Death in the substantia nigra: a motor tragedy

References

• MacMahon DG, Findley L, Holmes J et al. The true economic impact of Parkinson’s disease: a research survey in the UK. Mov. Disord.15, P861 178 (2000).
   Google Scholar
• Jarman B, Hurwitz B, Cook A, Bajekal M, Lee A. Effects of community based nurses specialising in Parkinson’s disease on health outcome and costs: randomised controlled trial. Br. Med. J.324, 1072–1075 (2002).
   PubMedGoogle Scholar
• Dowding CH, Shenton CL, Salek SS. A review of the health-related quality of life and economic impact of Parkinson’s disease. Drugs Aging23, 693–721 (2006).
   PubMed Web of Science ®Google Scholar
• Sian J, Gerlach M, Youdim MB, Riederer P. Parkinson’s disease: a major hypokinetic basal ganglia disorder. J. Neural. Transm.106, 443–476 (1999).
   PubMed Web of Science ®Google Scholar
• Bernheimer H, Birkmayer W, Hornykiewicz O, Jellinger K, Seitelberger F. Brain dopamine and the syndromes of Parkinson and Huntington. Clinical, morphological and neurochemical correlations. J. Neurol. Sci.20, 415–455 (1973).
   PubMed Web of Science ®Google Scholar
• Ehringer H, Hornykiewicz O. Distribution of noradrenaline and dopamine (3-hydroxytyramine) in the human brain and their behavior in diseases of the extrapyramidal system. Klin. Wochenschr.38, 1236–1239 (1960).
   PubMed Web of Science ®Google Scholar
• Riederer P, Wuketich S. Time course of nigrostriatal degeneration in Parkinson’s disease: a detailed study of influential factors in human brain amine analysis. J. Neural. Transm.38, 277–301 (1976).
   PubMed Web of Science ®Google Scholar
• Utter AA, Basso MA. The basal ganglia: an overview of circuits and function? Neurosci. Biobehav. Rev. (2007) (In press).
   PubMed Web of Science ®Google Scholar
• Hornykiewics O. Neurochemical pathology and etiology of Parkinson’s disease: basic facts and hypothetical possibilities. Mt Sinai J. Med.55, 11–20 (1988).
   PubMedGoogle Scholar
• Yurek DM, Sladek JR. Dopamine cell replacement: Parkinson’s disease. Ann. Rev. Neurosci.13, 415–440 (1990).
   PubMed Web of Science ®Google Scholar
• Braak H, Ghebremedhin E, Rub U, Bratzke H, Del Tredici K. Stages in the development of Parkinson’s disease-related pathology. Cell Tissue Res.318, 121–134 (2004).
   PubMed Web of Science ®Google Scholar
• Stocchi F. Optimising levodopa therapy for the management of Parkinson’s disease. J. Neurol.252, IV43–IV48 (2005).
   PubMedGoogle Scholar
• Schapira AH. Present and future drug treatment for Parkinson’s disease. J. Neurol. Neurosurg. Psychiatry76, 1472–1478 (2005).
   PubMed Web of Science ®Google Scholar
• Hirsch EC, Hunot S, Damier P, Faucheux B. Glial cells and inflammation in Parkinson’s disease: a role in neurodegeneration? Ann. Neurol.44, S115–S120 (1998).
   PubMedGoogle Scholar
• Jellinger KA. Cell death mechanisms in Parkinson’s disease. J. Neural. Transm.107, 1–29 (2000).
   PubMed Web of Science ®Google Scholar
• Gebicke-Haerter PJ. Microglia in neurodegeneration: molecular aspects. Microsc. Res. Tech.54, 47–58 (2001).
   PubMed Web of Science ®Google Scholar
• Jenner P, Olanow CW. The pathogenesis of cell death in Parkinson’s disease. Neurology66(10 Suppl. 4), S24–S36 (2006).
   PubMed Web of Science ®Google Scholar
• Novikova L, Garris BL, Garris DR, Lau YS. Early signs of neuronal apoptosis in the substantia nigra pars compacta of the progressive neurodegenerative mouse 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine/probenecid model of Parkinson’s disease. Neuroscience140, 67–76 (2006).
   PubMed Web of Science ®Google Scholar
• Nair VD, McNaught KS, Gonzalez-Maeso J, Sealfon SC, Olanow CW. p53 mediates non-transcriptional cell death in dopaminergic cells in response to proteasome inhibition. J. Biol. Chem.281(51) 39550–39560 (2007).
   Web of Science ®Google Scholar
• Hartmann A, Hirsch EC. Parkinson’s disease. The apoptosis hypothesis revisited. Adv. Neurol.86, 143–153 (2001).
   PubMedGoogle Scholar
• Scholtissen B, Verhey FR, Steinbusch HW, Leentjens AF. Serotonergic mechanisms in Parkinson’s disease: opposing results from preclinical and clinical data. J. Neural. Transm.113, 59–73 (2006).
   PubMed Web of Science ®Google Scholar
• Waldmeier P, Bozyczko-Coyne D, Williams M, Vaught JL. Recent clinical failures in Parkinson’s disease with apoptosis inhibitors underline the need for a paradigm shift in drug discovery for neurodegenerative diseases. Biochem. Pharmacol.72, 1197–1206 (2006).
   PubMed Web of Science ®Google Scholar
• Cossette M, Lecomte F, Parent A. Morphology and distribution of dopaminergic neurons intrinsic to the human striatum. J. Chem. Neuroanat.29, 1–11 (2005).
   PubMed Web of Science ®Google Scholar
• Baker H, Kobayashi K, Okano H, Saino-Saito S. Cortical and striatal expression of tyrosine hydroxylase mRNA in neonatal and adult mice. Cell Mol. Neurobiol.23, 507–518 (2003).
   PubMed Web of Science ®Google Scholar
• Tashiro Y, Sugimoto T, Hattori T et al. Tyrosine hydroxylase-like immunoreactive neurons in the striatum of the rat. Neurosci. Lett.97, 6–10 (1989).
   PubMed Web of Science ®Google Scholar
• Dubach M, Schmidt R, Kunkel D, Bowden DM, Martin R, German DC. Primate neostriatal neurons containing tyrosine hydroxylase: immunohistochemical evidence. Neurosci. Lett.75, 205–210 (1987).
   PubMed Web of Science ®Google Scholar
• Bjorklund A, Dunnett SB. Dopamine neuron systems in the brain: an update. Trends Neurosci.30(5), 194–202 (2007).
   PubMed Web of Science ®Google Scholar
• Andén NE, Carlsson A, Dahlstroem A, Fuxe K, Hillarp NA, Larsson K. Demonstration and mapping out of nigro-neostriatal dopamine neurons. Life Sci.3, 523–530 (1964).
   Web of Science ®Google Scholar
• Danner H, Pfister C. 7 types of neurons in the substantia nigra of the rat. Golgi rapid-impregnation study. J. Hirnforsch.23, 553–556 (1982).
   PubMedGoogle Scholar
• Yelnik J, Francois C, Percheron G, Heyner S. Golgi study of the primate substantia nigra. I. Quantitative morphology and typology of nigral neurons. J. Comp. Neurol.265, 455–472 (1987).
