Skip to main content
Key Specialties
Cardiology Diabetology Endocrinology Gastroenterology Geriatrics and Gerontology Gynecology and Obstetrics Hematology Infectious Disease Internal Medicine Nephrology Neurology Oncology Pediatrics Respiratory Medicine Rheumatology Surgery
Congress Coverage
2024 ACC Congress 2023 ESMO Congress 2023 EASD Congress 2023 ERS Congress 2023 ESC Congress
Clinical Collections
Advances in Alzheimer’s

Keynote webinar | Spotlight on medication adherence

LIVE: Thursday 27th June 2024, 18:00-19:30 (CEST)
Join our expert panel to discover why you need to understand the drivers of non-adherence in your patients, and how you can optimize medication adherence in your clinics to drastically improve patient outcomes.
ADVANCED SEARCH
Log in
Top
Molecular Neurodegeneration
Published in: Molecular Neurodegeneration 1/2012

Open Access 01-12-2012 | Research article

Wld S but not Nmnat1 protects dopaminergic neurites from MPP+neurotoxicity

Authors: Jo Ann V Antenor-Dorsey, Karen L O'Malley

Published in: Molecular Neurodegeneration | Issue 1/2012

Login to get access

Abstract

Background

The Wld S mouse mutant ("Wallerian degeneration-slow") delays axonal degeneration in a variety of disorders including in vivo models of Parkinson's disease. The mechanisms underlying Wld S -mediated axonal protection are unclear, although many studies have attributed Wld S neuroprotection to the NAD+-synthesizing Nmnat1 portion of the fusion protein. Here, we used dissociated dopaminergic cultures to test the hypothesis that catalytically active Nmnat1 protects dopaminergic neurons from toxin-mediated axonal injury.

Results

Using mutant mice and lentiviral transduction of dopaminergic neurons, the present findings demonstrate that Wld S but not Nmnat1, Nmnat3, or cytoplasmically-targeted Nmnat1 protects dopamine axons from the parkinsonian mimetic N-methyl-4-phenylpyridinium (MPP+). Moreover, NAD+ synthesis is not required since enzymatically-inactive Wld S still protects. In addition, NAD+ by itself is axonally protective and together with Wld S is additive in the MPP+ model.

