The Degeneration of Dopamine Neurons in Parkinson's Disease: Insights from Embryology and Evolution of the Mesostriatocortical System
Identifieur interne : 001F00 ( Istex/Corpus ); précédent : 001E99; suivant : 001F01The Degeneration of Dopamine Neurons in Parkinson's Disease: Insights from Embryology and Evolution of the Mesostriatocortical System
Auteurs : Philippe Vernier ; Frederic Moret ; Sophie Callier ; Marina Snapyan ; Christophe Wersinger ; Anita SidhuSource :
- Annals of the New York Academy of Sciences [ 0077-8923 ] ; 2004-12.
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Abstract
Abstract: Parkinson's disease (PD) is, to a large extent, specific to the human species. Most symptoms are the consequence of the preferential degeneration of the dopamine‐synthesizing cells of the mesostriatal‐mesocortical neuronal pathway. Reasons for that can be traced back to the evolutionary mechanisms that shaped the dopamine neurons in humans. In vertebrates, dopamine‐containing neurons and nuclei do not exhibit homogenous phenotypes. In this respect, mesencephalic dopamine neurons of the substantia nigra and ventral tegmental area are characterized by a molecular combination (tyrosine hydroxylase, aromatic amino acid decarboxylase, monoamine oxidase, vesicular monoamine transporter, dopamine transporter—to name a few), which is not found in other dopamine‐containing neurons of the vertebrate brain. In addition, the size of these mesencephalic DA nuclei is tremendously expanded in humans as compared to other vertebrates. Differentiation of the mesencephalic neurons during development depends on genetic mechanisms, which also differ from those of other dopamine nuclei. In contrast, pathophysiological approaches to PD have highlighted the role of ubiquitously expressed molecules such as a‐synuclein, parkin, and microtubule‐associated proteins. We propose that the peculiar phenotype of the dopamine mesencephalic neurons, which has been selected during vertebrate evolution and reshaped in the human lineage, has also rendered these neurons particularly prone to oxidative stress, and thus, to the fairly specific neurodegeneration of PD. Numerous evidence has been accumulated to demonstrate that perturbed regulation of DAT‐dependent dopamine uptake, DAT‐dependent accumulation of toxins, dysregulation of TH activity as well as high sensitivity of DA mesencephalic neurons to oxidants are key components of the neurodegeneration process of PD. This view points to the contribution of nonspecific mechanisms (α‐synuclein aggregation) in a highly specific cellular environment (the dopamine mesencephalic neurons) and provides a robust framework to develop novel and rational therapeutic schemes in PD.
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DOI: 10.1196/annals.1332.015
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<front><div type="abstract">Abstract: Parkinson's disease (PD) is, to a large extent, specific to the human species. Most symptoms are the consequence of the preferential degeneration of the dopamine‐synthesizing cells of the mesostriatal‐mesocortical neuronal pathway. Reasons for that can be traced back to the evolutionary mechanisms that shaped the dopamine neurons in humans. In vertebrates, dopamine‐containing neurons and nuclei do not exhibit homogenous phenotypes. In this respect, mesencephalic dopamine neurons of the substantia nigra and ventral tegmental area are characterized by a molecular combination (tyrosine hydroxylase, aromatic amino acid decarboxylase, monoamine oxidase, vesicular monoamine transporter, dopamine transporter—to name a few), which is not found in other dopamine‐containing neurons of the vertebrate brain. In addition, the size of these mesencephalic DA nuclei is tremendously expanded in humans as compared to other vertebrates. Differentiation of the mesencephalic neurons during development depends on genetic mechanisms, which also differ from those of other