   PubMed Web of Science ®Google Scholar
• McRitchie DA, Halliday GM. Calbindin D28k-containing neurons are restricted to the medial substantia nigra in humans. Neuroscience65, 87–91 (1995).
   PubMed Web of Science ®Google Scholar
• McRitchie DA, Halliday GM, Pamphlett R. Diagnostic evaluation of the substantia nigra. Neuropathol. Appl. Neurobiol.22, 228–232 (1996).
   PubMed Web of Science ®Google Scholar
• Dahlstrom A, Fuxe K. Localization of monoamines in the lower brain stem. Experientia20, 398–399 (1964).
   PubMedGoogle Scholar
• Hokfelt T, Johansson O, Goldstein M. Chemical anatomy of the brain. Science225, 1326–1334 (1984).
   PubMed Web of Science ®Google Scholar
• Oertel WH, Mugnaini E. Immunocytochemical studies of GABAergic neurons in rat basal ganglia and their relations to other neuronal systems. Neurosci. Lett.47, 233–238 (1984).
   PubMed Web of Science ®Google Scholar
• Smith DE, Saji M, Joh TH, Reis DJ, Pickel VM. Ibotenic acid-induced lesions of striatal target and projection neurons: ultrastructural manifestations in dopaminergic and non-dopaminergic neurons and in glia. Histol. Histopathol.2, 251–263 (1987).
   PubMed Web of Science ®Google Scholar
• Ficalora AS, Mize RR. The neurons of the substantia nigra and zona incerta which project to the cat superior colliculus are GABA immunoreactive: a double-label study using GABA immunocytochemistry and lectin retrograde transport. Neuroscience29, 567–581 (1989).
   PubMed Web of Science ®Google Scholar
• German DC, Manaye KF. Midbrain dopaminergic neurons (nuclei A8, A9, and A10): three-dimensional reconstruction in the rat. J. Comp. Neurol.331, 297–309 (1993).
   PubMed Web of Science ®Google Scholar
• Nelson EL, Liang CL, Sinton CM, German DC. Midbrain dopaminergic neurons in the mouse: computer-assisted mapping. J. Comp. Neurol.369, 361–371 (1996).
   PubMed Web of Science ®Google Scholar
• Tepper JM, Sawyer SF, Groves PM. Electrophysiologically identified nigral dopaminergic neurons intracellularly labeled with HRP: light microscopic analysis? Neuroscience7, 2794–2806 (1987).
   PubMed Web of Science ®Google Scholar
• Di Giovanni G, De Deurwaerdere P, Di Mascio M, Di Matteo V, Esposito E, Spampinato U. Selective blockade of serotonin-2C/2B receptors enhances mesolimbic and mesostriatal dopaminergic function: a combined in vivo electrophysiological and microdialysis study. Neuroscience91, 587–597 (1999).
   PubMed Web of Science ®Google Scholar
• Berretta N, Freestone PS, Guatteo E et al. Acute effects of 6-hydroxydopamine on dopaminergic neurons of the rat substantia nigra pars compacta in vitro.Neurotoxicology26, 869–881 (2005).
   PubMed Web of Science ®Google Scholar
• Seroogy KB, Dangaran K, Lim S, Haycock JW, Fallon JH. Ventral mesencephalic neurons containing both cholecystokinin- and tyrosine hydroxylase-like immunoreactivities project to forebrain regions. J. Comp. Neurol.279, 397–414 (1989).
   PubMed Web of Science ®Google Scholar
• McRitchie DA, Hardman CD, Halliday GM. Cytoarchitectural distribution of calcium binding proteins in midbrain dopaminergic regions of rats and humans. J. Comp. Neurol.364, 121–150 (1996).
   PubMed Web of Science ®Google Scholar
• Lee CR, Tepper JM. Morphological and physiological properties of parvalbumin- and calretinin-containing γ-aminobutyric acidergic neurons in the substantia nigra. J. Comp. Neurol.500, 958–972 (2007).
   PubMed Web of Science ®Google Scholar
• González-Hernández T, Rodríguez M. Compartmental organization and chemical profile of dopaminergic and GABAergic neurons in the substantia nigra of the rat. J. Comp. Neurol.421, 107–135 (2000).
   PubMed Web of Science ®Google Scholar
• Forno LS, DeLanney LE, Irwin I, Langston JW. Evolution of nerve fiber degeneration in the striatum in the MPTP-treated squirrel monkey. Mol. Neurobiol.9, 163–170 (1994).
   PubMed Web of Science ®Google Scholar
• Damier P, Hirsch EC, Agid Y, Graybiel AM. The substantia nigra of the human brain. II. Patterns of loss of dopamine-containing neurones in Parkinson’s disease. Brain122, 1437–1448 (1999).
   PubMed Web of Science ®Google Scholar
• Damier P, Hirsch EC, Agid Y, Graybiel AM. The substantia nigra of the human brain. I. Nigrosomes and the nigral matrix, a compartmental organization based on calbindin D (28K) immunohistochemistry. Brain122, 1421–1436 (1999).
   PubMed Web of Science ®Google Scholar
• Smidt MP, Burbach JP. How to make a mesodiencephalic dopaminergic neurone. Nat. Rev. Neurosci.8, 21–32 (2007).
   PubMed Web of Science ®Google Scholar
• Gates MA, Torres EM, White A, Fricker-Gates RA, Dunnett SB. Re-examining the ontogeny of substantia nigra dopamine neurons. Eur. J. Neurosci.23, 1384–1390 (2006).
   PubMed Web of Science ®Google Scholar
• Riddle R., Pollock JD. Making connections: the development of mesencephalic dopaminergic neurones. Dev. Brain Res.147, 3–21 (2003).
   PubMedGoogle Scholar
• Smits SM, Burbach JPH, Smidt MP. Developmental origin and fate of meso-diencephalic dopamine neurons. Progr. Neurobiol.78, 1–26 (2006).
   PubMed Web of Science ®Google Scholar
• Prakash N, Wurst W. Genetic networks controlling the development of midbrain dopaminergic neurons. J. Physiol.575, 403–410 (2006).
   PubMed Web of Science ®Google Scholar
• Zetterstrom RH, Solomin L, Jansson L, Hoffer BJ, Olson L, Perlmann T. Dopamine neuron agenesis in Nurr1-deficient mice. Science276, 248–250 (1997).
   PubMed Web of Science ®Google Scholar
• Smidt MP, Asbreuk CH, Cox JJ, Chen H, Johnson RL, Burbach JP. A second independent pathway for development of mesencephalic dopaminergic neurons requires Lmx1b. Nat. Neurosci.3, 337–341 (2000).
   PubMed Web of Science ®Google Scholar
• Martinat C, Bacci JJ, Leete T et al. Cooperative transcription activation by Nurr1 and Pitx3 induces embryonic stem cell maturation to the midbrain dopamine neuron phenotype. Proc. Natl Acad. Sci. USA103, 2874–2879 (2006).
   PubMed Web of Science ®Google Scholar
• Burbach JP, Smidt MP. Molecular programming of stem cells into mesodiencephalic dopaminergic neurones. Trends Neurosci.29, 601–603 (2006).
