reed D, et al. Cigarette smoking and protection from Parkinson’s disease: false association or etiologic clue? Neurology 1995; 45(6): 1041–51PubMedCrossRef Morens DM, Grandinetti A, Reed D, et al. Cigarette smoking and protection from Parkinson’s disease: false association or etiologic clue? Neurology 1995; 45(6): 1041–51PubMedCrossRef
12.
Zurück zum Zitat Grandinetti A, Morens DM, Reed D, et al. Prospective study of cigarette smoking and the risk of developing idiopathic Parkinson’s disease. Am J Epidemiol 1994; 139(12): 1129–38PubMed Grandinetti A, Morens DM, Reed D, et al. Prospective study of cigarette smoking and the risk of developing idiopathic Parkinson’s disease. Am J Epidemiol 1994; 139(12): 1129–38PubMed
13.
Zurück zum Zitat Gorell JM, Rybicki BA, Johnson CC, et al. Smoking and Parkinson’s disease: a dose-response relationship. Neurology 1999; 52(1): 115–9PubMedCrossRef Gorell JM, Rybicki BA, Johnson CC, et al. Smoking and Parkinson’s disease: a dose-response relationship. Neurology 1999; 52(1): 115–9PubMedCrossRef
14.
Zurück zum Zitat Hellenbrand W, Seidler A, Robra BP, et al. Smoking and Parkinson’s disease: a case-control study in Germany. Int J Epidemiol 1997; 26(2): 328–39PubMedCrossRef Hellenbrand W, Seidler A, Robra BP, et al. Smoking and Parkinson’s disease: a case-control study in Germany. Int J Epidemiol 1997; 26(2): 328–39PubMedCrossRef
15.
Zurück zum Zitat Smargiassi A, Mutti A, De Rosa A, et al. A case-control study of occupational and environmental risk factors for Parkinson’s disease in the Emilia-Romagna region of Italy. Neurotoxicology 1998; 19(4–5): 709–12PubMed Smargiassi A, Mutti A, De Rosa A, et al. A case-control study of occupational and environmental risk factors for Parkinson’s disease in the Emilia-Romagna region of Italy. Neurotoxicology 1998; 19(4–5): 709–12PubMed
16.
Zurück zum Zitat Chan DK, Woo J, Ho SC, et al. Genetic and environmental risk factors for Parkinson’s disease in a Chinese population. J Neurol Neurosurg Psychiatry 1998; 65(5): 781–4PubMedCrossRef Chan DK, Woo J, Ho SC, et al. Genetic and environmental risk factors for Parkinson’s disease in a Chinese population. J Neurol Neurosurg Psychiatry 1998; 65(5): 781–4PubMedCrossRef
17.
Zurück zum Zitat Liou HH, Tsai MC, Chen CJ, et al. Environmental risk factors and Parkinson’s disease: a case-control study in Taiwan. Neurology 1997; 48(6): 1583–8PubMedCrossRef Liou HH, Tsai MC, Chen CJ, et al. Environmental risk factors and Parkinson’s disease: a case-control study in Taiwan. Neurology 1997; 48(6): 1583–8PubMedCrossRef
18.
Zurück zum Zitat Werneck AL, Alvarenga H. Genetics, drugs and environmental factors in Parkinson’s disease. A case-control study. Arq Neuropsiquiatr 1999; 57(2B): 347–55PubMedCrossRef Werneck AL, Alvarenga H. Genetics, drugs and environmental factors in Parkinson’s disease. A case-control study. Arq Neuropsiquiatr 1999; 57(2B): 347–55PubMedCrossRef
20.
Zurück zum Zitat Sorenson EM, Shiroyama T, Kitai ST. Postsynaptic nicotinic receptors on dopaminergic neurons in the substantia nigra pars compacta of the rat. Neuroscience 1998; 87(3): 659–73PubMedCrossRef Sorenson EM, Shiroyama T, Kitai ST. Postsynaptic nicotinic receptors on dopaminergic neurons in the substantia nigra pars compacta of the rat. Neuroscience 1998; 87(3): 659–73PubMedCrossRef
21.
Zurück zum Zitat Clarke PB, Schwartz RD, Paul SM, et al. Nicotinic binding in rat brain: autoradiographic comparison of [3H]acetylcholine, [3H]nicotine, and [125I]-alpha-bungarotoxin. J Neurosci 1985; 5(5): 1307–15PubMed Clarke PB, Schwartz RD, Paul SM, et al. Nicotinic binding in rat brain: autoradiographic comparison of [3H]acetylcholine, [3H]nicotine, and [125I]-alpha-bungarotoxin. J Neurosci 1985; 5(5): 1307–15PubMed
22.
Zurück zum Zitat Newhouse PA, Potter A, Levin ED. Nicotinic system involvement in Alzheimer’s and Parkinson’s diseases: implications for therapeutics. Drugs Aging 1997; 11(3): 206–28PubMedCrossRef Newhouse PA, Potter A, Levin ED. Nicotinic system involvement in Alzheimer’s and Parkinson’s diseases: implications for therapeutics. Drugs Aging 1997; 11(3): 206–28PubMedCrossRef
23.
