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Immunomodulators as Therapeutic Agents in Mitigating the Progression of Parkinson’s Disease

Grimmig, Bethany, Morganti, Josh, Nash, Kevin, Bickford, Paula·2016·Brain Sciences

Abstract

Parkinson’s disease (PD) is a common neurodegenerative disorder that primarily afflicts the elderly. It is characterized by motor dysfunction due to extensive neuron loss in the substantia nigra pars compacta. There are multiple biological processes that are negatively impacted during the pathogenesis of PD, and are implicated in the cell death in this region. Neuroinflammation is evidently involved in PD pathology and mitigating the inflammatory cascade has been a therapeutic strategy. Age is the number one risk factor for PD and thus needs to be considered in the context of disease pathology. Here, we discuss the role of neuroinflammation within the context of aging as it applies to the development of PD, and the potential for two representative compounds, fractalkine and astaxanthin, to attenuate the pathophysiology that modulates neurodegeneration that occurs in Parkinson’s disease.

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Research works printed but not linked: 59

  1. Kowal, 2013, The current and projected economic burden of Parkinson’s disease in the United States, Mov. Disord., 28, 311, 10.1002/mds.25292 · DOI · Paper page
  2. Braak, 2004, Stages in the development of Parkinson’s disease-related pathology, Cell Tissue Res., 318, 121, 10.1007/s00441-004-0956-9 · DOI · Paper page
  3. Stefanovic, 2014, α-Synuclein oligomers distinctively permeabilize complex model membranes, FEBS J., 281, 2838, 10.1111/febs.12824 · DOI
  4. Danzer, 2007, Different species of alpha-synuclein oligomers induce calcium influx and seeding, J. Neurosci., 27, 9220, 10.1523/JNEUROSCI.2617-07.2007 · DOI · Paper page
  5. Luth, 2014, Soluble, prefibrillar α-synuclein oligomers promote complex I-dependent, Ca2+-induced mitochondrial dysfunction, J. Biol. Chem., 289, 21490, 10.1074/jbc.M113.545749 · DOI
  6. Gamble, 2014, Formation of α-synuclein Lewy neurite-like aggregates in axons impedes the transport of distinct endosomes, Mol. Biol. Cell, 25, 4010, 10.1091/mbc.e14-02-0741 · DOI
  7. Lashuel, 2002, Alpha-synuclein, especially the Parkinson’s disease-associated mutants, forms pore-like annular and tubular protofibrils, J. Mol. Biol., 322, 1089, 10.1016/S0022-2836(02)00735-0 · DOI
  8. Hurtig, 2000, Alpha-synuclein cortical Lewy bodies correlate with dementia in Parkinson’s disease, Neurology, 54, 1916, 10.1212/WNL.54.10.1916 · DOI
  9. Tanaka, 2004, Aggresomes formed by alpha-synuclein and synphilin-1 are cytoprotective, J. Biol. Chem., 279, 4625, 10.1074/jbc.M310994200 · DOI
  10. Reeve, 2014, Ageing and Parkinson’s disease: Why is advancing age the biggest risk factor?, Ageing Res. Rev., 14, 19, 10.1016/j.arr.2014.01.004 · DOI
  11. Dias, 2013, The role of oxidative stress in Parkinson’s disease, J. Parkinsons Dis., 3, 461, 10.3233/JPD-130230 · DOI · Paper page
  12. Bharath, 2002, Glutathione, iron and Parkinson’s disease, Biochem. Pharmacol., 64, 1037, 10.1016/S0006-2952(02)01174-7 · DOI
  13. Venkateshappa, 2012, Increased oxidative damage and decreased antioxidant function in aging human substantia nigra compared to striatum: Implications for Parkinson’s disease, Neurochem. Res., 37, 358, 10.1007/s11064-011-0619-7 · DOI
  14. Paolicelli, 2011, Microglia in development: Linking brain wiring to brain environment, Neuron Glia Biol., 7, 77, 10.1017/S1740925X12000105 · DOI
  15. Jurgens, 2012, Dysregulated neuronal-microglial cross-talk during aging, stress and inflammation, Exp. Neurol., 233, 40, 10.1016/j.expneurol.2010.11.014 · DOI · Paper page
  16. Lee, 2013, Aging enhances classical activation but mitigates alternative activation in the central nervous system, Neurobiol. Aging, 34, 1610, 10.1016/j.neurobiolaging.2012.12.014 · DOI
  17. Hickman, 2013, The microglial sensome revealed by direct RNA sequencing, Nat. Neurosci., 16, 1896, 10.1038/nn.3554 · DOI · Paper page