   PubMed Web of Science ®Google Scholar
• Storch A, Sabolek M, Milosevic J, Schwarz SC, Schwarz J. Midbrain-derived neural stem cells: from basic science to therapeutic approaches. Cell Tissue Res.318, 15–22 (2004).
   PubMed Web of Science ®Google Scholar
• Bogerts B, Hantsch J, Herzer M. A morphometric study of the dopamine-containing cell groups in the mesencephalon of normals, Parkinson patients, and schizophrenics. Biol. Psychiatry18, 951–969 (1983).
   PubMed Web of Science ®Google Scholar
• Fearnley JM, Lees AJ. Ageing and Parkinson’s disease: substantia nigra regional selectivity. Brain114, 2283–2301 (1991).
   PubMed Web of Science ®Google Scholar
• Teismann P, Tieu K, Choi DK et al. Cyclooxygenase-2 is instrumental in Parkinson’s disease neurodegeneration. Proc. Natl Acad. Sci. USA100, 5473–5478 (2003).
   PubMed Web of Science ®Google Scholar
• Asanuma M, Miyazaki I. Nonsteroidal anti-inflammatory drugs in Parkinson’s disease: possible involvement of quinone formation. Expert Rev. Neurother.6, 1313–1325 (2006).
   PubMed Web of Science ®Google Scholar
• Rabinovic AD, Lewis DA, Hastings TG. Role of oxidative changes in the degeneration of dopamine terminals after injection of neurotoxic levels of dopamine. Neuroscience101, 67–76 (2000).
   PubMed Web of Science ®Google Scholar
• Lawson LJ, Perry VH, Dri P, Gordon S. Heterogeneity in the distribution and morphology of microglia in the normal adult mouse brain. Neuroscience39, 151–170 (1990).
   PubMed Web of Science ®Google Scholar
• Kim WG, Mohney RP, Wilson B, Jeohn GH, Liu B, Hong JS. Regional difference in susceptibility to lipopolysaccharide-induced neurotoxicity in the rat brain: role of microglia. J. Neurosci.20, 6309–6316 (2000).
   PubMed Web of Science ®Google Scholar
• Hutchinson M, Raff U. Structural changes of the substantia nigra in Parkinson’s disease as revealed by MR imaging. AJNR Am. J. Neuroradiol.21, 697–701 (2000).
   PubMed Web of Science ®Google Scholar
• Lu L, Neff F, Fischer DA et al. Regional vulnerability of mesencephalic dopaminergic neurones prone to degenerate in Parkinson’s disease: a post-mortem study in human control subjects. Neurobiol. Dis.23, 409–421 (2006).
   PubMed Web of Science ®Google Scholar
• Iravani MM, Syed E, Jackson MJ et al. A modified MPTP treatment regime produces reproducible partial nigrostriatal lesions in common marmosets. J. Neurosci.21, 841–854 (2005).
   Web of Science ®Google Scholar
• Chung S, Hedlund E, Hwang M et al. The homeodomain transcription factor Pitx3 facilitates differentiation of mouse embryonic stem cells into AHD2-expressing dopaminergic neurons. Mol. Cell. Neurosci.28, 241–252 (2005).
   PubMed Web of Science ®Google Scholar
• Greene JG, Dingledine R, Greenamyre JT. Gene expression profiling of rat midbrain dopamine neurons: implications for selective vulnerability in parkinsonism. Neurobiol. Dis.18, 19–31 (2005).
   PubMed Web of Science ®Google Scholar
• McCormack AL, Atienza JG, Langston JW, Di Monte DA. Decreased susceptibility to oxidative stress underlies the resistance of specific dopaminergic cell populations to paraquat-induced degeneration. Neuroscience141, 929–937 (2006).
   PubMed Web of Science ®Google Scholar
• Double KL, Halliday GM. New face of neuromelanin. J. Neural. Transm.70(Suppl.), 119–123 (2006).
   Google Scholar
• Zecca L, Zucca FA, Albertini A, Rizzio E, Fariello RG. A proposed dual role of neuromelanin in the pathogenesis of Parkinson’s disease. Neurology67, S8–S11 (2006).
   PubMed Web of Science ®Google Scholar
• Liang CL, Nelson O, Yazdani U, Pasbakhsh P, German DC. Inverse relationship between the contents of neuromelanin pigment and the vesicular monoamine transporter-2: human midbrain dopamine neurones. J. Comp. Neurol.473, 97–106 (2004).
   PubMed Web of Science ®Google Scholar
• Graham DG. Oxidative pathways for catecholamines in the genesis of neuromelanin and cytotoxic quinones. Mol. Pharmacol.14, 633–643 (1978).
   PubMed Web of Science ®Google Scholar
• Mann DM, Yates PO. Possible role of neuromelanin in the pathogenesis of Parkinson’s disease. Mech. Ageing Dev.21, 193–203 (1983).
   PubMed Web of Science ®Google Scholar
• Ellis RJ. Macromolecular crowding: obvious but underappreciated. Trends Biochem. Sci.26, 597–604 (2001).
   PubMed Web of Science ®Google Scholar
• Pothos EN, Larsen KE, Krantz DE et al. Synaptic vesicle transporter expression regulates vesicle phenotype and quantal size. J. Neurosci.20, 7297–7306 (2000).
   PubMed Web of Science ®Google Scholar
• Halliday GM, Ophof A, Broe M et al. α-synuclein redistributes to neuromelanin lipid in the substantia nigra early in Parkinson’s disease. Brain128, 2654–2664 (2005).
   PubMed Web of Science ®Google Scholar
• Shtilerman MD, Ding TT, Lansbury PT. Molecular crowding accelerates fibrillization of α-synuclein: could an increase in the cytoplasmic protein concentration induce Parkinson’s disease? Biochemistry41, 3855–3860 (2002).
   PubMed Web of Science ®Google Scholar
• Takahashi H, Wakabyashi K. The cellular pathology of Parkinson’s disease. Neuropathology21, 315–322 (2001).
   PubMed Web of Science ®Google Scholar
• Zhang W, Wang T, Pei Z et al. Aggregated α-synuclein activates microglia: a process leading to disease progression in Parkinson’s disease. FASEB J.19, 533–542 (2005).
   PubMed Web of Science ®Google Scholar
• Sulzer D, Bogulavsky J, Larsen KE et al. Neuromelanin biosynthesis is driven by excess cytosolic catecholamines not accumulated by synaptic vesicles. Proc. Natl Acad. Sci. USA97, 11869–11874 (2000).
   PubMed Web of Science ®Google Scholar
• McCormack AL, Delfani K, Janson AM, Langston JW, Di Monte DA. Neuronal vulnerability to MPTP injury: roles of aging and neuromelanin. Abstr. Soc. Neurosci.31, 386 (2001).
   Google Scholar
• Conway KA, Rochet J-C, Bieganski RM, Lansbury PT. Kinetic stabilization of the α-synuclein protofibril by a dopamine-α-synuclein adduct. Science294, 1346–1349 (2001).
   PubMed Web of Science ®Google Scholar
• Langston JW, Ballard P, Tetrud JW, Irwin I. Chronic parkinsonism in humans due to a product of meperidine-analog synthesis. Science219, 979–980 (1983).