Zurück zum Zitat Seppa T, Ahtee L. Comparison of the effects of epibatidine and nicotine on the output of dopamine in the dorsal and ventral striatum of freely-moving rats. Naunyn Schmiedebergs Arch Pharmacol 2000; 362(4–5): 444–7PubMed Seppa T, Ahtee L. Comparison of the effects of epibatidine and nicotine on the output of dopamine in the dorsal and ventral striatum of freely-moving rats. Naunyn Schmiedebergs Arch Pharmacol 2000; 362(4–5): 444–7PubMed
24.
Zurück zum Zitat Clarke PB, Kumar R. The effects of nicotine on locomotor activity in non-tolerant and tolerant rats. Br J Pharmacol 1983; 78(2): 329–37PubMedCrossRef Clarke PB, Kumar R. The effects of nicotine on locomotor activity in non-tolerant and tolerant rats. Br J Pharmacol 1983; 78(2): 329–37PubMedCrossRef
25.
Zurück zum Zitat Sershen H, Hashim A, Lajtha A. Behavioral and biochemical effects of nicotine in an MPTP-induced mouse model of Parkinson’s disease. Pharmacol Biochem Behav 1987; 28(2): 299–303PubMedCrossRef Sershen H, Hashim A, Lajtha A. Behavioral and biochemical effects of nicotine in an MPTP-induced mouse model of Parkinson’s disease. Pharmacol Biochem Behav 1987; 28(2): 299–303PubMedCrossRef
26.
Zurück zum Zitat Ishikawa A, Miyatake T. Effects of smoking in patients with early-onset Parkinson’s disease. J Neurol Sci 1993; 117(1–2): 28–32PubMedCrossRef Ishikawa A, Miyatake T. Effects of smoking in patients with early-onset Parkinson’s disease. J Neurol Sci 1993; 117(1–2): 28–32PubMedCrossRef
27.
Zurück zum Zitat Fagerstrom KO, Pomerleau O, Giordani B, et al. Nicotine may relieve symptoms of Parkinson’s disease. Psychopharmacology (Berl) 1994; 116(1): 117–9CrossRef Fagerstrom KO, Pomerleau O, Giordani B, et al. Nicotine may relieve symptoms of Parkinson’s disease. Psychopharmacology (Berl) 1994; 116(1): 117–9CrossRef
28.
Zurück zum Zitat Kelton MC, Kahn HJ, Conrath CL, et al. The effects of nicotine on Parkinson’s disease. Brain Cogn 2000; 43(1–3): 274–82PubMed Kelton MC, Kahn HJ, Conrath CL, et al. The effects of nicotine on Parkinson’s disease. Brain Cogn 2000; 43(1–3): 274–82PubMed
29.
Zurück zum Zitat Clemens P, Baron JA, Coffey D, et al. The short-term effect of nicotine chewing gum in patients with Parkinson’s disease. Psychopharmacology (Berl) 1995; 117(2): 253–6CrossRef Clemens P, Baron JA, Coffey D, et al. The short-term effect of nicotine chewing gum in patients with Parkinson’s disease. Psychopharmacology (Berl) 1995; 117(2): 253–6CrossRef
30.
Zurück zum Zitat Ebersbach G, Stock M, Muller J, et al. Worsening of motor performance in patients with Parkinson’s disease following transdermal nicotine administration. Mov Disord 1999; 14(6): 1011–3PubMedCrossRef Ebersbach G, Stock M, Muller J, et al. Worsening of motor performance in patients with Parkinson’s disease following transdermal nicotine administration. Mov Disord 1999; 14(6): 1011–3PubMedCrossRef
31.
Zurück zum Zitat Nishimura H, Tachibana H, Okuda B, et al. Transient worsening of Parkinson’s disease after cigarette smoking. Intern Med 1997; 36(9): 651–3PubMedCrossRef Nishimura H, Tachibana H, Okuda B, et al. Transient worsening of Parkinson’s disease after cigarette smoking. Intern Med 1997; 36(9): 651–3PubMedCrossRef
32.
Zurück zum Zitat Janson AM, Moller A. Chronic nicotine treatment counteracts nigral cell loss induced by a partial mesodiencephalic hemitransection: an analysis of the total number and mean volume of neurons and glia in substantia nigra of the male rat. Neuroscience 1993; 57(4): 931–41PubMedCrossRef Janson AM, Moller A. Chronic nicotine treatment counteracts nigral cell loss induced by a partial mesodiencephalic hemitransection: an analysis of the total number and mean volume of neurons and glia in substantia nigra of the male rat. Neuroscience 1993; 57(4): 931–41PubMedCrossRef
33.
Zurück zum Zitat Carr LA, Rowell PP. Attenuation of 1 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced neurotoxicity by tobacco smoke. Neuropharmacology 1990; 29(3): 311–4PubMedCrossRef Carr LA, Rowell PP. Attenuation of 1 -methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced neurotoxicity by tobacco smoke. Neuropharmacology 1990; 29(3): 311–4PubMedCrossRef
34.
Zurück zum Zitat Fung YK, Fiske LA, Lau YS. Chronic administration of nicotine fails to alter the MPTP-induced neurotoxicity in mice. Gen Pharmacol 1991; 22(4): 669–72PubMedCrossRef Fung YK, Fiske LA, Lau YS. Chronic administration of nicotine fails to alter the MPTP-induced neurotoxicity in mice. Gen Pharmacol 1991; 22(4): 669–72PubMedCrossRef
35.