Conclusions

Our data suggest that NAD+ and Wld S act through separate and possibly parallel mechanisms to protect dopamine axons. As MPP+ is thought to impair mitochondrial function, these results suggest that Wld S might be involved in preserving mitochondrial health or maintaining cellular metabolism.
Appendix
Available only for authorised users
Literature
1.
Dauer W, Przedborski S: Parkinson's disease: mechanisms and models. Neuron. 2003, 39: 889-909. 10.1016/S0896-6273(03)00568-3.CrossRefPubMed
2.
Blum D, Torch S, Lambeng N, Nissou M, Benabid AL, Sadoul R, Verna JM: Molecular pathways involved in the neurotoxicity of 6-OHDA, dopamine and MPTP: contribution to the apoptotic theory in Parkinson's disease. Prog Neurobiol. 2001, 65: 135-172. 10.1016/S0301-0082(01)00003-X.CrossRefPubMed
3.
Braak H, Ghebremedhin E, Rub U, Bratzke H, Del Tredici K: Stages in the development of Parkinson's disease-related pathology. Cell Tissue Res. 2004, 318: 121-134. 10.1007/s00441-004-0956-9.CrossRefPubMed
4.
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. 1973, 20: 415-455. 10.1016/0022-510X(73)90175-5.CrossRefPubMed
5.
Scherman D, Desnos C, Darchen F, Pollak P, Javoy-Agid F, Agid Y: Striatal dopamine deficiency in Parkinson's disease: role of aging. Ann Neurol. 1989, 26: 551-557. 10.1002/ana.410260409.CrossRefPubMed
6.
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. 1976, 38: 277-301. 10.1007/BF01249445.CrossRefPubMed
7.
Cheng HC, Ulane CM, Burke RE: Clinical progression in Parkinson disease and the neurobiology of axons. Ann Neurol. 2010, 67: 715-725. 10.1002/ana.21995.PubMedCentralCrossRefPubMed
8.
Fearnley JM, Lees AJ: Ageing and Parkinson's disease: substantia nigra regional selectivity. Brain. 1991, 114 (Pt 5): 2283-2301.CrossRefPubMed
9.
Kramer ML, Schulz-Schaeffer WJ: Presynaptic alpha-synuclein aggregates, not Lewy bodies, cause neurodegeneration in dementia with Lewy bodies. J Neurosci. 2007, 27: 1405-1410. 10.1523/JNEUROSCI.4564-06.2007.CrossRefPubMed
10.
Saha AR, Hill J, Utton MA, Asuni AA, Ackerley S, Grierson AJ, Miller CC, Davies AM, Buchman VL, Anderton BH, Hanger DP: Parkinson's disease alpha-synuclein mutations exhibit defective axonal transport in cultured neurons. J Cell Sci. 2004, 117: 1017-1024. 10.1242/jcs.00967.CrossRefPubMed
11.
Li Y, Liu W, Oo TF, Wang L, Tang Y, Jackson-Lewis V, Zhou C, Geghman K, Bogdanov M, Przedborski S, Beal MF, Burke RE, Li C: Mutant LRRK2(R1441G) BAC transgenic mice recapitulate cardinal features of Parkinson's disease. Nat Neurosci. 2009, 12: 826-828. 10.1038/nn.2349.PubMedCentralCrossRefPubMed
12.
Kitada T, Asakawa S, Hattori N, Matsumine H, Yamamura Y, Minoshima S, Yokochi M, Mizuno Y, Shimizu N: Mutations in the parkin gene cause autosomal recessive juvenile parkinsonism. Nature. 1998, 392: 605-608. 10.1038/33416.CrossRefPubMed
13.
Weihofen A, Thomas KJ, Ostaszewski BL, Cookson MR, Selkoe DJ: Pink1 forms a multiprotein complex with Miro and Milton, linking Pink1 function to mitochondrial trafficking. Biochemistry. 2009, 48: 2045-2052. 10.1021/bi8019178.PubMedCentralCrossRefPubMed
14.
Mortiboys H, Thomas KJ, Koopman WJ, Klaffke S, Abou-Sleiman P, Olpin S, Wood NW, Willems PH, Smeitink JA, Cookson MR, Bandmann O: Mitochondrial function and morphology are impaired in parkin-mutant fibroblasts. Ann Neurol. 2008, 64: 555-565. 10.1002/ana.21492.PubMedCentralCrossRefPubMed