dopamine nuclei. In contrast, pathophysiological approaches to PD have highlighted the role of ubiquitously expressed molecules such as a‐synuclein, parkin, and microtubule‐associated proteins. We propose that the peculiar phenotype of the dopamine mesencephalic neurons, which has been selected during vertebrate evolution and reshaped in the human lineage, has also rendered these neurons particularly prone to oxidative stress, and thus, to the fairly specific neurodegeneration of PD. Numerous evidence has been accumulated to demonstrate that perturbed regulation of DAT‐dependent dopamine uptake, DAT‐dependent accumulation of toxins, dysregulation of TH activity as well as high sensitivity of DA mesencephalic neurons to oxidants are key components of the neurodegeneration process of PD. This view points to the contribution of nonspecific mechanisms (α‐synuclein aggregation) in a highly specific cellular environment (the dopamine mesencephalic neurons) and provides a robust framework to develop novel and rational therapeutic schemes in PD.</div>
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<abstract>Abstract: Parkinson's disease (PD) is, to a large extent, specific to the human species. Most symptoms are the consequence of the preferential degeneration of the dopamine‐synthesizing cells of the mesostriatal‐mesocortical neuronal pathway. Reasons for that can be traced back to the evolutionary mechanisms that shaped the dopamine neurons in humans. In vertebrates, dopamine‐containing neurons and nuclei do not exhibit homogenous phenotypes. In this respect, mesencephalic dopamine neurons of the substantia nigra and ventral tegmental area are characterized by a molecular combination (tyrosine hydroxylase, aromatic amino acid decarboxylase, monoamine oxidase, vesicular monoamine transporter, dopamine transporter—to name a few), which is not found in other dopamine‐containing neurons of the vertebrate brain. In addition, the size of these mesencephalic DA nuclei is tremendously expanded in humans as compared to other vertebrates. Differentiation of the mesencephalic neurons during development depends on genetic mechanisms, which also differ from those of other dopamine nuclei. In contrast, pathophysiological approaches to PD have highlighted the role of ubiquitously expressed molecules such as a‐synuclein, parkin, and microtubule‐associated proteins. We propose that the peculiar phenotype of the dopamine mesencephalic neurons, which has been selected during vertebrate evolution and reshaped in the human lineage, has also rendered these neurons particularly prone to oxidative stress, and thus, to the fairly specific neurodegeneration of PD. Numerous evidence has been accumulated to demonstrate that perturbed regulation of DAT‐dependent dopamine uptake, DAT‐dependent accumulation of toxins, dysregulation of TH activity as well as high sensitivity of DA mesencephalic neurons to oxidants are key components of the neurodegeneration process of PD. This view points to the contribution of nonspecific mechanisms (α‐synuclein aggregation) in a highly specific cellular environment (the dopamine mesencephalic neurons) and provides a robust framework to develop novel and rational therapeutic schemes in PD.</abstract>
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<refBibs><json:item><author><json:item><name>J.M. Fearnley</name>
</json:item>
</author>
<host><volume>114</volume>
<pages><last>2301</last>
<first>2283</first>
</pages>
<author></author>
<title>Brain</title>
</host>
<title>Ageing and Parkinson's disease: substantia nigra regional selectivity</title>
</json:item>
<json:item><author><json:item><name>G.C. Cotzias</name>
</json:item>
</author>
<host><volume>276</volume>
<pages><last>379</last>
<first>374</first>
</pages>
<author></author>
<title>N. Engl. J. Med.</title>
</host>
<title>Aromatic amino acids and modification of parkinsonism</title>
</json:item>
<json:item><host><author></author>