Zurück zum Zitat Behmand RA, Harik SI. Nicotine enhances 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine neurotoxicity. J Neurochem 1992; 58(2): 776–9PubMedCrossRef Behmand RA, Harik SI. Nicotine enhances 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine neurotoxicity. J Neurochem 1992; 58(2): 776–9PubMedCrossRef
36.
Zurück zum Zitat Costa G, Abin-Carriquiry JA, Dajas F. Nicotine prevents striatal dopamine loss produced by 6-hydroxydopamine lesion in the substantia nigra (1). Brain Res 2001; 888(2): 336–42PubMedCrossRef Costa G, Abin-Carriquiry JA, Dajas F. Nicotine prevents striatal dopamine loss produced by 6-hydroxydopamine lesion in the substantia nigra (1). Brain Res 2001; 888(2): 336–42PubMedCrossRef
37.
Zurück zum Zitat Ryan RE, Ross SA, Drago J, et al. Dose-related neuroprotective effects of chronic nicotine in 6-hydroxydopamine treated rats, and loss of neuroprotection in alpha4 nicotinic receptor subunit knockout mice. Br J Pharmacol 2001; 132(8): 1650–6PubMedCrossRef Ryan RE, Ross SA, Drago J, et al. Dose-related neuroprotective effects of chronic nicotine in 6-hydroxydopamine treated rats, and loss of neuroprotection in alpha4 nicotinic receptor subunit knockout mice. Br J Pharmacol 2001; 132(8): 1650–6PubMedCrossRef
38.
Zurück zum Zitat Akaike A, Tamura Y, Yokota T, et al. Nicotine-induced protection of cultured cortical neurons against N- methyl-D-aspartate receptor-mediated glutamate cytotoxicity. Brain Res 1994; 644(2): 181–7PubMedCrossRef Akaike A, Tamura Y, Yokota T, et al. Nicotine-induced protection of cultured cortical neurons against N- methyl-D-aspartate receptor-mediated glutamate cytotoxicity. Brain Res 1994; 644(2): 181–7PubMedCrossRef
39.
Zurück zum Zitat Shimohama S, Akaike A, Kimura J. Nicotine-induced protection against glutamate cytotoxicity. Nicotinic cholinergic receptor-mediated inhibition of nitric oxide formation. Ann N Y Acad Sci 1996; 777: 356–61PubMedCrossRef Shimohama S, Akaike A, Kimura J. Nicotine-induced protection against glutamate cytotoxicity. Nicotinic cholinergic receptor-mediated inhibition of nitric oxide formation. Ann N Y Acad Sci 1996; 777: 356–61PubMedCrossRef
40.
Zurück zum Zitat Kaneko S, Maeda T, Kume T, et al. Nicotine protects cultured cortical neurons against glutamate-induced cytotoxicity via alpha7-neuronal receptors and neuronal CNS receptors. Brain Res 1997; 765(1): 135–40PubMedCrossRef Kaneko S, Maeda T, Kume T, et al. Nicotine protects cultured cortical neurons against glutamate-induced cytotoxicity via alpha7-neuronal receptors and neuronal CNS receptors. Brain Res 1997; 765(1): 135–40PubMedCrossRef
41.
Zurück zum Zitat Zamani MR, Allen YS, Owen GP, et al. Nicotine modulates the neurotoxic effect of beta-amyloid protein (25–35) in hippocampal cultures. Neuroreport 1997; 8(2): 513–7PubMedCrossRef Zamani MR, Allen YS, Owen GP, et al. Nicotine modulates the neurotoxic effect of beta-amyloid protein (25–35) in hippocampal cultures. Neuroreport 1997; 8(2): 513–7PubMedCrossRef
42.
Zurück zum Zitat Minana MD, Montoliu C, Llansola M, et al. Nicotine prevents glutamate-induced proteolysis of the microtubule- associated protein MAP-2 and glutamate neurotoxicity in primary cultures of cerebellar neurons. Neuropharmacology 1998; 37(7): 847–57PubMedCrossRef Minana MD, Montoliu C, Llansola M, et al. Nicotine prevents glutamate-induced proteolysis of the microtubule- associated protein MAP-2 and glutamate neurotoxicity in primary cultures of cerebellar neurons. Neuropharmacology 1998; 37(7): 847–57PubMedCrossRef
43.
Zurück zum Zitat Marin P, Maus M, Desagher S, et al. Nicotine protects cultured striatal neurones against N-methyl-D-aspartate receptor-mediated neurotoxicity. Neuroreport 1994; 5(15): 1977–80PubMedCrossRef Marin P, Maus M, Desagher S, et al. Nicotine protects cultured striatal neurones against N-methyl-D-aspartate receptor-mediated neurotoxicity. Neuroreport 1994; 5(15): 1977–80PubMedCrossRef
44.
Zurück zum Zitat Quik M, Jeyarasasingam G. Nicotinic receptors and Parkinson’s disease. Eur J Pharmacol 2000; 393(1–3): 223–30PubMedCrossRef Quik M, Jeyarasasingam G. Nicotinic receptors and Parkinson’s disease. Eur J Pharmacol 2000; 393(1–3): 223–30PubMedCrossRef
45.