   PubMed Web of Science ®Google Scholar
• Betarbet R, Sherer TB, MacKenzie G, Garcia-Osuna M, Panov AV, Greenmyre JT. Chronic systemic pesticide exposure reproduces features of Parkinson’s disease. Nat. Neurobiol.3, 1301–1306 (2000).
   Google Scholar
• Kubo S, Hattori N, Mizuno Y. Recessive Parkinson’s disease. Mov. Disord.21, 885–893 (2006).
   PubMed Web of Science ®Google Scholar
• Bonifati V. Genetics of Parkinson’s disease. Minerva Med.96, 175–186 (2005).
   PubMedGoogle Scholar
• Bonifati V, Oostra BA, Heutink P. Unraveling the pathogenesis of Parkinson’s disease: the contribution of monogenic forms. Cell. Mol. Life Sci.61, 1729–1750 (2004).
   PubMed Web of Science ®Google Scholar
• Grandhi S, Wood NW. Molecular pathogenesis of Parkinson’s disease. Human Mol. Genet.14, 2749–2755 (2005).
   Google Scholar
• Abeliovich A, Flint Beal M. Parkinsonism genes: culprits and clues. J. Neurochem.99, 1062–1072 (2006).
   PubMed Web of Science ®Google Scholar
• McGeer PL, Yasojima K, McGeer EG. Inflammation in Parkinson’s disease. Adv. Neurol.86, 83–89 (2001).
   PubMed Web of Science ®Google Scholar
• Kim YS, Joh TH. Microglia, major player in the brain inflammation: their roles in the pathogenesis of Parkinson’s disease. Exp. Mol. Med.38, 333–347 (2006).
   PubMed Web of Science ®Google Scholar
• Kim W, De Vellis S. Microglia in health and disease. J. Neurosci. Res.81, 302–313 (2005).
   PubMed Web of Science ®Google Scholar
• Beyer ML, Sherer TB, MacKenzie G, Garcia-Osuna M, Panov AV, Greenamyre JT. Phagocytosis of neuronal or glial debris by microglial cells: upregulation of MHC Class I expression and multinuclear giant cell formation in vitro.Glia31, 262–266 (2000).
   PubMed Web of Science ®Google Scholar
• Hald A, Lotharius J. Oxidative stress and inflammation in Parkinson’s disease: is there a causal link? Exp. Neurol.193, 279–290 (2005).
   PubMed Web of Science ®Google Scholar
• McGeer PL, McGeer EG. Inflammation and neurodegeneration in Parkinson’s disease. Parkinsonism Relat. Disord.10, S3–S7 (2004).
   PubMed Web of Science ®Google Scholar
• Minghetti L. Role of inflammation in neurodegenerative diseases. Curr. Opin. Neurol.18, 315–321 (2005).
   PubMed Web of Science ®Google Scholar
• Marchetti B, Abbracchio MP. To be or not to be (inflamed) – is that the question in anti-inflammatory drug therapy of neurodegenerative disorders? Trends Pharmacol. Sci.26, 517–525 (2005).
   PubMed Web of Science ®Google Scholar
• McGeer PL, Itagaki S, Boyes BE, McGeer EG. Reactive microglia are positive for HLA-DR in the substantia nigra of Parkinson’s and Alzheimer’s disease brains. Neurology38, 1285–1291 (1988).
   PubMed Web of Science ®Google Scholar
• Czonkowska I, Kurkowska-Jastrzbska A, Czonkowski PD, Stefano GB. Immune processes in the pathogenesis of Parkinson’s disease – a potential role for microglia and nitric oxide. Med. Sci. Monit.8, RA165–RA177 (2002).
   PubMedGoogle Scholar
• McGeer PL, Schwab C, Parent A, Doudet D. Presence of reactive microglia in monkey substantia nigra years after 1-methyl-4-phenil-1,2,3,6-tetrahydropyridine administration. Ann. Neurol.54, 599–604 (2003).
   PubMed Web of Science ®Google Scholar
• Sugama S, Cho BP, Degiorgio LA et al. Temporal and sequential analysis of microglia in the substantia nigra following medial forebrain bundle axotomy in rat. Neuroscience116, 925–933 (2003).
   PubMed Web of Science ®Google Scholar
• de Meira Santos Lima M, Braga Reksidler A, Marques Zanata S, Bueno Machado H, Tufik S, Vital MA. Different parkinsonism models produce a time-dependent induction of COX-2 in the substantia nigra of rats. Brain Res.1101, 117–125 (2006).
   PubMed Web of Science ®Google Scholar
• Przybykowski A, Kurkowska-Jastrz bska I, Joniec I, Ciesielska A, Czonkowska A, Czonkowski A. Cyclooxygenases mRNA and protein expression in striata in the experimental mouse model of Parkinson’s disease induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine administration to mouse. Brain Res.1019, 144–151 (2004).
   PubMed Web of Science ®Google Scholar
• Kaku K, Shikimi T, Kamisaki Y et al. Elevation of striatal interleukin-6 and serum corticosterone contents in MPTP-treated mice. Clin. Exp. Pharmacol. Physiol.26, 680–683 (1999).
   PubMed Web of Science ®Google Scholar
• Mogi M, Togari A, Ogawa M et al. Effects of repeated systemic administration of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to mice on interleukin-1β and nerve growth factor in the striatum. Neurosci. Lett.250, 25–28 (1998).
   PubMed Web of Science ®Google Scholar
• Iravani MM, Kashefi K, Mander P, Rose S, Jenner P. Involvement of inducible nitric oxide synthase in inflammation-induced dopaminergic neurodegeneration. Neuroscience110, 49–58 (2002).
   PubMed Web of Science ®Google Scholar
• Kataoka M, Tonooka K, Ando T, Imai K, Aimoto T. Hydroxyl radical scavenging activity of nonsteroidal anti-inflammatory drugs. Free Radic. Res.27, 419–427 (1997).
   PubMed Web of Science ®Google Scholar
• Knott C, Stern G, Wilkin GP. Inflammatory regulators in Parkinson’s disease: iNOS, lipocortin-1, and cyclooxygenases-1 and -2. Mol. Cell. Neurosci.16, 724–739 (2000).
   PubMed Web of Science ®Google Scholar
• Kurkowska-Jastrzębska A, Wronska M, Kohutnicka A, Człokowski A, Członkowska A. The inflammatory reaction following 1-methyl-4-phenyl-1,2,3, 6-tetrahydropyridine intoxication in mouse. Exp. Neurol.156, 50–61 (1999).
   PubMed Web of Science ®Google Scholar
• Takeuchi H, Mizuno T, Zhang G et al. Neuritic beading induced by activated microglia is an early feature of neuronal dysfunction toward neuronal death by inhibition of mitochondrial respiration and axonal transport. J. Biol. Chem.280, 10444–10454 (2005).
   PubMed Web of Science ®Google Scholar
• Schiefer J, Kampe K, Dodt HU, Zieglgansberger W, Kreutzberg GW. Microglial motility in the rat facial nucleus following peripheral axotomy. J. Neurocytol.28, 439–453 (1999).