15.
Ren Y, Liu W, Jiang H, Jiang Q, Feng J: Selective vulnerability of dopaminergic neurons to microtubule depolymerization. J Biol Chem. 2005, 280: 34105-34112. 10.1074/jbc.M503483200.CrossRefPubMed
16.
Cappelletti G, Pedrotti B, Maggioni MG, Maci R: Microtubule assembly is directly affected by MPP(+)in vitro. Cell Biol Int. 2001, 25: 981-984. 10.1006/cbir.2001.0772.CrossRefPubMed
17.
Cartelli D, Ronchi C, Maggioni MG, Rodighiero S, Giavini E, Cappelletti G: Microtubule dysfunction precedes transport impairment and mitochondria damage in MPP+ -induced neurodegeneration. J Neurochem. 2010, 115: 247-258. 10.1111/j.1471-4159.2010.06924.x.CrossRefPubMed
18.
Morfini G, Pigino G, Opalach K, Serulle Y, Moreira JE, Sugimori M, Llinas RR, Brady ST: 1-Methyl-4-phenylpyridinium affects fast axonal transport by activation of caspase and protein kinase C. Proc Natl Acad Sci USA. 2007, 104: 2442-2447. 10.1073/pnas.0611231104.PubMedCentralCrossRefPubMed
19.
Kim-Han JS, Antenor-Dorsey JA, O'Malley KL: The Parkinsonian Mimetic, MPP+, Specifically Impairs Mitochondrial Transport in Dopamine Axons. J Neurosci. 2011, 31: 7212-7221. 10.1523/JNEUROSCI.0711-11.2011.PubMedCentralCrossRefPubMed
20.
Coleman MP, Freeman MR: Wallerian degeneration, wld(s), and nmnat. Annu Rev Neurosci. 2010, 33: 245-267. 10.1146/annurev-neuro-060909-153248.CrossRefPubMed
21.
Mi W, Beirowski B, Gillingwater TH, Adalbert R, Wagner D, Grumme D, Osaka H, Conforti L, Arnhold S, Addicks K, Wada K, Ribchester RR, Coleman MP: The slow Wallerian degeneration gene, WldS, inhibits axonal spheroid pathology in gracile axonal dystrophy mice. Brain. 2005, 128: 405-416.CrossRefPubMed
22.
Sajadi A, Schneider BL, Aebischer P: Wlds-mediated protection of dopaminergic fibers in an animal model of Parkinson disease. Curr Biol. 2004, 14: 326-330.CrossRefPubMed
23.
Hasbani DM, O'Malley KL: Wld(S) mice are protected against the Parkinsonian mimetic MPTP. Exp Neurol. 2006, 202: 93-99. 10.1016/j.expneurol.2006.05.017.CrossRefPubMed
24.
Mack TG, Reiner M, Beirowski B, Mi W, Emanuelli M, Wagner D, Thomson D, Gillingwater T, Court F, Conforti L, Fernando FS, Tarlton A, Andressen C, Addicks K, Magni G, Ribchester RR, Perry VH, Coleman MP: Wallerian degeneration of injured axons and synapses is delayed by a Ube4b/Nmnat chimeric gene. Nat Neurosci. 2001, 4: 1199-1206.CrossRefPubMed
25.
Coleman MP, Conforti L, Buckmaster EA, Tarlton A, Ewing RM, Brown MC, Lyon MF, Perry VH: An 85-kb tandem triplication in the slow Wallerian degeneration (Wlds) mouse. Proc Natl Acad Sci USA. 1998, 95: 9985-9990. 10.1073/pnas.95.17.9985.PubMedCentralCrossRefPubMed
26.
Conforti L, Wilbrey A, Morreale G, Janeckova L, Beirowski B, Adalbert R, Mazzola F, Di Stefano M, Hartley R, Babetto E, Smith T, Gilley J, Billington RA, Genazzani AA, Ribchester RR, Magni G, Coleman M: Wld S protein requires Nmnat activity and a short N-terminal sequence to protect axons in mice. J Cell Biol. 2009, 184: 491-500. 10.1083/jcb.200807175.PubMedCentralCrossRefPubMed
27.
Araki T, Sasaki Y, Milbrandt J: Increased nuclear NAD biosynthesis and SIRT1 activation prevent axonal degeneration. Science. 2004, 305: 1010-1013. 10.1126/science.1098014.CrossRefPubMed