Zurück zum Zitat Foley P, Riederer P. Influence of neurotoxins and oxidative stress on the onset and progression of Parkinson’s disease. J Neurol 2000; 247 Suppl 2: II82–94CrossRef Foley P, Riederer P. Influence of neurotoxins and oxidative stress on the onset and progression of Parkinson’s disease. J Neurol 2000; 247 Suppl 2: II82–94CrossRef
46.
Zurück zum Zitat Alexi T, Borlongan CV, Faull RL, et al. Neuroprotective strategies for basal ganglia degeneration: Parkinson’s and Huntington’s diseases. Prog Neurobiol 2000; 60(5): 409–70PubMedCrossRef Alexi T, Borlongan CV, Faull RL, et al. Neuroprotective strategies for basal ganglia degeneration: Parkinson’s and Huntington’s diseases. Prog Neurobiol 2000; 60(5): 409–70PubMedCrossRef
47.
Zurück zum Zitat Olanow CW, Arendash GW. Metals and free radicals in neu-rodegeneration. Curr Opin Neurol 1994; 7(6): 548–58PubMedCrossRef Olanow CW, Arendash GW. Metals and free radicals in neu-rodegeneration. Curr Opin Neurol 1994; 7(6): 548–58PubMedCrossRef
48.
Zurück zum Zitat Ferger B, Spratt C, Earl CD, et al. Effects of nicotine on hydroxyl free radical formation in vitro and on MPTP-induced neurotoxicity in vivo. Naunyn Schmiedebergs Arch Pharmacol 1998; 358(3): 351–9PubMedCrossRef Ferger B, Spratt C, Earl CD, et al. Effects of nicotine on hydroxyl free radical formation in vitro and on MPTP-induced neurotoxicity in vivo. Naunyn Schmiedebergs Arch Pharmacol 1998; 358(3): 351–9PubMedCrossRef
49.
Zurück zum Zitat Linert W, Bridge MH, Huber M, et al. In vitro and in vivo studies investigating possible antioxidant actions of nicotine: relevance to Parkinson’s and Alzheimer’s diseases. Biochim Biophys Acta 1999; 1454(2): 143–52PubMed Linert W, Bridge MH, Huber M, et al. In vitro and in vivo studies investigating possible antioxidant actions of nicotine: relevance to Parkinson’s and Alzheimer’s diseases. Biochim Biophys Acta 1999; 1454(2): 143–52PubMed
50.
Zurück zum Zitat Fowler JS, Volkow ND, Wang GJ, et al. Inhibition of monoamine oxidase B in the brains of smokers. Nature 1996; 379(6567): 733–6PubMedCrossRef Fowler JS, Volkow ND, Wang GJ, et al. Inhibition of monoamine oxidase B in the brains of smokers. Nature 1996; 379(6567): 733–6PubMedCrossRef
51.
Zurück zum Zitat Maggio R, Riva M, Vaglini F, et al. Nicotine prevents experimental parkinsonism in rodents and induces striatal increase of neurotrophic factors. J Neurochem 1998; 71(6): 2439–46PubMedCrossRef Maggio R, Riva M, Vaglini F, et al. Nicotine prevents experimental parkinsonism in rodents and induces striatal increase of neurotrophic factors. J Neurochem 1998; 71(6): 2439–46PubMedCrossRef
52.
Zurück zum Zitat Belluardo N, Blum M, Mudo G, et al. Acute intermittent nicotine treatment produces regional increases of basic fibroblast growth factor messenger RNA and protein in the tel- and diencephalon of the rat. Neuroscience 1998; 83(3): 723–40PubMedCrossRef Belluardo N, Blum M, Mudo G, et al. Acute intermittent nicotine treatment produces regional increases of basic fibroblast growth factor messenger RNA and protein in the tel- and diencephalon of the rat. Neuroscience 1998; 83(3): 723–40PubMedCrossRef
53.
Zurück zum Zitat Bean AJ, Elde R, Cao YH, et al. Expression of acidic and basic fibroblast growth factors in the substantia nigra of rat, monkey, and human. Proc Natl Acad Sci U S A 1991; 88(22): 10237–41PubMedCrossRef Bean AJ, Elde R, Cao YH, et al. Expression of acidic and basic fibroblast growth factors in the substantia nigra of rat, monkey, and human. Proc Natl Acad Sci U S A 1991; 88(22): 10237–41PubMedCrossRef
54.
Zurück zum Zitat Otto D, Unsicker K. Basic FGF reverses chemical and morphological deficits in the nigrostriatal system of MPTP-treated mice. J Neurosci 1990; 10(6): 1912–21PubMed Otto D, Unsicker K. Basic FGF reverses chemical and morphological deficits in the nigrostriatal system of MPTP-treated mice. J Neurosci 1990; 10(6): 1912–21PubMed
55.
Zurück zum Zitat Tooyama I, Kawamata T, Walker D, et al. Loss of basic fibroblast growth factor in substantia nigra neurons in Parkinson’s disease [published erratum in Neurology 1993 Apr; 43 (4): 815-6]. Neurology 1993; 43(2): 372–6PubMedCrossRef Tooyama I, Kawamata T, Walker D, et al. Loss of basic fibroblast growth factor in substantia nigra neurons in Parkinson’s disease [published erratum in Neurology 1993 Apr; 43 (4): 815-6]. Neurology 1993; 43(2): 372–6PubMedCrossRef
56.