   PubMedGoogle Scholar
• Isacson O, Brundin P, Gage FH, Bjorklund A. Neural grafting in a rat model of Huntington’s disease: progressive neurochemical changes after neostriatal ibotenate lesions and striatal tissue grafting. Neuroscience16, 799–817 (1985).
   PubMed Web of Science ®Google Scholar
• Vijitruth R, Liu M, Choi DY, Nguyen XV, Hunter RL, Bing G. Cyclooxygenase-2 mediates microglial activation and secondary dopaminergic cell death in the mouse MPTP model of Parkinson’s disease. J. Neuroinflammation3, 6 (2006).
   PubMed Web of Science ®Google Scholar
• Wang, T, Pei Z, Zhang W et al. MPP+-induced COX-2 activation and subsequent dopaminergic neurodegeneration. FASEB J.19, 1134–1136 (2005).
   PubMed Web of Science ®Google Scholar
• Dehmer T, Heneka MT, Sastre M, Dichgans J, Schulz JB. Protection by pioglitazone in the MPTP model of Parkinson’s disease correlates with IκBα induction and block of NFκB and iNOS activation. J. Neurochem.88, 494–501 (2004).
   PubMed Web of Science ®Google Scholar
• Baeuerle PA, Baichwal VR. NF-κB as a frequent target for immunosuppressive and anti-inflammatory molecules. Adv. Immunol.65, 111–137 (1997).
   PubMed Web of Science ®Google Scholar
• Dugan LL, Choi DW. Hypoxic-ischemic brain injury and oxidative stress. In: Basic Neurochemistry. Siegel GJ. Agranoff BW, Albers RW, Fisher SK, Uhler MD (Eds). Raven Press, NY, USA 711–730 (1999).
   Google Scholar
• Adams J, Collaco-Moraes Y, De Belleroche J. Cyclooxygenase-2 induction in cerebral cortex: an intracellular response to synaptic excitation. J. Neurochem.66, 6–13 (1996).
   PubMed Web of Science ®Google Scholar
• Westwick JK, Weitzel C, Minden A, Karin M, Brenner DA. Tumor necrosis factor α stimulates AP-1 activity through prolonged activation of the c-Jun kinase. J. Biol. Chem.269, 26396–26401 (1994).
   PubMed Web of Science ®Google Scholar
• McCarty MF. Down-regulation of microglial activation may represent a practical strategy for combating neurodegenerative disorders. Med. Hypotheses67, 251–269 (2006).
   PubMed Web of Science ®Google Scholar
• Gao HM, Liu B, Zhang W, Hong JS. Novel anti-inflammatory therapy for Parkinson’s disease. Trends Pharmacol. Sci.24, 395–401 (2003).
   PubMed Web of Science ®Google Scholar
• Klegeris A, McGeer PL. Non-steroidal anti-inflammatory drugs (NSAIDs) and other anti-inflammatory agents in the treatment of neurodegenerative disease. Curr. Alzheimer Res.2, 355–365 (2005).
   PubMedGoogle Scholar
• Kopp E, Ghosh S. Inhibition of NF-κB by sodium salicylate and aspirin. Science265, 956–959 (1994).
   Google Scholar
• Grilli M, Pizzi M, Memo M, Spano P. Neuroprotection by aspirin and sodium salicylate through blockade of NF-κB activation. Science274, 1383–1385 (1996).
   PubMed Web of Science ®Google Scholar
• Dong Z, Huang C, Brown RE, Ma WY. Inhibition of activator protein 1 activity and neoplastic transformation by aspirin. J. Biol. Chem.272, 9962–9970 (1997).
   PubMed Web of Science ®Google Scholar
• Vane JR, Botting RM. Inflammation and the mechanism of action of anti-inflammatory drugs. FASEB J.1, 89–96 (1987).
   PubMed Web of Science ®Google Scholar
• Weissmann G. Aspirin. Sci. Am.264, 58–64 (1991).
   PubMed Web of Science ®Google Scholar
• Mitchell JA, Saunders M, Barnes PJ, Newton R, Belvisi MG. Sodium salicylate inhibits cyclo-oxygenase-2 activity independently of transcription factor (nuclear factor κB) activation: role of arachidonic acid. Mol. Pharmacol.51, 907–912 (1997).
   PubMed Web of Science ®Google Scholar
• Amann R, Egger, T, Schuligoi R, Heinemann A, Peskar BA. Sodium salicylate enhances the expression of cyclooxygenase-2 in endotoxin-stimulated human mononuclear cells. Eur. J. Pharmacol.433, 129–134 (2001).
   PubMed Web of Science ®Google Scholar
• Vaux DL, Strasser A, The molecular biology of apoptosis. Proc. Natl Acad. Sci. USA93, 2239–2244 (1996).
   PubMed Web of Science ®Google Scholar
• Xu XM, Sansores-Garcia L, Chen XM, Matijevic-Aleksic N, Du M, Wu KK. Suppression of inducible cyclooxygenase 2 gene transcription by aspirin and sodium salicylate. Proc. Natl Acad. Sci. USA96, 5292–5297 (1999).
   PubMed Web of Science ®Google Scholar
• Wu KK. Aspirin and other cyclooxygenase inhibitors: new therapeutic insights. Semin. Vasc. Med.3, 107–112 (2003).
   PubMedGoogle Scholar
• Asanuma M, Nishibayashi-Asanuma S, Miyazaki I, Kohno M, Ogawa N. Neuroprotective effects of non-steroidal anti-inflammatory drugs by direct scavenging of nitric oxide radicals. J. Neurochem.76, 1895–1904 (2001).
   PubMed Web of Science ®Google Scholar
• Farivar RS, Chobanian AV, Brecher P. Salicylate or aspirin inhibits the induction of the inducible nitric oxide synthase in rat cardiac fibroblasts. Circ. Res.78, 759–768 (1996).
   PubMed Web of Science ®Google Scholar
• Chen TG, Chen JZ, Xie XD. Effects of aspirin on number, activity and inducible nitric oxide synthase of endothelial progenitor cells from peripheral blood. Acta Pharmacol. Sin.27, 430–436 (2006).
   PubMedGoogle Scholar
• Di Matteo V, Pierucci M, Di Giovanni G et al. Aspirin protects striatal dopaminergic neurones from neurotoxin-induced degeneration: an in vivo microdialysis study. Brain Res.1095, 167–177 (2006).
   PubMed Web of Science ®Google Scholar
• Di Matteo V, Benigno A, Pierucci M et al. 7-nitroindazole protects striatal dopaminergic neurons against MPP+-induced degeneration: an in vivo microdialysis study. Ann. NY Acad. Sci.1089, 462–471 (2006).
   PubMed Web of Science ®Google Scholar
• Lehmann, JM, Lenhard JM, Oliver BB, Ringold GM, Kliewer SA. Peroxisome proliferator-activated receptors α and γ are activated by indomethacin and other non-steroidal anti-inflammatory drugs. J. Biol. Chem.272, 3406–3410 (1997).
   PubMed Web of Science ®Google Scholar
• Lemberger T, Desvergne B, Wahli W. Peroxisome proliferator-activated receptors: a nuclear receptor signaling pathway in lipid physiology. Ann. Rev. Cell Dev. Biol.12, 335–363 (1996).