<title>Przedborski, S., V. Kostic, N. Giladi, et al. 2003. Dopaminergic systems in Parkinson's disease, in dopamine receptors and transporters. A. Sidhu, M. Laruelle & P. Vernier, Eds.: 363–402. Marcel Dekker. New York.</title>
</host>
</json:item>
<json:item><author><json:item><name>W. Dauer</name>
</json:item>
</author>
<host><volume>39</volume>
<pages><last>909</last>
<first>889</first>
</pages>
<author></author>
<title>Neuron</title>
</host>
<title>Parkinson's disease: mechanisms and models</title>
</json:item>
<json:item><author><json:item><name>G. Wick</name>
</json:item>
</author>
<host><volume>38</volume>
<pages><last>25</last>
<first>13</first>
</pages>
<author></author>
<title>Exp. Gerontol.</title>
</host>
<title>A Darwinian‐evolutionary concept of age‐related diseases</title>
</json:item>
<json:item><author><json:item><name>M. Rose</name>
</json:item>
</author>
<host><volume>36</volume>
<pages><last>1297</last>
<first>1293</first>
</pages>
<author></author>
<title>Free Radical Res.</title>
</host>
<title>Pharmacology, genomics, and the evolutionary biology of ageing</title>
</json:item>
<json:item><author><json:item><name>S. Stearns</name>
</json:item>
</author>
<host><volume>76</volume>
<pages><last>432</last>
<first>417</first>
</pages>
<author></author>
<title>Q. Rev. Biol.</title>
</host>
<title>Evolution in health and disease: work in progress</title>
</json:item>
<json:item><author><json:item><name>H. Ehringer</name>
</json:item>
</author>
<host><volume>38</volume>
<pages><last>1239</last>
<first>1236</first>
</pages>
<author></author>
<title>Klin. Wschr.</title>
</host>
<title>Verteilung von noradrenalin und dopamine 3‐hydroxy‐tyramin in Gehirn des Menschen und ihr Verhalten by Erkrankungen des Extrapyramidalen systems</title>
</json:item>
<json:item><author><json:item><name>M. Foix</name>
</json:item>
</author>
<host><volume>28</volume>
<pages><last>600</last>
<first>593</first>
</pages>
<author></author>
<title>Rev. Neurol.</title>
</host>
<title>Les lésions anatomiques de la Maladie de Parkinson</title>
</json:item>
<json:item><author><json:item><name>A. Samii</name>
</json:item>
</author>
<host><volume>363</volume>
<pages><last>1793</last>
<first>1783</first>
</pages>
<author></author>
<title>Lancet</title>
</host>
<title>Parkinson's disease</title>
</json:item>
<json:item><author><json:item><name>H. Braak</name>
</json:item>
</author>
<host><volume>24</volume>
<pages><last>211</last>
<first>197</first>
</pages>
<author></author>
<title>Neurobiol. Aging</title>
</host>
<title>Staging of brain pathology associated to sporadic Parkinson's disease</title>
</json:item>
<json:item><host><author></author>
<title>Hirsch, E.C., G. Hoglinger, E. Rousselet, et al. 2003 Animal models of Parkinson's disease in rodents induced by toxins: an update. J. Neural Trans. suppl. 65: 89–100.</title>
</host>
</json:item>
<json:item><host><author></author>
<title>Dawson, T. M., & V.L. Dawson. 2003 Molecular pathways of neurodegeneration in Parkinson's disease. Science 302: 819–822.</title>
</host>
</json:item>
<json:item><host><author></author>
<title>Sidhu, A., C. Wersinger & P. Vernier. 2004 Does α‐synuclein modulate dopaminergic synaptic content and tone at the synapse? FASEB J. 18: 637–647.</title>
</host>
</json:item>
<json:item><host><volume>114</volume>
<pages><last>8</last>
<first>1</first>
</pages>
<author></author>
<title>Are ubiquitination pathways central to Parkinson's disease? Cell</title>
</host>
</json:item>
<json:item><author><json:item><name>M. Baba</name>
</json:item>
</author>
<host><volume>152</volume>
<pages><last>884</last>
<first>879</first>
</pages>
<author></author>
<title>Am. J. Pathol.</title>
</host>
<title>Aggregation of alpha‐synuclein in Lewy bodies of sporadic Parkinson's disease and dementia with Lewy bodies</title>
</json:item>
<json:item><author><json:item><name>K.A. Conway</name>
</json:item>
</author>
<host><volume>294</volume>
<pages><last>1349</last>
<first>1346</first>