Zurück zum Zitat Belluardo N, Mudo G, Blum M, et al. The nicotinic acetylcholine receptor agonist (+/-)-epibatidine increases FGF-2 mRNA and protein levels in the rat brain. Brain Res Mol Brain Res 1999; 74(1–2): 98–110PubMedCrossRef Belluardo N, Mudo G, Blum M, et al. The nicotinic acetylcholine receptor agonist (+/-)-epibatidine increases FGF-2 mRNA and protein levels in the rat brain. Brain Res Mol Brain Res 1999; 74(1–2): 98–110PubMedCrossRef
57.
Zurück zum Zitat Linville DG, Arneric SP. Cortical cerebral blood flow governed by the basal forebrain: age-related impairments. Neurobiol Aging 1991; 12(5): 503–10PubMedCrossRef Linville DG, Arneric SP. Cortical cerebral blood flow governed by the basal forebrain: age-related impairments. Neurobiol Aging 1991; 12(5): 503–10PubMedCrossRef
58.
Zurück zum Zitat Linville DG, Williams S, Raszkiewicz JL, et al. Nicotinic agonists modulate basal forebrain control of cortical cerebral blood flow in anesthetized rats. J Pharmacol Exp Ther 1993; 267(1): 440–8PubMed Linville DG, Williams S, Raszkiewicz JL, et al. Nicotinic agonists modulate basal forebrain control of cortical cerebral blood flow in anesthetized rats. J Pharmacol Exp Ther 1993; 267(1): 440–8PubMed
59.
Zurück zum Zitat Uchida S, Kagitani F, Nakayama H, et al. Effect of stimulation of nicotinic cholinergic receptors on cortical cerebral blood flow and changes in the effect during aging in anesthetized rats. Neurosci Lett 1997; 228(3): 203–6PubMedCrossRef Uchida S, Kagitani F, Nakayama H, et al. Effect of stimulation of nicotinic cholinergic receptors on cortical cerebral blood flow and changes in the effect during aging in anesthetized rats. Neurosci Lett 1997; 228(3): 203–6PubMedCrossRef
60.
Zurück zum Zitat Marenco T, Bernstein S, Cumming P, et al. Effects of nicotine and chlorisondamine on cerebral glucose utilization in immobilized and freely-moving rats. Br J Pharmacol 2000; 129(1): 147–55PubMedCrossRef Marenco T, Bernstein S, Cumming P, et al. Effects of nicotine and chlorisondamine on cerebral glucose utilization in immobilized and freely-moving rats. Br J Pharmacol 2000; 129(1): 147–55PubMedCrossRef
61.
Zurück zum Zitat Grunwald F, Schrock H, Kuschinsky W. The effect of an acute nicotine infusion on the local cerebral glucose utilization of the awake rat. Klin Wochenschr 1988; 66(Suppl. 11): 37–41PubMed Grunwald F, Schrock H, Kuschinsky W. The effect of an acute nicotine infusion on the local cerebral glucose utilization of the awake rat. Klin Wochenschr 1988; 66(Suppl. 11): 37–41PubMed
62.
Zurück zum Zitat Morioka C, Kondo H, Akashi K, et al. The continuous and simultaneous blood flow velocity measurement of four cerebral vessels and a peripheral vessel during cigarette smoking. Psychopharmacology (Berl) 1997; 131(3): 220–9CrossRef Morioka C, Kondo H, Akashi K, et al. The continuous and simultaneous blood flow velocity measurement of four cerebral vessels and a peripheral vessel during cigarette smoking. Psychopharmacology (Berl) 1997; 131(3): 220–9CrossRef
63.
Zurück zum Zitat Boyajian RA, Otis SM. Acute effects of smoking on humancerebral blood flow: a transcranial Doppler ultrasonography study. J Neuroimaging 2000; 10(4): 204–8PubMed Boyajian RA, Otis SM. Acute effects of smoking on humancerebral blood flow: a transcranial Doppler ultrasonography study. J Neuroimaging 2000; 10(4): 204–8PubMed
64.
Zurück zum Zitat Domino EF, Minoshima S, Guthrie S, et al. Nicotine effects on regional cerebral blood flow in awake, resting tobacco smokers. Synapse 2000; 38(3): 313–21PubMedCrossRef Domino EF, Minoshima S, Guthrie S, et al. Nicotine effects on regional cerebral blood flow in awake, resting tobacco smokers. Synapse 2000; 38(3): 313–21PubMedCrossRef
65.
Zurück zum Zitat Nehlig A, Daval JL, Debry G. Caffeine and the cental nervous system: mechanisms of action, biochemical, metabolic and psychostimulant effects. Brain Res Brain Res Rev 1992; 17(2): 139–70PubMedCrossRef Nehlig A, Daval JL, Debry G. Caffeine and the cental nervous system: mechanisms of action, biochemical, metabolic and psychostimulant effects. Brain Res Brain Res Rev 1992; 17(2): 139–70PubMedCrossRef
66.
