Neuroprotection in Parkinson’s disease: love story or mission impossible?

References

• Langston JVV, Ballard PA, Tetrud JVV, Irwin I. Chronic parkinsonism in humans due to a product of meperidine analog synthesis. Science 219,979–980 (1983).
   PubMed Web of Science ®Google Scholar
• Olanow CW, Tatton WG. Etiology and pathogenesis of Parkinson's disease. Ann. Rev Neurosci. 22,123–144 (1999).
   PubMed Web of Science ®Google Scholar
• ••Comprehensive review of theetiopathogenesis of PD.
   Google Scholar
• Gasser T. Is Parkinson's disease an inherited condition?. Adv. Neurol. 80,143–152 (1999).
   Google Scholar
• ••Excellent review of the genetic basis ofPD.
   Google Scholar
• Goedert M. Alpha-synuclein and neurodegenerative diseases. Nat. Rev Neurosci. 2,492–501 (2001).
   PubMed Web of Science ®Google Scholar
• Shimura H, Scholssmacher MG, Hattori N et al. Ubiquitination of a new form of a-syn by parkin from human brain: implications for Parkinson's disease. Science 293,263–269 (2001).
   Google Scholar
• Tanner CM, Aston DA. Epidemiology of Parkinson's disease and akinetic syndromes. CUIT: Opin. Neurol. 13,427–430 (2000).
   Google Scholar
• Betarbet R, Sherer TB, MacKenzie G, Garda-Osuna M, Panov AV, Greenamyre JT. Chronic pesticide exposure reproduces features of Parkinson's disease. Nat. Neurosci. 3,1301–1306 (2000).
   Google Scholar
• ••First description of rotenone-inducedparkinsonism in rats with remarkable pathological similarities with PD. This paper reinforces the role of environmental toxins in the origin of PD.
   Google Scholar
• Giasson BI, Lee VM. A new link between pesticides and Parkinson's disease. Nat. Neurosci. 3,1227–1228 (2000).
   PubMedGoogle Scholar
• Sveinbjornsdottir S, Hicks AD, Jonsson T et al. Familial aggregation of Parkinson's disease in Iceland. N Engl. J Med. 343, 2239–2244 (2000).
   Google Scholar
• Johnson WG. Late-onset neurodegenerative diseases-the role of protein insolubility. J Anat. 196,609–616 (2000).
   Google Scholar
• Dunnett SB, Björklund A. Prospects for new restorative and neuroprotective treatments in Parkinson's disease. Nature 399(Suppl.), A32—A39 (1999).
   Google Scholar
• Sherman MY, Goldberg AL. Cellular defenses against unfolded proteins: A cell biologist thinks about neurodegenerative diseases. Neurone 29,15–32 (2001).
   PubMed Web of Science ®Google Scholar
• ••Excellent review about the role ofunfolded proteins in the origin of neurodegenerative diseases.
   Google Scholar
• Kopito RR. Aggresomes, inclusion bodies and protein aggregation. Trends Cell Biol. 10,524–530 (2000).
   PubMed Web of Science ®Google Scholar
• McNaught KS, Olanow CW, Halliwell B, Isacson 0, Jenner P Failure of the ubiquitin-proteasome system in Parkinson's disease. Nat. Rev Neurosci. 2,589-594 (2001).
   Google Scholar
• ••Review of the role of the UPS in thepathogenesis of PD.
   Google Scholar
• Chung KKK, Dawson VL, Dawson TM. The role of the ubiquitin-proteasomal pathway in Parkinson's disease and other neurodegenerative disorders. Trends Neurosci. 24 (Suppl.), S7—S14 (2001).
   Google Scholar
• ••Review of the role of UPS in thepathogenesis of PD.
   Google Scholar
• McNaught KP, Jenner P Proteasomal function is impaired in substantia nigra in Parkinson's disease. Neurosci. Lett. 297, 191–194 (2001).
   PubMed Web of Science ®Google Scholar
• ••First report of the failure of the UPS insporadic PD.
   Google Scholar
• Schapira AHV, Cooper JM, Dexter D, Clark JB, Jenner P, Marsden CD. Mitochondrial complex I deficiency in Parkinson's disease. J Neurochem. 54,823–827 (1990).
   PubMed Web of Science ®Google Scholar
• Giasson BI, Duda JE, Murray IVJ et al. Oxidative damage linked to neurodegeneration by selective a-synuclein nitration in synucleinopathy lesions. Science 290,985–989 (2000).
   PubMed Web of Science ®Google Scholar
• Tofaris GK, Layfield R, Spillantini MG. A-synuclein metabolism and aggregation is linked to ubiquitin-independent degradation by the proteasome. FEBS Lett. 509,22–26 (2001).