</pages>
<author></author>
<title>Science</title>
</host>
<title>Kinetic stabilization of the alpha‐synuclein protofibril by a dopamine‐alpha‐synuclein adduct</title>
</json:item>
<json:item><host><author></author>
<title>Sidhu, A., C. Wersinger & P. Vernier. 2004 Alpha‐synuclein regulation of the dopaminergic transporter: a possible role in the pathogenesis of Parkinson's disease. FEBS Lett. 265: 1–5.</title>
</host>
</json:item>
<json:item><author><json:item><name>R.G. Perez</name>
</json:item>
</author>
<host><volume>22</volume>
<pages><last>3099</last>
<first>3090</first>
</pages>
<author></author>
<title>J. Neurosci.</title>
</host>
<title>A role for alpha‐synuclein in the regulation of dopamine biosynthesis</title>
</json:item>
<json:item><host><author></author>
<title>Lotharius, J., S. Barg, P. Wiekop, et al. 2002 Effect of mutant alpha‐synuclein on dopamine homeostasis in a new human mesencephalic cell line. J. Biol. Hematol. 277: 38884–38894.</title>
</host>
</json:item>
<json:item><author><json:item><name>J. Lotharius</name>
</json:item>
</author>
<host><volume>3</volume>
<pages><last>942</last>
<first>932</first>
</pages>
<author></author>
<title>Nat. Rev. Neurosci.</title>
</host>
<title>Pathogenesis of Parkinson's disease: dopamine, vesicles and alpha‐synuclein</title>
</json:item>
<json:item><author><json:item><name>C. Wersinger</name>
</json:item>
</author>
<host><volume>24</volume>
<pages><last>105</last>
<first>91</first>
</pages>
<author></author>
<title>Mol. Cell Neurosci.</title>
</host>
<title>Mutations in the lipid‐binding domain of alpha‐synuclein confer overlapping, yet distinct, functional properties in the regulation of dopamine transporter activity</title>
</json:item>
<json:item><host><author></author>
<title>El‐Agnaf, O.M. & G.B. Irvine. 2002 Aggregation and neurotoxicity of alpha‐synuclein and related peptides. Biochem. Soc. Trans. 30: 559–565.</title>
</host>
</json:item>
<json:item><host><author></author>
<title>Lucking, C.B. & A. Brice. 2000 Alpha‐synuclein and Parkinson's disease. Cell. Mol. Life Sci. 57: 1894–1908.</title>
</host>
</json:item>
<json:item><host><author></author>
<title>Hökfelt, T., R. Martensson, A. Björklund, et al. 1984 Distributional maps of tyrosine hydroxylase‐immunoreactive neurons in the rat brain. In Handbook of Chemical Neuroanatomy. T. Hökfelt, Ed.: 277–386. Elsevier. Amsterdam.</title>
</host>
</json:item>
<json:item><author><json:item><name>L. Puelles</name>
</json:item>
</author>
<host><volume>16</volume>
<pages><last>479</last>
<first>472</first>
</pages>
<author></author>
<title>Trends Neurosci.</title>
</host>
<title>Expression patterns of homeobox and other putative regulatory genes in the embryonic mouse forebrain suggest a neuromeric organization</title>
</json:item>
<json:item><author><json:item><name>L. Puelles</name>
</json:item>
</author>
<host><volume>26</volume>
<pages><last>476</last>
<first>469</first>
</pages>
<author></author>
<title>Trends Neurosci.</title>
</host>
<title>Forebrain gene expression domains and the evolving prosomeric model</title>
</json:item>
<json:item><host><author></author>
<title>Wullimann, M.L. & L. Puelles. 1999 Postembryonic neural proliferation in the zebrafish forebrainand its relationships to prosomeric domains. Anat. Embryol. 201: 329–348.</title>
</host>
</json:item>
<json:item><host><author></author>
<title>Smeets, WJ. & A. Reiner. 1994. Phylogeny and development of catecholamine systems in the CNS of vertebrates. Cambridge University Press. London.</title>
</host>
</json:item>
<json:item><author><json:item><name>W.J. Smeets</name>
</json:item>
</author>
<host><volume>33</volume>
<pages><last>379</last>
<first>308</first>
</pages>
<author></author>
<title>Brain Res. Rev.</title>
</host>
<title>Catecholamine systems in the brain of vertebrates: new perspectives through a comparative approach</title>
</json:item>
<json:item><host><author></author>