28.
Sasaki Y, Araki T, Milbrandt J: Stimulation of nicotinamide adenine dinucleotide biosynthetic pathways delays axonal degeneration after axotomy. J Neurosci. 2006, 26: 8484-8491. 10.1523/JNEUROSCI.2320-06.2006.CrossRefPubMed
29.
Avery MA, Sheehan AE, Kerr KS, Wang J, Freeman MR: WldS requires Nmnat1 enzymatic activity and N16-VCP interactions to suppress Wallerian degeneration. J Cell Biol. 2009, 184: 501-513. 10.1083/jcb.200808042.PubMedCentralCrossRefPubMed
30.
Zhai RG, Zhang F, Hiesinger PR, Cao Y, Haueter CM, Bellen HJ: NAD synthase NMNAT acts as a chaperone to protect against neurodegeneration. Nature. 2008, 452: 887-891. 10.1038/nature06721.PubMedCentralCrossRefPubMed
31.
Wen Y, Parrish JZ, He R, Zhai RG, Kim MD: Nmnat exerts neuroprotective effects in dendrites and axons. Mol Cell Neurosci. 2011
32.
Zhai RG, Cao Y, Hiesinger PR, Zhou Y, Mehta SQ, Schulze KL, Verstreken P, Bellen HJ: Drosophila NMNAT maintains neural integrity independent of its NAD synthesis activity. PLoS Biol. 2006, 4: e416-10.1371/journal.pbio.0040416.PubMedCentralCrossRefPubMed
33.
Lotharius J, Dugan LL, O'Malley KL: Distinct mechanisms underlie neurotoxin-mediated cell death in cultured dopaminergic neurons. J Neurosci. 1999, 19: 1284-1293.PubMed
34.
Babetto E, Beirowski B, Janeckova L, Brown R, Gilley J, Thomson D, Ribchester RR, Coleman MP: Targeting NMNAT1 to axons and synapses transforms its neuroprotective potency in vivo. J Neurosci. 2010, 30: 13291-13304. 10.1523/JNEUROSCI.1189-10.2010.CrossRefPubMed
35.
Sasaki Y, Milbrandt J: Axonal degeneration is blocked by nicotinamide mononucleotide adenylyltransferase (Nmnat) protein transduction into transected axons. J Biol Chem. 2010, 285: 41211-41215. 10.1074/jbc.C110.193904.PubMedCentralCrossRefPubMed
36.
Press C, Milbrandt J: Nmnat delays axonal degeneration caused by mitochondrial and oxidative stress. J Neurosci. 2008, 28: 4861-4871. 10.1523/JNEUROSCI.0525-08.2008.PubMedCentralCrossRefPubMed
37.
Verghese PB, Sasaki Y, Yang D, Stewart F, Sabar F, Finn MB, Wroge CM, Mennerick S, Neil JJ, Milbrandt J, Holtzman DM: Nicotinamide mononucleotide adenylyl transferase 1 protects against acute neurodegeneration in developing CNS by inhibiting excitotoxic-necrotic cell death. Proc Natl Acad Sci USA. 2011, 108: 19054-19059. 10.1073/pnas.1107325108.PubMedCentralCrossRefPubMed
38.
Sasaki Y, Vohra BP, Lund FE, Milbrandt J: Nicotinamide mononucleotide adenylyl transferase-mediated axonal protection requires enzymatic activity but not increased levels of neuronal nicotinamide adenine dinucleotide. J Neurosci. 2009, 29: 5525-5535. 10.1523/JNEUROSCI.5469-08.2009.PubMedCentralCrossRefPubMed
39.
Sasaki Y, Vohra BP, Baloh RH, Milbrandt J: Transgenic mice expressing the Nmnat1 protein manifest robust delay in axonal degeneration in vivo. J Neurosci. 2009, 29: 6526-6534. 10.1523/JNEUROSCI.1429-09.2009.PubMedCentralCrossRefPubMed
40.
Wishart TM, Pemberton HN, James SR, McCabe CJ, Gillingwater TH: Modified cell cycle status in a mouse model of altered neuronal vulnerability (slow Wallerian degeneration; Wlds). Genome Biol. 2008, 9: R101-10.1186/gb-2008-9-6-r101.PubMedCentralCrossRefPubMed
41.