   PubMed Web of Science ®Google Scholar
• Jiang C, Ting AT, Seed B. PPAR-γ agonists inhibit production of monocyte inflammatory cytokines. Nature391, 82–86 (1998).
   PubMedGoogle Scholar
• Ricote M, Li AC, Willson TM, Kelly CJ, Glass CK. The peroxisome proliferator-activated receptor-γ is a negative regulator of macrophage activation. Nature391, 79–82 (1998).
   PubMed Web of Science ®Google Scholar
• Bishop-Bailey D, Warner TD. PPARγ ligands induce prostaglandin production in vascular smooth muscle cells: indomethacin acts as a peroxisome proliferator-activated receptor-γ antagonist. FASEB J.17, 1925–1927 (2003).
   PubMed Web of Science ®Google Scholar
• Heneka MT, Sastre M, Dumitrescu-Ozimek L et al. Acute treatment with the PPARγ agonist pioglitazone and ibuprofen reduces glial inflammation and Aβ1-42 levels in APPV717I transgenic mice. Brain128, 1442–1453 (2005).
   PubMed Web of Science ®Google Scholar
• Sastre M, Dewachter I, Rossner S et al. Nonsteroidal anti-inflammatory drugs repress β-secretase gene promoter activity by the activation of PPARγ. Proc. Natl Acad. Sci. USA103, 443–448 (2006).
   PubMed Web of Science ®Google Scholar
• Aubin N, Curet O, Deffois A, Carter C. Aspirin and salicylate protect against MPTP-induced dopamine depletion in mice. J. Neurochem.71, 1635–1642 (1998).
   PubMed Web of Science ®Google Scholar
• Ferger B, Teismann P, Earl CD, Kuschinsky K, Oertel WH. Salicylate protects against MPTP-induced impairments in dopaminergic neurotransmission at the striatal and nigral level in mice. Naunyn Schmiedebergs Arch. Pharmacol.360, 256–261 (1999).
   PubMed Web of Science ®Google Scholar
• Mohanakumar KP, Muralikrishnan D, Thomas B. Neuroprotection by sodium salicylate against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced neurotoxicity. Brain Res.864, 281–290 (2000).
   PubMed Web of Science ®Google Scholar
• Sairam, K, Saravanan KS, Banerjee R, Mohanakumar KP. Non-steroidal anti-inflammatory drug sodium salicylate, but not diclofenac or celecoxib, protects against 1-methyl-4-phenyl pyridinium-induced dopaminergic neurotoxicity in rats. Brain Res.966, 245–252 (2003).
   PubMed Web of Science ®Google Scholar
• Maharaj DS, Saravanan KS, Maharaj H, Mohanakumar KP, Daya S. Acetaminophen and aspirin inhibit superoxide anion generation and lipid peroxidation, and protect against 1-methyl-4-phenyl pyridinium-induced dopaminergic neurotoxicity in rats. Neurochem. Int.44, 355–360 (2004).
   PubMed Web of Science ®Google Scholar
• Carrasco E, Camper D, Werner P. Dopaminergic neurotoxicity by 6-OHDA and MPP+: differential requirement for neuronal cyclooxygenase activity. J. Neurosci. Res.81, 121–131 (2005).
   Google Scholar
• Maharaj H, Maharaj DS, Daya S. Acetylsalicylic acid and acetaminophen protect against MPP+-induced mitochondrial damage and superoxide anion generation. Life Sci.78, 2438–2443 (2006).
   PubMed Web of Science ®Google Scholar
• Kurkowska-Jastrzębska I, Babiuch M, Joniec I, Przybyłkowski A, Członkowski A, Członkowska, A. Indomethacin protects against neurodegeneration caused by MPTP intoxication in mice. Int. Immunopharmacol.2, 1213–1218 (2002).
   PubMed Web of Science ®Google Scholar
• Teismann P, Ferger B. Inhibition of the cyclooxygenase isoenzymes COX-1 and COX-2 provide neuroprotection in the MPTP-mouse model of Parkinson’s disease. Synapse39, 167–174 (2001).
   PubMed Web of Science ®Google Scholar
• Wyss M, Kaddurah-Daouk R. Creatine and creatinine metabolism. Physiol. Rev.80, 1107–1213 (2000).
   PubMed Web of Science ®Google Scholar
• Klivenyi P, Gardian G, Calingasan NY, Yang L, Beal MF. Additive neuroprotective effects of creatine and a cyclooxygenase 2 inhibitor against dopamine depletion in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of Parkinson’s disease. J. Mol. Neurosci.21, 191–198 (2003).
   PubMed Web of Science ®Google Scholar
• Sánchez-Pernaute R, Ferree A, Cooper O, Yu M, Brownell AL, Isacson O. Selective COX-2 inhibition prevents progressive dopamine neuron degeneration in a rat model of Parkinson’s disease. J. Neuroinflammation1, 6 (2004).
   PubMedGoogle Scholar
• Reksidler AB, Lima MM, Zanata SM et al. The COX-2 inhibitor parecoxib produces neuroprotective effects in MPTP-lesioned rats. Eur. J. Pharmacol.560, 163–175 (2007).
   PubMed Web of Science ®Google Scholar
• Chen H, Zhang S, Herna MA et al. Nonsteroidal anti-inflammatory drugs and the risk of Parkinson disease. Arch. Neurol.60, 1059–1064 (2003).
   PubMed Web of Science ®Google Scholar
• Chen H, Jacobs E, Schwarzschild MA et al. Nonsteroidal antiinflammatory drug use and the risk for Parkinson’s disease. Ann. Neurol.58, 963–967 (2005).
   PubMed Web of Science ®Google Scholar
• Hernán MA, Logroscino G, García Rodríguez LA. Nonsteroidal anti-inflammatory drugs and the incidence of Parkinson disease. Neurology66, 1097–1099 (2006).
   PubMed Web of Science ®Google Scholar
• Bower JH, Maraganore DM, Peterson BJ, Ahlskog JE, Rocca WA. Immunologic diseases, anti-inflammatory drugs, and Parkinson disease: a case–control study. Neurology67, 494–496 (2006).
   PubMed Web of Science ®Google Scholar
• McGeer EG, McGeer PL. The role of the immune system in neurodegenerative disorders. Mov. Disord.12, 855–858 (1997).
   PubMed Web of Science ®Google Scholar
• Ton TG, Heckbert SR, Longstreth WT et al. Nonsteroidal anti-inflammatory drugs and risk of Parkinson’s disease. Mov. Disord.21, 964–969 (2006).
   PubMed Web of Science ®Google Scholar
• Hancock DB, Martin ER, Stajich JM et al. Smoking, caffeine, and nonsteroidal anti-inflammatory drugs in families with Parkinson disease. Arch. Neurol.64, 576–580 (2007).
   PubMed Web of Science ®Google Scholar
• Golstein P, Kroemer G. Cell death by necrosis: towards a molecular definition. Trends Biochem. Sci.32, 37–43 (2007).
   PubMed Web of Science ®Google Scholar
• Nicotera P, Leist M, Fava E, Berliocchi L, Vollbrecht C. Energy requirement for caspase activation and neuronal cell death. Brain Pathol.10, 276–282 (2000).