   Google Scholar
• Clarke G, Collins RA, Leavitt BR et al. A one hit model of cell death in inherited neuronal degenerations. Nature 406,195–199 (2000).
   PubMed Web of Science ®Google Scholar
• Kanda S, Bishop JF, Eglitis MA, Yang Y, Mouradian MM. Enhanced vulnerability to oxidative stress by a-synuclein mutations and c-terminal truncation. Neuroscience 97, 279–284 (2000).
   Google Scholar
• Tanner CM, Ottman R, Goldman SM et al. Parkinson's disease in twins: an etiologic study. JAMA 281,341–346 (1999).
   PubMed Web of Science ®Google Scholar
• Scott WK, Nance MA, Watts RL et al. Complete genomic screen in PD: Evidence for multiple genes. JAMA 286,2239–2244 (2001).
   PubMed Web of Science ®Google Scholar
• Armstrong RJE, Barker RA. Neurodegeneration: a failure of neuroregeneration? Lancet 358,1174–1176 (2001).
   PubMed Web of Science ®Google Scholar
• Green DR, Reed JC. Mitochondria and apoptosis. Science 281,1309–1312 (1998).
   PubMed Web of Science ®Google Scholar
• Tatton WG, Olanow CW Apoptosis in neurodegenerative diseases: the role of mitochondria. Biochimica et Biophysica Acta 1410,195–213 (1999).
   PubMed Web of Science ®Google Scholar
• •Comprehensive review of the role of mitochondria and apoptosis in neuronal death.
   Google Scholar
• Jellinger KA, Stadelmann C. Mechanisms of cell death in neurodegenerative disorders. J Neural. Transm. 59 (Suppl.), 95–114 (2000).
   Google Scholar
• Shoulson I. Protective therapy for Parkinson's disease. In 'Movement Disorders 3: Marsden CD, Fahn S (Eds.) Butterworth, London, UK 167–180 (1994).
   Google Scholar
• Schapira AHV. Science, medicine and the future: Parkinson's disease. Br. Med. J. 338, 311–314 (1999).
   Google Scholar
• Fearnley JM, Lees AJ. Ageing and Parkinson's disease: substantia nigra regional selectivity. Brain 114,2283–2291 (1991).
   PubMed Web of Science ®Google Scholar
• Morrish PK, Rakshi JS, Sawle GW, Brooks DJ. Measuring the rate of progression and estimating the preclinical period of Parkinson's disease with 18Fdopa PET. J Neurol. Neurosurg. Psychiatry 64,314–319 (1998).
   Google Scholar
• Piccini P, Burn DJ, Caravolo R, Maraganore D, Brooks DJ. The role of inheritance in sporadic Parkinson's disease: evidence from a longitudinal study of dopaminergic function in twins. Ann. Neurol. 45,577-582 (1999).
   Google Scholar
• Kruger R, Kuhn W, Leenders KL et al. Familial parkinsonism with synuclein pathology: Clinical and PET studies of A3OP mutation carriers. Neurology 56 1355–1362 (2001).
   PubMedGoogle Scholar
• Montgomery EB, Jr., Baker KB, Lyons K, Koller WC. Abnormal performance on the PD test battery by asymptomatic first-degree relatives. Neurology 52,757–762 (1999).
   Google Scholar
• Deng Y, Rajput A, Miyashita H, Rajput A, Birdi S, Hornykiewicz 0. Increased concentrations of a novel compound, 1-acetyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline, in parkinsonian brains. Ann. Neurol. 50 (Suppl.), S20 (2001).
   Google Scholar
• Morrish PK, Rakshi JS, Brooks DJ. Can the neuroprotective efficacy of an agent ever be conclusively proven? Eur. j Neurol. 4\(Suppl. 3), S19—S24 (1997).
   Google Scholar
• Zetusky WJ, Jankovic J, Pirozzolo FJ. The heterogeneity of Parkinson's disease: clinical and prognostic implications. Neurology 35 522–526 (1985).
   PubMed Web of Science ®Google Scholar
• Stoessl AJ. Assessing the integrity of the dopamine system in Parkinson's disease: How best to do it? Mov. Disord. 16, 804–806 (2001).
   Google Scholar
• Yee RE, Irwin I, Milonas C etal. Novel observations with FDOPA-PET imaging after early nigrostriatal damage. Mov. Disord. 16, 838–848 (2001).
   Google Scholar
• Snow BJ, Tooyama I, McGeer EG eta]. Human positron emission tomographic 18Ffluorodopa studies correlate with dopamine cell counts and levels. Ann. Neurol. 34, 324–330 (1993).