  18. Cho, 2015, SIRT1 deficiency in microglia contributes to cognitive decline in aging and neurodegeneration via epigenetic regulation of IL-1β, J. Neurosci., 35, 807, 10.1523/JNEUROSCI.2939-14.2015 · DOI · Paper page
  19. McGeer, 1988, Rate of cell death in parkinsonism indicates active neuropathological process, Ann. Neurol., 24, 574, 10.1002/ana.410240415 · DOI
  20. Knott, 2000, Inflammatory regulators in Parkinson’s disease: iNOS, lipocortin-1, and cyclooxygenases-1 and -2, Mol. Cell. Neurosci., 16, 724, 10.1006/mcne.2000.0914 · DOI · Paper page
  21. Goldman, 2006, Head injury and Parkinson’s disease risk in twins, Ann. Neurol., 60, 65, 10.1002/ana.20882 · DOI · Paper page
  22. Lawson, 1990, Heterogeneity in the distribution and morphology of microglia in the normal adult mouse brain, Neuroscience, 39, 151, 10.1016/0306-4522(90)90229-W · DOI · Paper page
  23. Sharma, 2015, Characterization of the lipopolysaccharide induced model of Parkinson’s disease: Role of oxidative stress and neuroinflammation, Neurochem. Int., 87, 92, 10.1016/j.neuint.2015.06.004 · DOI
  24. Reynolds, 2008, Nitrated alpha-synuclein-activated microglial profiling for Parkinson’s disease, J. Neurochem., 104, 1504, 10.1111/j.1471-4159.2007.05087.x · DOI
  25. Cao, 2010, Fcγ receptors are required for NF-κB signaling, microglial activation and dopaminergic neurodegeneration in an AAV-synuclein mouse model of Parkinson’s disease, Mol. Neurodegener., 5, 42, 10.1186/1750-1326-5-42 · DOI
  26. Cao, 2012, The gamma chain subunit of Fc receptors is required for alpha-synuclein-induced pro-inflammatory signaling in microglia, J. Neuroinflamm., 9, 259, 10.1186/1742-2094-9-259 · DOI
  27. Polinski, 2015, Recombinant adenoassociated virus 2/5-mediated gene transfer is reduced in the aged rat midbrain, Neurobiol. Aging, 36, 1110, 10.1016/j.neurobiolaging.2014.07.047 · DOI
  28. Nash, 2015, Fractalkine over expression suppresses α-synuclein-mediated neurodegeneration, Mol. Ther., 23, 17, 10.1038/mt.2014.175 · DOI
  29. Morganti, 2012, The soluble isoform of CX3CL1 is necessary for neuroprotection in a mouse model of Parkinson’s disease, J. Neurosci., 32, 14592, 10.1523/JNEUROSCI.0539-12.2012 · DOI
  30. Rees, 2011, Non-steroidal anti-inflammatory drugs as disease-modifying agents for Parkinson’s disease: Evidence from observational studies, Cochrane Database Syst. Rev., 11, CD008454
  31. Du, 2001, Minocycline prevents nigrostriatal dopaminergic neurodegeneration in the MPTP model of Parkinson’s disease, Proc. Natl. Acad. Sci. USA, 98, 14669, 10.1073/pnas.251341998 · DOI · Paper page
  32. Lee, 2004, Minocycline inhibits apoptotic cell death via attenuation of TNF-alpha expression following iNOS/NO induction by lipopolysaccharide in neuron/glia co-cultures, J. Neurochem., 91, 568, 10.1111/j.1471-4159.2004.02780.x · DOI
  33. Jones, 2010, Fractalkine/CX3CL1: A potential new target for inflammatory diseases, Mol. Interv., 10, 263, 10.1124/mi.10.5.3 · DOI
  34. Thome, A.D., Standaert, D.G., and Harms, A.S. (2015). Fractalkine signaling regulates the inflammatory response in an α-synuclein model of Parkinson disease. PLoS ONE, 10. · DOI
  35. Lee, 2014, Opposing effects of membrane-anchored CX3CL1 on amyloid and tau pathologies via the p38 MAPK pathway, J. Neurosci., 34, 12538, 10.1523/JNEUROSCI.0853-14.2014 · DOI · Paper page
  36. Norden, 2013, Review: Microglia of the aged brain: Primed to be activated and resistant to regulation, Neuropathol. Appl. Neurobiol., 39, 19, 10.1111/j.1365-2990.2012.01306.x · DOI · Paper page
  37. Bachstetter, 2011, Fractalkine and CX 3 CR1 regulate hippocampal neurogenesis in adult and aged rats, Neurobiol. Aging, 32, 2030, 10.1016/j.neurobiolaging.2009.11.022 · DOI · Paper page
  38. Surmeier, 2010, Calcium, cellular aging, and selective neuronal vulnerability in Parkinson’s disease, Cell Calcium, 47, 175, 10.1016/j.ceca.2009.12.003 · DOI
  39. Surmeier, 2010, What causes the death of dopaminergic neurons in Parkinson’s Disease?, Prog. Brain Res., 183, 59, 10.1016/S0079-6123(10)83004-3 · DOI
  40. Kim, 2010, Down-regulation of IL-6 production by astaxanthin via ERK-, MSK-, and NF-κB-mediated signals in activated microglia, Int. Immunopharmacol., 10, 1560, 10.1016/j.intimp.2010.09.007 · DOI