   PubMed Web of Science ®Google Scholar
• Krantic S, Mechawar N, Reix S, Quirion R. Molecular basis of programmed cell death involved in neurodegeneration. Trends Neurosci.28, 670–676 (2005).
   PubMed Web of Science ®Google Scholar
• Bredesen DE. Key note lecture: toward a mechanistic taxonomy for cell death programs. Stroke38, 652–660 (2007).
   PubMed Web of Science ®Google Scholar
• Leist M, Nicotera P. Apoptosis, excitotoxicity, and neuropathology. Exp. Cell. Res.239, 183–201 (1998).
   PubMed Web of Science ®Google Scholar
• Roth KA, D’Sa C. Apoptosis and brain development. Ment. Retard. Dev. Disabil. Res. Rev.7, 261–266 (2001).
   PubMedGoogle Scholar
• Mogi M, Kondo T, Mizuno Y, Nagatsu T. p53 protein, interferon-γ, and NF-κB levels are elevated in the parkinsonian brain. Neurosci. Lett.414, 94–97 (2007).
   PubMed Web of Science ®Google Scholar
• Mochizuki H, Goto K, Mori H, Mizuno Y. Histochemical detection of apoptosis in Parkinson’s disease. J. Neurol. Sci.137, 120–123 (1996).
   PubMed Web of Science ®Google Scholar
• Anglade P, Vyas S, Javoy-Agid F et al. Apoptosis and autophagy in nigral neurons of patients with Parkinson’s disease. Histol. Histopathol.2, 25–31 (1997).
   Google Scholar
• Tatton WG, Chalmers-Redman R, Brown D, Tatton N. Apoptosis in Parkinson’s disease: signals for neuronal degradation. Ann. Neurol.53, S61–S70 (2003).
   PubMed Web of Science ®Google Scholar
• Banati RB, Daniel SE, Path MRC, Blunt SB. Glial pathology but absence of apoptotic nigral neurones in long-standing Parkinson’s disease. Mov. Disord.13, 221–227 (1998).
   PubMed Web of Science ®Google Scholar
• Graeber MB, Grasbon-Frodl E, Abell-Aleff P, Kösel S. Nigral neurones are likely to die of a mechanism other than classical apoptosis in Parkinson’s disease. Parkinsonism Relat. Disord.5, 187–192 (1999).
   PubMed Web of Science ®Google Scholar
• Wüllner U, Kornhuber J, Weller M, Schulz JB, Löschmann PA, Riederer P. Cell death and apoptosis regulating proteins in Parkinson’s disease – a cautionary note. Acta Neuropathol.97, 408–412 (1999).
   PubMed Web of Science ®Google Scholar
• Kösel S, Egensperger R, von Eitzen U, Mehraein P, Graeber M. On the question of apoptosis in the parkinsonian substantia nigra. Acta Neuropathol.93, 105–108 (1997).
   PubMed Web of Science ®Google Scholar
• He XJ, Nakayama H, Dong M et al. Evidence of apoptosis in the subventricular zone and rostral migratory stream in the MPTP mouse model of Parkinson disease. J. Neuropathol. Exp. Neurol.65, 873–882 (2006).
   PubMed Web of Science ®Google Scholar
• Kaul S, Kanthasamy A, Kitazawa M, Anantharam V, Kanthasamy AG. Caspase-3 dependent proteolytic activation of protein kinase C delta mediates and regulates 1-methyl-4-phenylpyridinium (MPP+)-induced apoptotic cell death in dopaminergic cells: relevance to oxidative stress in dopaminergic degeneration. Eur. J. Neurosci.18, 1387–1401 (2003).
   PubMed Web of Science ®Google Scholar
• Saporito MS, Thomas BA, Scott RW. MPTP activates c-Jun NH2-terminal kinase (JNK) and its upstream regulatory kinase MKK4 in nigrostriatal neurons in vivo.J. Neurochem.75, 1200–1208 (2000).
   PubMed Web of Science ®Google Scholar
• Blum D, Torch S, Lambeng N et al. Molecular pathways involved in the neurotoxicity of 6-OHDA, dopamine and MPTP: contribution to the apoptotic theory in Parkinson’s disease. Prog. Neurobiol.65, 135–172 (2001).
   PubMed Web of Science ®Google Scholar
• Mladenovic A, Perovic M, Raicevic N, Kanazir S, Rakic L, Ruzdijic S. 6-Hydroxydopamine increases the level of TNFα and bax mRNA in the striatum and induces apoptosis of dopaminergic neurons in hemiparkinsonian rats. Brain Res.996, 237–245 (2004).
   PubMed Web of Science ®Google Scholar
• Choi WS, Yoon SY, Oh TH, Choi EJ, O’Malley KL, Oh YJ. Two distinct mechanisms are involved in 6-hydroxydopamine- and MPP+- induced dopaminergic neuronal cell death: role of caspases, ROS, and JNK. J. Neurosci. Res.57, 86–94 (1999).
   PubMed Web of Science ®Google Scholar
• O’Malley KL, Liu J, Lotharius J, Holtz W. Targeted expression of BCL-2 attenuates MPP+ but not 6-OHDA induced cell death in dopaminergic neurons. Neurobiol. Dis.14, 43–51 (2003).
   PubMed Web of Science ®Google Scholar
• Alvarez-Buylla A, Lim DA. For the long run: maintaining germinal niches in the adult brain. Neuron41(5), 683–686 (2004).
   PubMed Web of Science ®Google Scholar
• Nilsson M, Perfilieva E, Johansson U, Orwar O, Eriksson PS. Enriched environment increases neurogenesis in the adult rat dentate gyrus and improves spatial memory. J. Neurobiol.39, 569–578 (1999).
   PubMedGoogle Scholar
• Santarelli L, Saxe M, Gross C et al. Requirement of hippocampal neurogenesis for the behavioral effects of antidepressants. Science301, 805–809 (2003).
   PubMed Web of Science ®Google Scholar
• Enwere E, Shingo T, Gregg C, Fujikawa H, Ohta S, Weiss S. Aging results in reduced epidermal growth factor receptor signaling, diminished olfactory neurogenesis, and deficits in fine olfactory discrimination. J. Neurosci.24, 8354–8365 (2004).
   PubMed Web of Science ®Google Scholar
• Kempermann G, Jessberger S, Steiner B, Kronenberg G. Milestones of neuronal development in the adult hippocampus. Trends Neurosci.27, 447–452 (2004).
   PubMed Web of Science ®Google Scholar
• Lie DC, Dziewczapolski G, Willhoite AR, Kaspar BK, Shults CW, Gage FH. The adult substantia nigra contains progenitor cells with neurogenic potential. J. Neurosci.22, 6639–6649 (2002).
   PubMed Web of Science ®Google Scholar
• Zhao M, Momma S, Delfani K et al. Evidence for neurogenesis in the adult mammalian substantia nigra. Proc. Natl Acad. Sci. USA100, 7925–7930 (2003).