Zurück zum Zitat Fredholm BB, Battig K, Holmen J, et al. Actions of caffeine in the brain with special reference to factors that contribute to its widespread use. Pharmacol Rev 1999; 51(1): 83–133PubMed Fredholm BB, Battig K, Holmen J, et al. Actions of caffeine in the brain with special reference to factors that contribute to its widespread use. Pharmacol Rev 1999; 51(1): 83–133PubMed
67.
Zurück zum Zitat Fuxe K, Ungerstedt U. Action of caffeine and theophyllamine on supersensitive dopamine receptors: considerable enhancement of receptor response to treatment with DOPA and dopamine receptor agonists. Med Biol 1974; 52(1): 48–54PubMed Fuxe K, Ungerstedt U. Action of caffeine and theophyllamine on supersensitive dopamine receptors: considerable enhancement of receptor response to treatment with DOPA and dopamine receptor agonists. Med Biol 1974; 52(1): 48–54PubMed
68.
Zurück zum Zitat Kartzinel R, Shoulson I, Calne DB. Studies with bromocriptine: III. Concomitant administration of caffeine to patients with idiopathic parkinsonism. Neurology 1976; 26(8): 741–3PubMedCrossRef Kartzinel R, Shoulson I, Calne DB. Studies with bromocriptine: III. Concomitant administration of caffeine to patients with idiopathic parkinsonism. Neurology 1976; 26(8): 741–3PubMedCrossRef
69.
Zurück zum Zitat Shoulson I, Chase T. Caffeine and the antiparkinsonian response to levodopa or piribedil. Neurology 1975; 25(8): 722–4PubMedCrossRef Shoulson I, Chase T. Caffeine and the antiparkinsonian response to levodopa or piribedil. Neurology 1975; 25(8): 722–4PubMedCrossRef
70.
Zurück zum Zitat Fall PA, Fredrikson M, Axelson O, et al. Nutritional and occupational factors influencing the risk of Parkinson’s disease: a case-control study in southeastern Sweden. Mov Disord 1999; 14(1): 28–37PubMedCrossRef Fall PA, Fredrikson M, Axelson O, et al. Nutritional and occupational factors influencing the risk of Parkinson’s disease: a case-control study in southeastern Sweden. Mov Disord 1999; 14(1): 28–37PubMedCrossRef
71.
Zurück zum Zitat Hellenbrand W, Seidler A, Boeing H, et al. Diet and Parkinson’s disease. I: a possible role for the past intake of specific foods and food groups. Results from a self-administered foodfrequency questionnaire in a case-control study. Neurology 1996; 47(3): 636–43PubMedCrossRef Hellenbrand W, Seidler A, Boeing H, et al. Diet and Parkinson’s disease. I: a possible role for the past intake of specific foods and food groups. Results from a self-administered foodfrequency questionnaire in a case-control study. Neurology 1996; 47(3): 636–43PubMedCrossRef
72.
Zurück zum Zitat Jimenez-Jimenez FJ, Mateo D, Gimenez-Roldan S. Premorbid smoking, alcohol consumption, and coffee drinking habits in Parkinson’s disease: a case-control study. Mov Disord 1992; 7(4): 339–44PubMedCrossRef Jimenez-Jimenez FJ, Mateo D, Gimenez-Roldan S. Premorbid smoking, alcohol consumption, and coffee drinking habits in Parkinson’s disease: a case-control study. Mov Disord 1992; 7(4): 339–44PubMedCrossRef
73.
Zurück zum Zitat Ross GW, Abbott RD, Petrovitch H, et al. Association of coffee and caffeine intake with the risk of Parkinson disease. JAMA 2000; 283(20): 2674–9PubMedCrossRef Ross GW, Abbott RD, Petrovitch H, et al. Association of coffee and caffeine intake with the risk of Parkinson disease. JAMA 2000; 283(20): 2674–9PubMedCrossRef
74.
Zurück zum Zitat Ascherio A, Zhang SM, Hernan MA, et al. Prospective study of caffeine consumption and risk of Parkinson’s disease in men and women. Ann Neurol 2001; 50(1): 56–63PubMedCrossRef Ascherio A, Zhang SM, Hernan MA, et al. Prospective study of caffeine consumption and risk of Parkinson’s disease in men and women. Ann Neurol 2001; 50(1): 56–63PubMedCrossRef
75.
Zurück zum Zitat Ferre S, Fredholm BB, Morelli M, et al. Adenosine-dopamine receptor-receptor interactions as an integrative mechanism in the basal ganglia. Trends Neurosci 1997; 20(10): 482–7PubMedCrossRef Ferre S, Fredholm BB, Morelli M, et al. Adenosine-dopamine receptor-receptor interactions as an integrative mechanism in the basal ganglia. Trends Neurosci 1997; 20(10): 482–7PubMedCrossRef
76.
Zurück zum Zitat Svenningsson P, Le Moine C, Fisone G, et al. Distribution, biochemistry and function of striatal adenosine A2A receptors. Prog Neurobiol 1999; 59(4): 355–96PubMedCrossRef Svenningsson P, Le Moine C, Fisone G, et al. Distribution, biochemistry and function of striatal adenosine A2A receptors. Prog Neurobiol 1999; 59(4): 355–96PubMedCrossRef
77.