  41. Liu, 2009, Astaxanthin inhibits reactive oxygen species-mediated cellular toxicity in dopaminergic SH-SY5Y cells via mitochondria-targeted protective mechanism, Brain Res., 1254, 18, 10.1016/j.brainres.2008.11.076 · DOI
  42. Lee, 2011, Astaxanthin protects against MPTP/MPP+-induced mitochondrial dysfunction and ROS production in vivo and in vitro, Food Chem. Toxicol., 49, 271, 10.1016/j.fct.2010.10.029 · DOI
  43. Kidd, 2011, Astaxanthin, a cell membrane nutrient with diverse clinical benefits and anti aging potential, Am. Med. Rev., 16, 355
  44. Park, 2012, Astaxanthin modulates age-associated mitochondrial dysfunction in healthy dogs, J. Anim. Sci., 91, 268275
  45. Otton, 2010, Astaxanthin ameliorates the redox imbalance in lymphocytes of experimental diabetic rats, Chem. Biol. Interact., 186, 306, 10.1016/j.cbi.2010.05.011 · DOI
  46. Augusti, 2012, Astaxanthin prevents changes in the activities of thioredoxin reductase and paraoxonase in hypercholesterolemic rabbits, J. Clin. Biochem. Nutr., 51, 42, 10.3164/jcbn.11-74 · DOI
  47. Li, 2013, Astaxanthin protects ARPE-19 cells from oxidative stress via upregulation of Nrf2-regulated phase II enzymes through activation of PI3K/Akt, Mol. Vis., 19, 1656
  48. Wang, 2010, Astaxanthin upregulates heme oxygenase-1 expression through ERK1/2 pathway and its protective effect against beta-amyloid-induced cytotoxicity in SH-SY5Y cells, Brain Res., 1360, 159, 10.1016/j.brainres.2010.08.100 · DOI
  49. Brunk, 2002, The mitochondrial-lysosomal axis theory of aging: Accumulation of damaged mitochondria as a result of imperfect autophagocytosis, Eur. J. Biochem., 269, 1996, 10.1046/j.1432-1033.2002.02869.x · DOI
  50. Collier, 2011, Ageing as a primary risk factor for Parkinson’s disease: Evidence from studies of non-human primates, Nat. Rev. Neurosci., 12, 359, 10.1038/nrn3039 · DOI
  51. Qin, 2015, Macrophage-microglia networks drive M1 microglia polarization after mycobacterium infection, Inflammation, 38, 1609, 10.1007/s10753-015-0136-y · DOI
  52. Minogue, 2014, Age-associated dysregulation of microglial activation is coupled with enhanced blood-brain barrier permeability and pathology in APP/PS1 mice, Neurobiol. Aging, 35, 1442, 10.1016/j.neurobiolaging.2013.12.026 · DOI
  53. Choi, 2008, Effects of astaxanthin on the production of NO and the expression of COX-2 and iNOS in LPS-stimulated BV2 microglial cells, J. Microbiol. Biotechnol., 18, 1990
  54. Guzman, 2014, Mitochondrial oxidant stress in locus coeruleus is regulated by activity and nitric oxide synthase, Nat. Neurosci., 17, 832, 10.1038/nn.3717 · DOI
  55. Dryanovski, 2013, Calcium entry and α-synuclein inclusions elevate dendritic mitochondrial oxidant stress in dopaminergic neurons, J. Neurosci., 33, 10154, 10.1523/JNEUROSCI.5311-12.2013 · DOI
  56. Surmeier, 2011, The role of calcium and mitochondrial oxidant stress in the loss of substantia nigra pars compacta dopaminergic neurons in Parkinson’s disease, Neuroscience, 198, 221, 10.1016/j.neuroscience.2011.08.045 · DOI · Paper page
  57. Parkinson Study Group (2013). Phase II safety, tolerability, and dose selection study of isradipine as a potential disease-modifying intervention in early Parkinson’s disease (STEADY-PD). Mov. Disord., 28, 1823–1831. · DOI
  58. Wolf, 2010, Astaxanthin protects mitochondrial redox state and functional integrity against oxidative stress, J. Nutr. Biochem., 21, 381, 10.1016/j.jnutbio.2009.01.011 · DOI
  59. Ye, Q., Huang, B., Zhang, X., Zhu, Y., and Chen, X. (2012). Astaxanthin protects against MPP(+)-induced oxidative stress in PC12 cells via the HO-1/NOX2 axis. BMC Neurosci., 13. · DOI

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Metadata

Authors
Grimmig, B., Morganti, J., Nash, K., & Bickford, P.
Venue
Brain Sciences
Publisher
MDPI AG
Published
2016-09-23
Volume
6
Issue
4
Pages
41
ISSN
2076-3425
Cited by
17
References
12
Language
en
Funders
  • National Institutes of Health (AG04418, AG044919)
  • Dept. Veterans Affairs (IO1BX000231)

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