<title>Kapsimali, M., F. Bourrat & P. Vernier. 2001 Distribution of the orphan nuclear receptor nurr1 in medaka Oryzias latipes: cues to the definition of homologous territories in the vertebrate brain. J. Comp. Neurol. 431: 276–292.</title>
</host>
</json:item>
<json:item><author><json:item><name>E. Rink</name>
</json:item>
</author>
<host><volume>57</volume>
<pages><last>387</last>
<first>385</first>
</pages>
<author></author>
<title>Brain Res. Bull.</title>
</host>
<title>Connections of the ventral telencephalon and tyrosine hydroxylase distribution in the zebrafish brain Danio rerio lead to identification of an ascending dopaminergic system in a teleost</title>
</json:item>
<json:item><author><json:item><name>L. Puelles</name>
</json:item>
</author>
<host><volume>394</volume>
<pages><last>308</last>
<first>283</first>
</pages>
<author></author>
<title>J. Comp. Neurol.</title>
</host>
<title>Early neuromeric distribution of tyrosine‐hydroxylase‐immunoreactive neurons in human embryos</title>
</json:item>
<json:item><host><author></author>
<title>Prensa, L. & A. Parent. 2001 The nigrostriatal pathway in the rat: a single‐axon study of the relationship between dorsal and ventral tier nigral neurons and the striosome/matrix striatal compartments. J. Neurosci. 21: 7247–7260.</title>
</host>
</json:item>
<json:item><author><json:item><name>C. Cerruti</name>
</json:item>
</author>
<host><volume>18</volume>
<pages><last>186</last>
<first>181</first>
</pages>
<author></author>
<title>Brain Res. Mol. Brain Res.</title>
</host>
<title>Dopamine transporter mRNA expression is intense in rat midbrain neurons and modest outside midbrain</title>
</json:item>
<json:item><host><author></author>
<title>Ciliax, B.J., C. Heilman, L.L. Demchyshyn, et al.. 1995 The dopamine transporter: immunochemical characterization and localization in brain. J. Neurosci. 15: 1714–1723.</title>
</host>
</json:item>
<json:item><author><json:item><name>B. Meister</name>
</json:item>
</author>
<host><volume>58</volume>
<pages><last>395</last>
<first>388</first>
</pages>
<author></author>
<title>Neuroendocrinology</title>
</host>
<title>Dopamine transporter mRNA in neurons of the rat hypothalamus</title>
</json:item>
<json:item><author><json:item><name>B.J. Ciliax</name>
</json:item>
</author>
<host><volume>409</volume>
<pages><last>56</last>
<first>38</first>
</pages>
<author></author>
<title>J. Comp. Neurol.</title>
</host>
<title>Immunocytochemical localization of the dopamine transporter in human brain</title>
</json:item>
<json:item><author><json:item><name>E. Weihe</name>
</json:item>
</author>
<host><volume>14</volume>
<pages><last>2449</last>
<first>2435</first>
</pages>
<author></author>
<title>FASEB J.</title>
</host>
<title>Chemical neuroanatomy of the vesicular amine transporters</title>
</json:item>
<json:item><author><json:item><name>J.C. Lin</name>
</json:item>
</author>
<host><volume>14</volume>
<pages><last>180</last>
<first>175</first>
</pages>
<author></author>
<title>Cell Dev. Biol.</title>
</host>
<title>Molecular mechanisms controlling the development of dopaminergic neurons</title>
</json:item>
<json:item><author><json:item><name>R. Riddle</name>
</json:item>
</author>
<host><volume>147</volume>
<pages><last>21</last>
<first>3</first>
</pages>
<author></author>
<title>Brain Res. Dev. Brain Res.</title>
</host>
<title>Making connections: the development of mesencephalic dopaminergic neurons</title>
</json:item>
<json:item><author><json:item><name>M. Smidt</name>
</json:item>
</author>
<host><volume>480</volume>
<pages><last>88</last>
<first>75</first>
</pages>
<author></author>
<title>Eur. J. Pharmacol.</title>
</host>
<title>Molecular mechanisms underlying midbrain dopamine neuron development and function</title>
</json:item>
<json:item><host><author></author>
<title>Hynes, M., J.A. Porter, C. Chiang, et al. 1995 Induction of midbrain dopaminergic neurons by Sonic hedgehog. Neuron 15: 35–44.</title>
</host>
</json:item>
<json:item><host><author></author>