Yan T, Feng Y, Zheng J, Ge X, Zhang Y, Wu D, Zhao J, Zhai Q: Nmnat2 delays axon degeneration in superior cervical ganglia dependent on its NAD synthesis activity. Neurochem Int. 2010, 56: 101-106. 10.1016/j.neuint.2009.09.007.CrossRefPubMed
42.
Conforti L, Fang G, Beirowski B, Wang MS, Sorci L, Asress S, Adalbert R, Silva A, Bridge K, Huang XP, Magni G, Glass JD, Coleman MP: NAD(+) and axon degeneration revisited: Nmnat1 cannot substitute for Wld(S) to delay Wallerian degeneration. Cell Death Differ. 2007, 14: 116-127. 10.1038/sj.cdd.4401944.CrossRefPubMed
43.
Yahata N, Yuasa S, Araki T: Nicotinamide mononucleotide adenylyltransferase expression in mitochondrial matrix delays Wallerian degeneration. J Neurosci. 2009, 29: 6276-6284. 10.1523/JNEUROSCI.4304-08.2009.CrossRefPubMed
44.
Kaneko S, Wang J, Kaneko M, Yiu G, Hurrell JM, Chitnis T, Khoury SJ, He Z: Protecting axonal degeneration by increasing nicotinamide adenine dinucleotide levels in experimental autoimmune encephalomyelitis models. J Neurosci. 2006, 26: 9794-9804. 10.1523/JNEUROSCI.2116-06.2006.CrossRefPubMed
45.
Yang J, Klaidman LK, Chang ML, Kem S, Sugawara T, Chan P, Adams JD: Nicotinamide therapy protects against both necrosis and apoptosis in a stroke model. Pharmacol Biochem Behav. 2002, 73: 901-910. 10.1016/S0091-3057(02)00939-5.CrossRefPubMed
46.
Sakakibara Y, Mitha AP, Ayoub IA, Ogilvy CS, Maynard KI: Delayed treatment with nicotinamide (vitamin B3) reduces the infarct volume following focal cerebral ischemia in spontaneously hypertensive rats, diabetic and non-diabetic Fischer 344 rats. Brain Res. 2002, 931: 68-73. 10.1016/S0006-8993(02)02263-1.CrossRefPubMed
47.
Demarin V, Podobnik SS, Storga-Tomic D, Kay G: Treatment of Alzheimer's disease with stabilized oral nicotinamide adenine dinucleotide: a randomized, double-blind study. Drugs Exp Clin Res. 2004, 30: 27-33.PubMed
48.
Birkmayer JG, Vrecko C, Volc D, Birkmayer W: Nicotinamide adenine dinucleotide (NADH)--a new therapeutic approach to Parkinson's disease. Comparison of oral and parenteral application. Acta Neurol Scand Suppl. 1993, 146: 32-35.PubMed
49.
Birkmayer JG: Coenzyme nicotinamide adenine dinucleotide: new therapeutic approach for improving dementia of the Alzheimer type. Ann Clin Lab Sci. 1996, 26: 1-9.PubMed
50.
Kuhn W, Muller T, Winkel R, Danielczik S, Gerstner A, Hacker R, Mattern C, Przuntek H: Parenteral application of NADH in Parkinson's disease: clinical improvement partially due to stimulation of endogenous levodopa biosynthesis. J Neural Transm. 1996, 103: 1187-1193. 10.1007/BF01271203.CrossRefPubMed
51.
Zhai RG, Rizzi M, Garavaglia S: Nicotinamide/nicotinic acid mononucleotide adenylyltransferase, new insights into an ancient enzyme. Cell Mol Life Sci. 2009, 66: 2805-2818. 10.1007/s00018-009-0047-x.CrossRefPubMed
52.
Ali YO, McCormack R, Darr A, Zhai RG: Nicotinamide Mononucleotide Adenylyltransferase Is a Stress Response Protein Regulated by the Heat Shock Factor/Hypoxia-inducible Factor 1α Pathway. J Biol Chem. 2011, 286: 19089-19099. 10.1074/jbc.M111.219295.PubMedCentralCrossRefPubMed
53.
Nicklas WJ, Vyas I, Heikkila RE: Inhibition of NADH-linked oxidation in brain mitochondria by 1-methyl-4-phenyl-pyridine, a metabolite of the neurotoxin, 1-methyl-4-phenyl-1,2,5,6-tetrahydropyridine. Life Sci. 1985, 36: 2503-2508. 10.1016/0024-3205(85)90146-8.CrossRefPubMed