   Google Scholar
• Booij J, Tissingh G, Boer GJ et al. 123IFP- CIT SPECT shows a pronounced decline of striatal dopamine transporter labelling in early and advanced Parkinson's disease. Neurol. Neurosurg. Psychiatry 62, 133–140 (1997).
   Google Scholar
• Olanow CW Attempts to obtain neuroprotection in Parkinson's disease. Neurology 49\(Suppl. 1), S26—S33 (1997).
   Google Scholar
• Marsden CD, Olanow CW. The causes of Parkinson's disease are being unravelled and rational neuroprotective therapy is close to reality. Ann. Neurol. 44\(Suppl. 1), S189—S196 (1998).
   Google Scholar
• ••Excellent review of the possibleneuroprotective strategies in PD.
   Google Scholar
• Burns RS, Markey SP, Phillips JM, Chiueh CC. The neurotoxicity of MPTP in the monkey and man. Can. j Neurol. Sci. 11, 166–168 (1984).
   PubMedGoogle Scholar
• Wadia JS, Chaimers-Redman RME, Ju WJH eta]. Mitochondrial membrane potential and nuclear changes in apoptosis caused by serum and nerve growth factor withdrawal: Time course and modification by (-) deprenyl. j Neurosci. 18, 932–947 (1998).
   PubMed Web of Science ®Google Scholar
• Naoi M, Maruyama W Future of neuroprotection in Parkinson's disease. Parkinsonism ReL Disord. 8, 139–145 (2001).
   PubMed Web of Science ®Google Scholar
• Waldmeier PC, Spooren WPJM, Hengerer B. CGP 3466 protects dopaminergic neurons in lesion models of Parkinson's disease. Arch. PharmacoL 362, 526–537 (2000).
   Google Scholar
• The Parkinson Study Group. Effect of tocopherol and deprenyl on the progression of disability in early Parkinson's disease. N EngL Med. 328, 176–183 (1993).
   PubMed Web of Science ®Google Scholar
• •• First, large-scale study conducted to demonstrate the potential neuroprotective effec of selegiline in PD.
   Google Scholar
• Effect of lazabemide on the progression of disability in early Parkinson's disease. Ann. Neurol. 40, 99–107 (1996).
   Google Scholar
• Olanow CW, Fahn S, Langston JVV, Goldbold J. Selegiline and mortality in Parkinson's disease. Ann. Neurol. 40, 841–845 (1996).
   Google Scholar
• Langston JVV, Tanner CM. Selegiline and Parkinson's disease. It's &Id vu-again. Neurology 55, 1770–1771 (2000).
   Google Scholar
• Olanow CW, Jenner P, Brooks DJ. Dopamine agonists and neuroprotection in Parkinson's disease. Ann. Neurol. 44\(Suppl. 1), S167-5174 (1998).
   Google Scholar
• Gassen M, Gross A, Youdim MBH. Apomorphine, a dopamine agonist with remarkable anti-oxidant and cytoprotective properties. Adv. Neurol. 80, 297–302 (1999).
   Google Scholar
• Kitamura Y, Kosaka T, Kakimura JI eta]. Protective effects of the antiparkinsonian drugs talipexole and pramipexole against MPTP apoptotic death in human neuroblastoma SH-SY5Y cells. MoL Pharmacol. 54, 1046–1054 (1998)
   Google Scholar
• Carvey PM, McGuire SO, Ling ZD. Neuroprotective effects of D3 dopamine receptor agonists. Parkinsonism Rel. Disord. 7, 213–223 (2001).
   Google Scholar
• Agid Y. Levodopa. Is toxicity a myth?. Neurology 50, 858–863 (1998).
   Google Scholar
• Jenner P, Brin ME Levodopa neurotoxicity. Experimental studies versus clinical relevance. Neurology50 (Suppl. 6), S39—S43 (1998).
   Google Scholar
• Murer MG, Dziewczapolski G, Menalled LB eta]. Chronic levodopa is not toxic for remaining dopamine neurons but instead promotes their recovery, in rats with moderate nigrostriatal lesions. Ann. Neurol. 43, 561–575 (1998).
   Google Scholar
• Fahn S. Parkinson's disease, the effect of levodopa and the ELLDOPA trial. Arch. Neurol. 56, 529–535 (1999).
   Google Scholar
• Linazasoro G. Mecanismos glutamatérgicos en la enfermedad de Parkinson. Neurdogia (Suppl. 6), 21–30 (2000).
   Google Scholar
• Albin RL, Greenamyre JT. Alternative excitotoxic hypothesis. Neurology 42 733–738 (1992).