<title>Kim, J., J. Auerbach, J. Rodriguez‐Gomez, et al. 2002 Dopamine neurons derived from embryonic stem cells function in an animal model of Parkinson's disease. Nature 418: 50–56.</title>
</host>
</json:item>
<json:item><host><author></author>
<title>Wurst, W. & L. Bally‐Cuif. 2001 Neural plate patterning: upstream and downstream of the isthmic organizer. Nat. Rev. Neurosci 2: 99–108.</title>
</host>
</json:item>
<json:item><author><json:item><name>G. Andrews</name>
</json:item>
</author>
<host><volume>23</volume>
<pages><last>120</last>
<first>107</first>
</pages>
<author></author>
<title>Mol. Cell Neurosci.</title>
</host>
<title>Dlx transcription factors regulate differentiation of dopaminergic neurons of the ventral thalamus</title>
</json:item>
<json:item><author><json:item><name>E. Rink</name>
</json:item>
</author>
<host><volume>137</volume>
<pages><last>100</last>
<first>89</first>
</pages>
<author></author>
<title>Brain Res. Dev. Brain Res.</title>
</host>
<title>Development of the catecholaminergic system in the early zebrafish brain: an immunohistochemical study</title>
</json:item>
<json:item><author><json:item><name>C. Verney</name>
</json:item>
</author>
<host><volume>429</volume>
<pages><last>44</last>
<first>22</first>
</pages>
<author></author>
<title>J. Comp. Neurol.</title>
</host>
<title>Structures of longitudinal brain zones that originate the substantia nigra and ventral tegmental area in human embryos, as revealed by cytoarchitecture, and tyrosine hydroxylase, calbindin, calretinin and GABA immunoreaction</title>
</json:item>
<json:item><author><json:item><name>J. Holzschuh</name>
</json:item>
</author>
<host><volume>23</volume>
<pages><last>5519</last>
<first>5507</first>
</pages>
<author></author>
<title>J. Neurosci.</title>
</host>
<title>Genetic analysis of the roles of Hh, FGF8, and nodal signaling during catecholaminergic system development in the zebrafish brain</title>
</json:item>
<json:item><author><json:item><name>R.H. Zetterstrom</name>
</json:item>
</author>
<host><volume>276</volume>
<pages><last>250</last>
<first>248</first>
</pages>
<author></author>
<title>Science</title>
</host>
<title>Dopamine neuron agenesis in Nurr1‐deficient mice</title>
</json:item>
<json:item><author><json:item><name>B. Joseph</name>
</json:item>
</author>
<host><volume>100</volume>
<pages><last>15624</last>
<first>15619</first>
</pages>
<author></author>
<title>Proc. Natl. Acad. Sci. USA</title>
</host>
<title>p57Kip2 cooperates with Nurr1 in developing dopamine cells</title>
</json:item>
<json:item><author><json:item><name>A. Abeliovich</name>
</json:item>
</author>
<host><volume>25</volume>
<pages><last>252</last>
<first>239</first>
</pages>
<author></author>
<title>Neuron</title>
</host>
<title>Mice lacking alpha‐synuclein display functional deficits in the nigrostriatal dopamine system</title>
</json:item>
<json:item><author><json:item><name>H. Simon</name>
</json:item>
</author>
<host><volume>21</volume>
<pages><last>3134</last>
<first>3126</first>
</pages>
<author></author>
<title>J. Neurosci.</title>
</host>
<title>Fate of midbrain dopamine neurons controlled by the Engrailed genes</title>
</json:item>
<json:item><author><json:item><name>O. Valdenaire</name>
</json:item>
</author>
<host><volume>220</volume>
<pages><last>584</last>
<first>577</first>
</pages>
<author></author>
<title>Eur. J. Biochem.</title>
</host>
<title>Transcription of the rat dopamine‐D2‐receptor gene from two promoters</title>
</json:item>
<json:item><author><json:item><name>H. Kawasaki</name>
</json:item>
</author>
<host><volume>99</volume>
<pages><last>1585</last>
<first>1580</first>
</pages>
<author></author>
<title>Proc. Natl. Acad. Sci. USA</title>
</host>
<title>Generation of dopaminergic neurons and pigmented epithelia from primate ES cells by stromal cell‐derived inducing activity</title>
</json:item>
<json:item><author><json:item><name>M.W. Moore</name>
</json:item>
</author>
<host><volume>382</volume>