54.
Ramsay RR, Krueger MJ, Youngster SK, Gluck MR, Casida JE, Singer TP: Interaction of 1-methyl-4-phenylpyridinium ion (MPP+) and its analogs with the rotenone/piericidin binding site of NADH dehydrogenase. J Neurochem. 1991, 56: 1184-1190. 10.1111/j.1471-4159.1991.tb11409.x.CrossRefPubMed
55.
Ramsay RR, Salach JI, Singer TP: Uptake of the neurotoxin 1-methyl-4-phenylpyridine (MPP+) by mitochondria and its relation to the inhibition of the mitochondrial oxidation of NAD+-linked substrates by MPP+. Biochem Biophys Res Commun. 1986, 134: 743-748. 10.1016/S0006-291X(86)80483-1.CrossRefPubMed
56.
Lotharius J, O'Malley KL: The parkinsonism-inducing drug 1-methyl-4-phenylpyridinium triggers intracellular dopamine oxidation. A novel mechanism of toxicity. J Biol Chem. 2000, 275: 38581-38588.CrossRefPubMed
57.
Chang GD, Ramirez VD: The mechanism of action of MPTP and MPP+ on endogenous dopamine release from the rat corpus striatum superfused in vitro. Brain Res. 1986, 368: 134-140. 10.1016/0006-8993(86)91050-4.CrossRefPubMed
58.
Cappelletti G, Surrey T, Maci R: The parkinsonism producing neurotoxin MPP+ affects microtubule dynamics by acting as a destabilising factor. FEBS Lett. 2005, 579: 4781-4786. 10.1016/j.febslet.2005.07.058.CrossRefPubMed
59.
Zhu JH, Horbinski C, Guo F, Watkins S, Uchiyama Y, Chu CT: Regulation of autophagy by extracellular signal-regulated protein kinases during 1-methyl-4-phenylpyridinium-induced cell death. Am J Pathol. 2007, 170: 75-86. 10.2353/ajpath.2007.060524.PubMedCentralCrossRefPubMed
60.
Barrientos SA, Martinez NW, Yoo S, Jara JS, Zamorano S, Hetz C, Twiss JL, Alvarez J, Court FA: Axonal degeneration is mediated by the mitochondrial permeability transition pore. J Neurosci. 2011, 31: 966-978. 10.1523/JNEUROSCI.4065-10.2011.PubMedCentralCrossRefPubMed
61.
Wishart TM, Paterson JM, Short DM, Meredith S, Robertson KA, Sutherland C, Cousin MA, Dutia MB, Gillingwater TH: Differential proteomics analysis of synaptic proteins identifies potential cellular targets and protein mediators of synaptic neuroprotection conferred by the slow Wallerian degeneration (Wlds) gene. Mol Cell Proteomics. 2007, 6: 1318-1330. 10.1074/mcp.M600457-MCP200.PubMedCentralCrossRefPubMed
62.
Miller BR, Press C, Daniels RW, Sasaki Y, Milbrandt J, DiAntonio A: A dual leucine kinase-dependent axon self-destruction program promotes Wallerian degeneration. Nat Neurosci. 2009, 12: 387-389. 10.1038/nn.2290.PubMedCentralCrossRefPubMed
63.
Surjana D, Halliday GM, Damian DL: Role of nicotinamide in DNA damage, mutagenesis, and DNA repair. J Nucleic Acids 2010. 2010
64.
Hisahara S, Chiba S, Matsumoto H, Horio Y: Transcriptional regulation of neuronal genes and its effect on neural functions: NAD-dependent histone deacetylase SIRT1 (Sir2α). J Pharmacol Sci. 2005, 98: 200-204. 10.1254/jphs.FMJ05001X2.CrossRefPubMed
65.
Wang J, Zhai Q, Chen Y, Lin E, Gu W, McBurney MW, He Z: A local mechanism mediates NAD-dependent protection of axon degeneration. J Cell Biol. 2005, 170: 349-355. 10.1083/jcb.200504028.PubMedCentralCrossRefPubMed
66.
Gillingwater TH, Haley JE, Ribchester RR, Horsburgh K: Neuroprotection after transient global cerebral ischemia in Wld(s) mutant mice. J Cereb Blood Flow Metab. 2004, 24: 62-66.CrossRefPubMed