   PubMed Web of Science ®Google Scholar
• Marey Semper I, Gelman M, Levi-Strauss M. A selective toxicity toward cultured mesencephalic dopaminergic neurons is induced by the synergistic effects of energy metabolism impairment and NMDA receptor activation. j Neurosci. 15, 5912–5918 (1995).
   Google Scholar
• Beal ME Excitotoxicity and nitric oxide in Parkinson's disease pathogenesis. Ann. Neurol. 44\(Suppl. 1), 110–114 (1998).
   Google Scholar
• •Review of the role of NO and glutamic acid in the pathogenesis of PD.
   Google Scholar
• Du Y, Ma Z, Lin S et al. Minocycline prevents nigrostriatal dopaminergic neurodegeneration in the MPTP model of Parkinson's disease. Proc. Natl Acad. Sci. USA 98, 14669–14674 (2001).
   PubMed Web of Science ®Google Scholar
• Rodriguez MC, Obeso JA, Olanow CW. Subthalamic nucleus-mediated excitotoxicity in Parkinson's disease. Ann. Neurol. 44\(Suppl. 1), S175—S188 (1998).
   Google Scholar
• Piallat B, Benazzouz A, Benabid AL. Subthalamic nucleus lesion in rats prevents dopaminergic nigral neurone degeneration after striatal 6–0HDA injection: behavioural and immunohistochemical studies. Eur. j Neurosci. 8, 1408–1414 (1996).
   Google Scholar
• Kreiss DS, Mastropietro CW, Rawji SS, Walters JR. The response of subthalamic nucleus neurons to dopamine receptor stimulation in a rodent model of Parkinson's disease. j Neurosci. 17, 6807–6819 (1997).
   PubMed Web of Science ®Google Scholar
• Ruiz Ortega JA, Linazasoro G, Ugedo L. Effects of systemic and intrasubthalamic dopaminergic drugs administration on the neurophysiological activity of the subthalamic nucleus of rats with moderate and severe lesions of the nigrostriatal pathway. (In preparation).
   Google Scholar
• Windels F, Bruet N, Poupard A, Savasta M. High frequency stimulation of the subthalamic nucleus increases extracellular contents of glutamate in substantia nigra and external pallidum. Mov. Disord. 15 (Suppl. 3), 15 (2000).
   Google Scholar
• Uiti RJ, Rajput AH, Ahlskog JE. Amantadine treatment is an independent predictor of improved survival in Parkinson's disease. Neurology 46, 1551–1556 (1996).
   Google Scholar
• Jones-Humble SA, Morgan PF, Cooper BR. The novel anticonvulsant lamotrigine prevents dopamine depletion in C57 black mice in the MPTP animal model of Parkinson's disease. Life Sci. 54, 245–252 (1994).
   Google Scholar
• Benazzouz A, Boraud T, Dubedat P, Boireau A, Stutzmann JM, Gross C. Riluzole prevents MPTP-induced parkinsonism in the rhesus monkey: a pilot study. Eur. j Pharmacol. 284, 299–307 (1995).
   PubMed Web of Science ®Google Scholar
• Parkinson Study Group. A multicenter randomized controlled trial of remacemide hydrochloride as monotherapy for Parkinson's disease. Neurology 54, 1583–1588 (2000).
   PubMed Web of Science ®Google Scholar
• Beal ME Energetics in the pathogenesis of neurodegenerative diseases. Trends Neurosci. 23, 298–303 (2000).
   Google Scholar
• Sluts CW, Haas RH, Beal ME A possible role of coenzyme Q10 in the etiology and treatment of Parkinson's disease. BioFactors 9, 267–272 (1999).
   Google Scholar
• Miyoshi Y, Zhiming Z, Ovadia A et al. Glial cell line-derived neurotrophic factor-levodopa interactions and reduction of side effects in parkinsonian monkeys. Ann. Neurol. 42, 208–214 (1997).
   PubMed Web of Science ®Google Scholar
• Kordower JH, Emborg ME, Bloch J et al. Neurodegeneration prevented by lentiviral vector delivery of GDNF in primate models of Parkinson's disease. Science 290, 767–773 (2000).
   PubMed Web of Science ®Google Scholar
• Nutt JG, Bronstein JM, Carter JH et al. Intraventricular administration of GDNF in the treatment of Parkinson's disease. Neurology 56\(Suppl. 3), A3751 (2001).
   Google Scholar
• Guo X, Dillman JF, Dawson VL, Dawson TM. Neuroimmunophilins: novel neuroprotective and neuroregenerative targets. Ann. Neurol. 50, 6–16 (2001).