<pages><last>79</last>
<first>76</first>
</pages>
<author></author>
<title>Nature</title>
</host>
<title>Renal and neural abnormalities in mice lacking GDNF</title>
</json:item>
<json:item><author><json:item><name>G. Castelo‐Branco</name>
</json:item>
</author>
<host><volume>100</volume>
<pages><last>12752</last>
<first>12747</first>
</pages>
<author></author>
<title>Proc. Natl. Acad. Sci. USA</title>
</host>
<title>Differential regulation of midbrain dopaminergic neuron development by Wnt‐1, Wnt‐3a, and Wnt‐5a</title>
</json:item>
<json:item><author><json:item><name>P. Damier</name>
</json:item>
</author>
<host><volume>122</volume>
<pages><last>1448</last>
<first>1437</first>
</pages>
<author></author>
<title>II. Patterns of loss of loss of dopamine-containing neurons. I. Parkinson's disease. Brain</title>
</host>
<title>The substantia nigra of the human brain</title>
</json:item>
</refBibs>
<genre><json:string>article</json:string>
</genre>
<host><volume>1035</volume>
<publisherId><json:string>NYAS</json:string>
</publisherId>
<pages><total>19</total>
<last>249</last>
<first>231</first>
</pages>
<issn><json:string>0077-8923</json:string>
</issn>
<issue>1</issue>
<genre><json:string>journal</json:string>
</genre>
<language><json:string>unknown</json:string>
</language>
<eissn><json:string>1749-6632</json:string>
</eissn>
<title>Annals of the New York Academy of Sciences</title>
<doi><json:string>10.1111/(ISSN)1749-6632</json:string>
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</host>
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<mods version="3.6"><titleInfo lang="en"><title>The Degeneration of Dopamine Neurons in Parkinson's Disease: Insights from Embryology and Evolution of the Mesostriatocortical System</title>
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<titleInfo type="alternative" contentType="CDATA" lang="en"><title>The Degeneration of Dopamine Neurons in Parkinson's Disease: Insights from Embryology and Evolution of the Mesostriatocortical System</title>
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<name type="personal"><namePart type="given">PHILIPPE</namePart>
<namePart type="family">VERNIER</namePart>
<affiliation>Development, Evolution, Plasticity of the Nervous System, Institute of Neurobiology A. Fessard, CNRS, 91198 Gif‐sur‐Yvette, France</affiliation>
<affiliation>E-mail: vernier@iaf.cnrs‐gif.fr</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">FREDERIC</namePart>
<namePart type="family">MORET</namePart>
<affiliation>Development, Evolution, Plasticity of the Nervous System, Institute of Neurobiology A. Fessard, CNRS, 91198 Gif‐sur‐Yvette, France</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">SOPHIE</namePart>
<namePart type="family">CALLIER</namePart>
<affiliation>Development, Evolution, Plasticity of the Nervous System, Institute of Neurobiology A. Fessard, CNRS, 91198 Gif‐sur‐Yvette, France</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">MARINA</namePart>
<namePart type="family">SNAPYAN</namePart>
<affiliation>Development, Evolution, Plasticity of the Nervous System, Institute of Neurobiology A. Fessard, CNRS, 91198 Gif‐sur‐Yvette, France</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">CHRISTOPHE</namePart>
<namePart type="family">WERSINGER</namePart>
<affiliation>Department of Pediatrics, Georgetown University, Washington, District of Columbia 20007, USA</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<name type="personal"><namePart type="given">ANITA</namePart>
<namePart type="family">SIDHU</namePart>
<affiliation>Department of Pediatrics, Georgetown University, Washington, District of Columbia 20007, USA</affiliation>
<role><roleTerm type="text">author</roleTerm>
</role>
</name>
<typeOfResource>text</typeOfResource>
<genre type="article" displayLabel="article"></genre>
<originInfo><publisher>Blackwell Publishing Ltd</publisher>
<place><placeTerm type="text">Oxford, UK</placeTerm>
</place>