Zurück zum Zitat Mally J, Stone TW. Potential of adenosine A2A receptor antagonists in the treatment of movement disorders. CNS Drugs 1998; 10(5): 311–20CrossRef Mally J, Stone TW. Potential of adenosine A2A receptor antagonists in the treatment of movement disorders. CNS Drugs 1998; 10(5): 311–20CrossRef
78.
Zurück zum Zitat Ongini E, Fredholm BB. Pharmacology of adenosine A2A receptors. Trends Pharmacol Sci 1996; 17(10): 364–72PubMed Ongini E, Fredholm BB. Pharmacology of adenosine A2A receptors. Trends Pharmacol Sci 1996; 17(10): 364–72PubMed
79.
Zurück zum Zitat Ferre S, von Euler G, Johansson B, et al. Stimulation of highaffinity adenosine A2 receptors decreases the affinity of dopamine D2 receptors in rat striatal membranes. Proc Natl Acad Sci U S A 1991; 88(16): 7238–41PubMedCrossRef Ferre S, von Euler G, Johansson B, et al. Stimulation of highaffinity adenosine A2 receptors decreases the affinity of dopamine D2 receptors in rat striatal membranes. Proc Natl Acad Sci U S A 1991; 88(16): 7238–41PubMedCrossRef
80.
Zurück zum Zitat Durcan MJ, Morgan PF. Evidence for adenosine A2 receptor involvement in the hypomobility effects of adenosine analogues in mice. Eur J Pharmacol 1989; 168(3): 285–90PubMedCrossRef Durcan MJ, Morgan PF. Evidence for adenosine A2 receptor involvement in the hypomobility effects of adenosine analogues in mice. Eur J Pharmacol 1989; 168(3): 285–90PubMedCrossRef
81.
Zurück zum Zitat Barraco RA, Martens KA, Parizon M, et al. Adenosine A2a receptors in the nucleus accumbens mediate locomotor depression [published erratum in Brain Res Bull 1993; 32 (2): 205]. Brain Res Bull 1993; 31(3–4): 397–404PubMedCrossRef Barraco RA, Martens KA, Parizon M, et al. Adenosine A2a receptors in the nucleus accumbens mediate locomotor depression [published erratum in Brain Res Bull 1993; 32 (2): 205]. Brain Res Bull 1993; 31(3–4): 397–404PubMedCrossRef
82.
Zurück zum Zitat Popoli P, Caporali MG, Scotti de Carolis A. Akinesia due to catecholamine depletion in mice is prevented by caffeine. Further evidence for an involvement of adenosinergic system in the control of motility. J Pharm Pharmacol 1991; 43(4): 280–1PubMedCrossRef Popoli P, Caporali MG, Scotti de Carolis A. Akinesia due to catecholamine depletion in mice is prevented by caffeine. Further evidence for an involvement of adenosinergic system in the control of motility. J Pharm Pharmacol 1991; 43(4): 280–1PubMedCrossRef
83.
Zurück zum Zitat Shiozaki S, Ichikawa S, Nakamura J, et al. Actions of adenosine A2A receptor antagonist KW-6002 on drug-induced catalepsy and hypokinesia caused by reserpine or MPTP. Psychopharmacology (Berl) 1999; 147(1): 90–5CrossRef Shiozaki S, Ichikawa S, Nakamura J, et al. Actions of adenosine A2A receptor antagonist KW-6002 on drug-induced catalepsy and hypokinesia caused by reserpine or MPTP. Psychopharmacology (Berl) 1999; 147(1): 90–5CrossRef
84.
Zurück zum Zitat Kuwana Y, Shiozaki S, Kanda T, et al. Antiparkinsonian activity of adenosine A2A antagonists in experimental models. Adv Neurol 1999; 80: 121–3PubMed Kuwana Y, Shiozaki S, Kanda T, et al. Antiparkinsonian activity of adenosine A2A antagonists in experimental models. Adv Neurol 1999; 80: 121–3PubMed
85.
Zurück zum Zitat Kanda T, Tashiro T, Kuwana Y, et al. Adenosine A2A receptors modify motor function in MPTP-treated common marmosets. Neuroreport 1998; 9(12): 2857–60PubMedCrossRef Kanda T, Tashiro T, Kuwana Y, et al. Adenosine A2A receptors modify motor function in MPTP-treated common marmosets. Neuroreport 1998; 9(12): 2857–60PubMedCrossRef
86.
Zurück zum Zitat Kanda T, Jackson MJ, Smith LA, et al. Adenosine A2A antagonist: a novel antiparkinsonian agent that does not provoke dyskinesia in parkinsonian monkeys. Ann Neurol 1998; 43(4): 507–13PubMedCrossRef Kanda T, Jackson MJ, Smith LA, et al. Adenosine A2A antagonist: a novel antiparkinsonian agent that does not provoke dyskinesia in parkinsonian monkeys. Ann Neurol 1998; 43(4): 507–13PubMedCrossRef
87.
Zurück zum Zitat Mally J, Stone TW. The effect of theophylline on parkinsonian symptoms. J Pharm Pharmacol 1994; 46(6): 515–7PubMedCrossRef Mally J, Stone TW. The effect of theophylline on parkinsonian symptoms. J Pharm Pharmacol 1994; 46(6): 515–7PubMedCrossRef
88.