   PubMed Web of Science ®Google Scholar
• Steiner JP, Hamilton GS, Ross GS eta]. Neurotrophic irnmunophilin ligands stimulate structural and functional recovery in neurodegenerative animal models. Proc. Natl Acad. Sci. USA 94, 2019–2024 (1997).
   Google Scholar
• Schneider JS, Roeltgen DP, Mancall EL, Chapas-Crilly J, Rothblat DS, Tatarian GT. Parkinson's disease: Improved function with GM1 ganglioside treatment in a randomized placebo-controlled study. Neurology50, 1630–1636 (1998).
   Google Scholar
• Vila M, Jackson-Lewis V, Vukosavic S et al. Bax ablation prevents dopaminergic neurodegeneration in the 1-methy1-4-pheny1-1,2,3,6-tetrahydropyridine mouse model of Parkinson's disease. Proc. Natl Acad. Sci. USA 98, 2837–2842 (2001).
   Google Scholar
• Michel PP, Lambeng N, Ruberg M. Neuropharmacologic aspects of apoptosis: significance for neurodegenerative diseases. Clin. Neuropharmacol. 22, 137–150 (1999).
   Google Scholar
• Thornberry NA, Lazebnik Y. Caspases: Enemies within. Science 281, 1312–1316 (1998).
   PubMed Web of Science ®Google Scholar
• Schierle GS, Hanson 0, Leist M, Nicotera P, Widner H, Brundin P. Caspase inhibition reduces apoptosis and increases survival of nigral transplants. Nat. Med. 5, 97–100 (1999).
   Google Scholar
• Prasad KN, Cole WC, Hovland AR et al. Multiple anti-oxidants in the prevention and treatment of neurodegenerative disease: analysis of biologic rationale. Curr. Opin. Neurol. 12, 761–770 (1999).
   PubMed Web of Science ®Google Scholar
• Dugan LL, Lovett EG, Quick KL, Lotharius J, Lin TT, O'Malley KL. Fullerene-based anti-oxidants and neurodegenerative disorders. Parkinsonism Rel. Disord 7, 243–247 (2001).
   PubMed Web of Science ®Google Scholar
• Wilkin GP, Knott C. Gila: a curtain raiser. Adv. Neurol. 80, 3–8 (1999).
   Google Scholar
• Vila M, Jackson-Lewis V, Guegan C et al. The role of glial cells in Parkinson's disease. CUIT: Opin. Neurol. 14, 483–490 (2001).
   Google Scholar
• Beal ME Experimental models of Parkinson's disease. Nat. Rev Neurosci. 2, 325–332 (2001).
   Google Scholar
• Dickson DW A-Synuclein and the Lewy body disorders. CUIT: Opin. Neurol. 14, 423–432 (2001).
   Google Scholar
• Klein WL, Krafft GA, Finch CE. Targetting small AB oligomers: the solution to an Alzheimer's disease conumdrum? Trends Neurosci. 24, 219–224 (2001).
   Google Scholar
• ••Review of the role of protofibrills andoligomers in the origin of AD.
   Google Scholar
• Nilsberth C, Westlind Danielson A, Eckman CB et al. The 'Arctic' APP mutation (E693G) causes Alzheimer's disease by enhanced AB protofibril formation. Nat. Neurosci. 4, 887–893 (2001).
   Google Scholar
• Dyer RB, McMurray CT. Mutant protein in Huntington's disease is resistant to proteolysis in affected brain. Nat. Genet. 29, 270–278 (2001).
   PubMedGoogle Scholar
• Conway KA, Lee SJ, Rochet JC, Ding TT, Williamson RE, Lansbury PT, Jr. Acceleration of oligomerization, not fibrillization, is a shared property of both a-synuclein mutations linked to early-onset Parkinson's disease: Implications for pathogenesis and therapy. Proc. Natl Acad. Sci. USA 97, 571–576 (2000).
   Google Scholar
• Masliah E, Rockenstein E, Veinbergs I eta]. B-amyloid peptides enhance a-synuclein accumulation and neuronal deficits in a transgenic mouse model linking Alzheimer's disease and Parkinson's disease. Proc. Natl Acad. Sci. USA 98, 12245–12250 (2001).
   Google Scholar
• ••This study suggests that PD and AD mayshare pathogenetic mechanisms and therapeutic opportunities.
   Google Scholar
• Morello JP, Petäjä-Repo UE, Bichet DG, Bouvier M. Pharmacological chaperones: a new twist on receptor folding. Trends Pharmacol. Sci. 21, 466–469 (2000).
   PubMed Web of Science ®Google Scholar