   PubMed Web of Science ®Google Scholar
• Fillmore HL, Holloway KL, Gillies GT. Cell replacement efforts to repair neuronal injury: a potential paradigm for the treatment of Parkinson’s disease. NeuroRehabilitation20, 233–242 (2005).
   PubMed Web of Science ®Google Scholar
• Lindvall O, Kokaia Z, Martinez-Serrano A. Stem cell therapy for human neurodegenerative disorders: how to make it work. Nat. Med.10, S42–S50 (2004).
   PubMed Web of Science ®Google Scholar
• Piper M, Abrams GM, Marks WJ. Deep brain stimulation for the treatment of Parkinson’s disease: overview and impact on gait and mobility. NeuroRehabilitation20, 223–232 (2005).
   PubMed Web of Science ®Google Scholar
• Borta A, Hoglinger GU. Dopamine and adult neurogenesis. J. Neurochem.100, 587–595 (2007).
   PubMed Web of Science ®Google Scholar
• Hirsch EC, Breidert T, Rousselet E, Hunot S, Hartmann A, Michel PP. The role of glial reaction and inflammation in Parkinson’s disease. Ann. NY Acad. Sci.991, 214–228 (2003).
   PubMed Web of Science ®Google Scholar
• Ho A, Blum M. Induction of interleukin-1 associated with compensatory dopaminergic sprouting in the denervated striatum of young mice: model of aging and neurodegenerative disease. J. Neurosci.18, 5614–5629 (1998).
   PubMed Web of Science ®Google Scholar
• Porritt MJ, Batchelor PE, Hughes AJ, Kalnins R, Donnan GA, Howells DW. New dopaminergic neurons in Parkinson’s disease striatum. Lancet356, 44–45 (2000).
   PubMed Web of Science ®Google Scholar
• Brbet R, Turner R, Chockkan V et al. Dopaminergic neurons intrinsic to the primate striatum. J. Neurosci.17, 6761–6768 (1997).
   PubMed Web of Science ®Google Scholar
• Palfi S, Leventhal L, Chu Y et al. Lentivirally delivered glial cell line-derived neurotrophic factor increases the number of striatal dopaminergic neurons in primate models of nigrostriatal degeneration. J. Neurosci.22, 4942–4954 (2002).
   PubMed Web of Science ®Google Scholar
• Meredith GE, Farrell T, Kellaghan P, Tan Y, Zahm DS, Totterdell S. Immunocytochemical characterization of catecholaminergic neurons in the rat striatum following dopamine-depleting lesions. Eur. J. Neurosci.11, 3585–3596 (1999).
   PubMed Web of Science ®Google Scholar
• Freundlieb N, Francois C, Tande D, Oertel WH, Hirsch EC, Hoglinger GU. Dopaminergic substantia nigra neurons project topographically organized to the subventricular zone and stimulate precursor cell proliferation in aged primates. J. Neurosci.26, 2321–2325 (2006).
   PubMed Web of Science ®Google Scholar
• Hoglinger GU, Rizk P, Muriel MP et al. Dopamine depletion impairs precursor cell proliferation in Parkinson disease. Nat. Neurosci.7, 726–735 (2004).
   PubMed Web of Science ®Google Scholar
• Shan X, Chi L, Bishop M et al. Enhanced de novo neurogenesis and dopaminergic neurogenesis in the substantia nigra of 1-methyl-4-phyenyl-1,2,3,6-tetrahydropyridine-induced Parkinson’s disease-like mice. Stem Cells24, 1280–1287 (2006).
   PubMed Web of Science ®Google Scholar
• Frielingsdorf H, Schwarz K, Brundin P, Mohapel P. No evidence for new dopaminergic neurones in the adult mammalian substantia nigra. Proc. Natl Acad. Sci. USA101, 10177–10182 (2004).
   PubMed Web of Science ®Google Scholar
• Steiner B, Winter C, Hosman K et al. Enriched environment induces cellular plasticity in the adult substantia nigra and improves motor behavior function in the 6-OHDA rat model of Parkinson’s disease. Exp. Neurol.199, 291–300 (2006).
   PubMed Web of Science ®Google Scholar
• Fallon J, Reid S, Kinyamu R et al.In vivo induction of massive proliferation, directed migration, and differentiation of neural cells in the adult mammalian brain. Proc. Natl Acad. Sci. USA97, 14686–14691 (2000).
   PubMed Web of Science ®Google Scholar
• Benraiss A, Chmielnicki E, Lerner K, Roh D, Goldman SA. Adenoviral brain-derived neurotrophic factor induces both neostriatal and olfactory neuronal recruitment from endogenous progenitor cells in the adult forebrain. J. Neurosci.21, 6718–6731 (2001).
   PubMed Web of Science ®Google Scholar
• Mohapel P, Frielingsdorf H, Haggblad J, Zachrisson O, Brundin P. Platelet-derived growth factor (PDGF-BB) and brain-derived neurotrophic factor (BDNF) induce striatal neurogenesis in adult rats with 6-hydroxydopamine lesions. Neuroscience132, 767–776 (2005).
   PubMed Web of Science ®Google Scholar
• Prodan CI, Monnot M, Ross ED, Coleman AE. Reversible dementia with parkinsonian features associated with budesonide use. Neurology67, 723 (2006).
   PubMed Web of Science ®Google Scholar
• Bonuccelli U, Del Dotto P. New pharmacologic horizons in the treatment of Parkinson disease. Neurology67, S30–S38 (2006).
   Google Scholar
• Di Giovanni G, Di Matteo V, Pierucci M, Benigno A, Esposito E. Serotonin involvement in the basal ganglia pathophysiology: could the 5-HT2C receptor be a new target for therapeutic strategies? Curr. Med. Chem.13, 3069–3081 (2006).
   PubMed Web of Science ®Google Scholar
• Schapira AH, Bezard E, Brotchie J et al. Novel pharmacological targets for the treatment of Parkinson’s disease. Nat. Rev. Drug Discov.5, 845–854 (2006).
   PubMed Web of Science ®Google Scholar
• Fernández-Ruiz J, García-Arencibia M, Sagredo O, Ramos JA. Role of endogenous cannabinoids in the control of basal ganglia activity. In: The Basal Ganglia Pathophysiology: Recent Advances. Di Giovanni G (Ed.). Transworld Research, Kerala, India 75–95 (2007).
   Google Scholar
• Del Bell E, Bermúdez-Echeverry M, Salum C, Raisman-Vozary R. Nitric oxide and basal ganglia physiopathology. In: The Basal Ganglia Pathophysiology: Recent Advances. Di Giovanni G (Ed.). Transworld Research, Kerala, India 129–158 (2007).
   Google Scholar
• Pinna A, Simola N, Morelli M. Adenosine A2A receptor antagonist treatment of Parkinson’s disease. In: The Basal Ganglia Pathophysiology: Recent Advances. Di Giovanni G (Ed.). Transworld Research, Kerala, India 191–223 (2007).
   Google Scholar
• Marchetti B. Estrogen, neuroinflammation and neuroprotection in Parkinson’s disease: key role of neuron-glia crosstalk. In: The Basal Ganglia Pathophysiology: Recent Advances. Di Giovanni G (Ed ). Transworld Research, Kerala, India 225–252 (2007).
   Google Scholar