Zurück zum Zitat Kostic VS, Svetel M, Sternic N, et al. Theophylline increases “on” time in advanced parkinsonian patients. Neurology 1999; 52(9): 1916PubMedCrossRef Kostic VS, Svetel M, Sternic N, et al. Theophylline increases “on” time in advanced parkinsonian patients. Neurology 1999; 52(9): 1916PubMedCrossRef
89.
Zurück zum Zitat Gao Y, Phillis JW. CGS 15943, an adenosine A2 receptor antagonist, reduces cerebral ischemic injury in the Mongolian gerbil. Life Sci 1994; 55(3): L61–5CrossRef Gao Y, Phillis JW. CGS 15943, an adenosine A2 receptor antagonist, reduces cerebral ischemic injury in the Mongolian gerbil. Life Sci 1994; 55(3): L61–5CrossRef
90.
Zurück zum Zitat Monopoli A, Casati C, Lozza G, et al. Cardiovascular pharmacology of the A2A adenosine receptor antagonist, SCH 58261, in the rat. J Pharmacol Exp Ther 1998; 285(1): 9–15PubMed Monopoli A, Casati C, Lozza G, et al. Cardiovascular pharmacology of the A2A adenosine receptor antagonist, SCH 58261, in the rat. J Pharmacol Exp Ther 1998; 285(1): 9–15PubMed
91.
Zurück zum Zitat Bona E, Aden U, Gilland E, et al. Neonatal cerebral hypoxiaischemia: the effect of adenosine receptor antagonists. Neuropharmacology 1997; 36(9): 1327–38PubMedCrossRef Bona E, Aden U, Gilland E, et al. Neonatal cerebral hypoxiaischemia: the effect of adenosine receptor antagonists. Neuropharmacology 1997; 36(9): 1327–38PubMedCrossRef
92.
Zurück zum Zitat Chen JF, Huang Z, Ma J, et al. A(2A) adenosine receptor deficiency attenuates brain injury induced by transient focal ischemia in mice. J Neurosci 1999; 19(21): 9192–200PubMed Chen JF, Huang Z, Ma J, et al. A(2A) adenosine receptor deficiency attenuates brain injury induced by transient focal ischemia in mice. J Neurosci 1999; 19(21): 9192–200PubMed
93.
Zurück zum Zitat Ongini E, Adami M, Ferri C, et al. Adenosine A2A receptors and neuroprotection. Ann N Y Acad Sci 1997; 825: 30–48PubMedCrossRef Ongini E, Adami M, Ferri C, et al. Adenosine A2A receptors and neuroprotection. Ann N Y Acad Sci 1997; 825: 30–48PubMedCrossRef
94.
Zurück zum Zitat Chen JF, Xu K, Petzer JP, et al. Neuroprotection by caffeine and A(2A) adenosine receptor inactivation in a model of Parkinson’s disease. J Neurosci 2001; 21(10): RC143PubMed Chen JF, Xu K, Petzer JP, et al. Neuroprotection by caffeine and A(2A) adenosine receptor inactivation in a model of Parkinson’s disease. J Neurosci 2001; 21(10): RC143PubMed
95.
Zurück zum Zitat Iida M, Miyazaki I, Tanaka K, et al. Dopamine D2 receptor-mediated antioxidant and neuroprotective effects of ropinirole, a dopamine agonist. Brain Res 1999; 838(1–2): 51–9PubMedCrossRef Iida M, Miyazaki I, Tanaka K, et al. Dopamine D2 receptor-mediated antioxidant and neuroprotective effects of ropinirole, a dopamine agonist. Brain Res 1999; 838(1–2): 51–9PubMedCrossRef
96.
Zurück zum Zitat Marek KL, Seibyl JP, Zoghbi SS, et al. [123I] beta-CIT/SPECT imaging demonstrates bilateral loss of dopamine transporters in hemi-Parkinson’s disease. Neurology 1996; 46(1): 231–7PubMedCrossRef Marek KL, Seibyl JP, Zoghbi SS, et al. [123I] beta-CIT/SPECT imaging demonstrates bilateral loss of dopamine transporters in hemi-Parkinson’s disease. Neurology 1996; 46(1): 231–7PubMedCrossRef
97.
Zurück zum Zitat Morrish PK, Sawle GV, Brooks DJ. Clinical and [18F] dopa PET findings in early Parkinson’s disease. J Neurol Neurosurg Psychiatry 1995; 59(6): 597–600PubMedCrossRef Morrish PK, Sawle GV, Brooks DJ. Clinical and [18F] dopa PET findings in early Parkinson’s disease. J Neurol Neurosurg Psychiatry 1995; 59(6): 597–600PubMedCrossRef
Metadaten
Titel
Current Evidence for Neuroprotective Effects of Nicotine and Caffeine Against Parkinson’s Disease
verfasst von
G. Webster Ross
Helen Petrovitch
Publikationsdatum
01.11.2001
Verlag
Springer International Publishing
Erschienen in
Drugs & Aging / Ausgabe 11/2001
Print ISSN: 1170-229X
Elektronische ISSN: 1179-1969
DOI
https://doi.org/10.2165/00002512-200118110-00001

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