67.
Ferri A, Sanes JR, Coleman MP, Cunningham JM, Kato AC: Inhibiting axon degeneration and synapse loss attenuates apoptosis and disease progression in a mouse model of motoneuron disease. Curr Biol. 2003, 13: 669-673. 10.1016/S0960-9822(03)00206-9.CrossRefPubMed
68.
Liang CL, Wang TT, Luby-Phelps K, German DC: Mitochondria mass is low in mouse substantia nigra dopamine neurons: implications for Parkinson's disease. Exp Neurol. 2007, 203: 370-380. 10.1016/j.expneurol.2006.08.015.CrossRefPubMed
69.
Hastings TG: The role of dopamine oxidation in mitochondrial dysfunction: implications for Parkinson's disease. J Bioenerg Biomembr. 2009, 41: 469-472. 10.1007/s10863-009-9257-z.CrossRefPubMed
70.
Surmeier DJ, Guzman JN, Sanchez-Padilla J, Goldberg JA: What causes the death of dopaminergic neurons in Parkinson's disease?. Prog Brain Res. 2010, 183: 59-77.CrossRefPubMed
71.
Dickson DW, Fujishiro H, Orr C, DelleDonne A, Josephs KA, Frigerio R, Burnett M, Parisi JE, Klos KJ, Ahlskog JE: Neuropathology of non-motor features of Parkinson disease. Parkinsonism Relat Disord. 2009, 15 (Suppl 3): S1-5.CrossRefPubMed
72.
Bernstein AI, Garrison SP, Zambetti GP, O'Malley KL: 6-OHDA generated ROS induces DNA damage and p53- and PUMA-dependent cell death. Mol Neurodegener. 2011, 6: 2-10.1186/1750-1326-6-2.PubMedCentralCrossRefPubMed
73.
Beirowski B, Babetto E, Gilley J, Mazzola F, Conforti L, Janeckova L, Magni G, Ribchester RR, Coleman MP: Non-nuclear Wld(S) determines its neuroprotective efficacy for axons and synapses in vivo. J Neurosci. 2009, 29: 653-668. 10.1523/JNEUROSCI.3814-08.2009.CrossRefPubMed
74.
Brown JA, Wysolmerski RB, Bridgman PC: Dorsal root ganglion neurons react to semaphorin 3A application through a biphasic response that requires multiple myosin II isoforms. Mol Biol Cell. 2009, 20: 1167-1179. 10.1091/mbc.E08-01-0065.PubMedCentralCrossRefPubMed
75.
Magni G, Amici A, Emanuelli M, Orsomando G, Raffaelli N, Ruggieri S: Enzymology of NAD+ homeostasis in man. Cell Mol Life Sci. 2004, 61: 19-34. 10.1007/s00018-003-3161-1.CrossRefPubMed
Metadata
Title
Wld S but not Nmnat1 protects dopaminergic neurites from MPP+neurotoxicity
Authors
Jo Ann V Antenor-Dorsey
Karen L O'Malley
Publication date
01-12-2012
Publisher
BioMed Central
Published in
Molecular Neurodegeneration / Issue 1/2012
Electronic ISSN: 1750-1326
DOI
https://doi.org/10.1186/1750-1326-7-5

Other articles of this Issue 1/2012

Molecular Neurodegeneration 1/2012 Go to the issue

Research article

Adeno-associated virus-mediated brain delivery of 5-lipoxygenase modulates the AD-like phenotype of APP mice

Research article

Loss of leucine-rich repeat kinase 2 causes age-dependent bi-phasic alterations of the autophagy pathway

Research article

Intraneuronal Aβ detection in 5xFAD mice by a new Aβ-specific antibody

Research article

Apoptosis-inducing factor downregulation increased neuronal progenitor, but not stem cell, survival in the neonatal hippocampus after cerebral hypoxia-ischemia

Methodology

Mass spectrometry quantification of clusterin in the human brain

Research article

Sorting nexin 12 interacts with BACE1 and regulates BACE1-mediated APP processing