<dateIssued encoding="w3cdtf">2004-12</dateIssued>
<copyrightDate encoding="w3cdtf">2004</copyrightDate>
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<language><languageTerm type="code" authority="rfc3066">en</languageTerm>
<languageTerm type="code" authority="iso639-2b">eng</languageTerm>
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<extent unit="figures">2</extent>
<extent unit="tables">1</extent>
<extent unit="references">58</extent>
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<abstract>Abstract: Parkinson's disease (PD) is, to a large extent, specific to the human species. Most symptoms are the consequence of the preferential degeneration of the dopamine‐synthesizing cells of the mesostriatal‐mesocortical neuronal pathway. Reasons for that can be traced back to the evolutionary mechanisms that shaped the dopamine neurons in humans. In vertebrates, dopamine‐containing neurons and nuclei do not exhibit homogenous phenotypes. In this respect, mesencephalic dopamine neurons of the substantia nigra and ventral tegmental area are characterized by a molecular combination (tyrosine hydroxylase, aromatic amino acid decarboxylase, monoamine oxidase, vesicular monoamine transporter, dopamine transporter—to name a few), which is not found in other dopamine‐containing neurons of the vertebrate brain. In addition, the size of these mesencephalic DA nuclei is tremendously expanded in humans as compared to other vertebrates. Differentiation of the mesencephalic neurons during development depends on genetic mechanisms, which also differ from those of other dopamine nuclei. In contrast, pathophysiological approaches to PD have highlighted the role of ubiquitously expressed molecules such as a‐synuclein, parkin, and microtubule‐associated proteins. We propose that the peculiar phenotype of the dopamine mesencephalic neurons, which has been selected during vertebrate evolution and reshaped in the human lineage, has also rendered these neurons particularly prone to oxidative stress, and thus, to the fairly specific neurodegeneration of PD. Numerous evidence has been accumulated to demonstrate that perturbed regulation of DAT‐dependent dopamine uptake, DAT‐dependent accumulation of toxins, dysregulation of TH activity as well as high sensitivity of DA mesencephalic neurons to oxidants are key components of the neurodegeneration process of PD. This view points to the contribution of nonspecific mechanisms (α‐synuclein aggregation) in a highly specific cellular environment (the dopamine mesencephalic neurons) and provides a robust framework to develop novel and rational therapeutic schemes in PD.</abstract>
<subject lang="en"><genre>keywords</genre>
<topic>Parkinson's disease (PD)</topic>
<topic>development</topic>
<topic>dopamine transporter</topic>
<topic>dopamine receptors</topic>
<topic>α‐synuclein</topic>
<topic>neuroprotection</topic>
</subject>
<relatedItem type="host"><titleInfo><title>Annals of the New York Academy of Sciences</title>
</titleInfo>
<genre type="journal">journal</genre>
<identifier type="ISSN">0077-8923</identifier>
<identifier type="eISSN">1749-6632</identifier>
<identifier type="DOI">10.1111/(ISSN)1749-6632</identifier>
<identifier type="PublisherID">NYAS</identifier>
<part><date>2004</date>
<detail type="title"><title>Protective Strategies for Neurodegenerative Diseases</title>
</detail>
<detail type="volume"><caption>vol.</caption>
<number>1035</number>
</detail>
<detail type="issue"><caption>no.</caption>
<number>1</number>
</detail>
<extent unit="pages"><start>231</start>
<end>249</end>
<total>19</total>
</extent>
</part>
</relatedItem>
<identifier type="istex">5B1D38C926A4F3FC8CDDF8DB627F9D146974C8D4</identifier>
<identifier type="DOI">10.1196/annals.1332.015</identifier>
<identifier type="ArticleID">NYAS231</identifier>
<recordInfo><recordContentSource>WILEY</recordContentSource>
<recordOrigin>Blackwell Publishing Ltd</recordOrigin>
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