350 rub
Journal Neurocomputers №1 for 2015 г.
Article in number:
Neurochemical mechanisms of forming the nervous system autoimmune diseases
Authors:
I. V. Kudaeva - Dr. Sc. (Med.), Associate Professor, Head of Clinical Diagnostic Biochemistry Laboratory, FSBI "East-Siberian Scientific Center of Human Ecology" SD RAMS (Angarsk)
Abstract:
The results of the experimental and clinical studies dealing with the pathogenesis of the autoimmune diseases of the nervous system are represented in this survey. The antibody synthesis is known to be the function of specific immunity. At the same time, in the recent years it was indicated that the cells of inborn immunity may be activated by the necrosis and apoptosis products promoting the activation of the autoimmune processes. At present, some pathogenetical concepts of the autoimmune processes in the nervous system are isolated. A special role in studying the problem above is.given to the function disorder of the hematoencephalic barrier which may occur both in the massive lesion of the brain matter and in the disfunction of the endothelium and astrocytes. Till present, the pathogenetical significance of the-higher level of the autoantibodies to the different antigens of the nervous system as well as the role of different biologically active substances, the growth factors and neuromediators remain not well studied. At the same time, the activation of cellular mechanisms of immunity may be very important in the development of autoimmune processes. The mitochondria disfunction, disorder of energetical metabolism in the neurones and astrocytes are considered as another mechanism of neurodegeneration development. The excitotoxicity, neurotoxicity of zinc, neurotoxicity of amyloid-β, role of cytokines, nitrogen oxide and growth factors may be isolated among the neurochemical mechanisms of the autoimmune disease development of the nervous system.
Pages: 16-24
References

 

  1. ZHirnova I. G., Larina I. V., Komelkova L. V., Careva M. I. Rol adgezivnykh svojjstv lejjkocitov i syvorotki krovi v patogeneze rassejannogo skleroza // ZHurnal nevrologii i psikhiatrii im. C.C. Korsakova. 2008. T. 108. № 4. S. 56-61.
  2. Srivastava R, Aslam M, Kalluri S., Schirmer L. et al. Potassium Channel KIR4.1 as an Immune Target in Multiple Sclerosis // N Engl J Med 2012. V. 367. P. 115-123.
  3. Dutta R., McDonough J., Yin X., Peterson J., et al. Mitochondrial dysfunction as a cause of axonal degeneration in multiple sclerosis patients. // Ann. Neurol. 2006. V.59. P.478-489. http://www.ncbi.nlm.nih.gov/pubmed/16392116
  4. Lu F., Selak M., O\'Connor J., Croul S., et al. Oxidative damage to mitochondrial DNA and activity of mitochondrial enzymes in chronic active lesions of multiple sclerosis. // J. Neurol. Sci. 2000. V. 177. P. 95-103. http://www.ncbi.nlm.nih.gov/pubmed/10980305
  5. Nikic I., Merkler D., Sorbara C., Brinkoetter M.,et al. A reversible form of axon damage in experimental autoimmune encephalomyelitis and multiple sclerosis. // Nat. Med. 2011. V. 17. P. 495-499. http://www.ncbi.nlm.nih.gov/pubmed/21441916
  6. Hoyer S, Frolich I. Dementia: the significance of cerebral metabolic disturbances in Alzheimer-s disease. Relation to Parkinson-s disease. In: Handbook of neurochemistry and molecular biology 3rd edition, degenerative diseases of the nervous system. New York: Springer; 2007. P. 189-232.
  7. Pappas B.A., Bayley P.J., Bui B.K., Hansen L.A. Choline acetyltransferase activity and cognitive domain scores of Alzheimer-s patients. // Neurobiol Aging. 2000. V. 21. P.11-17. http://www.ncbi.nlm.nih.gov/pubmed/10794843
  8. Szutowicz A., Bielarczyk H., Gul S., Ronowska A. et al. Phenotype-dependent susceptibility of cholinergic neuroblastoma cells to neurotoxic inputs. // Metab Brain Dis. 2006. V.21. P. 149-161. http://www.ncbi.nlm.nih.gov/pubmed/16724269
  9. Martin L.J. Mitochondrial pathobiology in Parkinson-s disease and amyotrophic lateral sclerosis. // J Alzheimer-s Dis. 2010. V. 20. P. 335-356. http://www.ncbi.nlm.nih.gov/pubmed/20413846
  10. Higgins G.C., Beart P.M., Shin Y.S., Chen M.J. et al. Oxidative stress: emerging mitochondrial and cellular themes and variations in neuronal injury. // J Alzheimer-s Dis. 2010. V. 20(2). P. 453-473. http://www.ncbi.nlm.nih.gov/pubmed/20463398
  11. Lin M. T., Beal M. F. Mitochondrial dysfunction and oxidative stress in neurodegenerative diseases. // Nature. 2006. V. 443. P. 787-795. http://www.ncbi.nlm.nih.gov/pubmed/17051205
  12. Moncada S., Bolanos J. P. Nitric oxide, cell bioenergetics and neurodegeneration. // J Neurochem. 2006. V. 97. P. 1676-1689. http://www.ncbi.nlm.nih.gov/pubmed/16805776
  13. Murphy M. P., LeVine H. Alzheimer-s disease and amyloid-βpeptide. // J Alzheimer-s Dis. 2010. V. 19. P. 311-323. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2813509/?report=reader
  14. Berridge M. J. Calcium signaling and Alzheimer-s disease. // Neurochem Res. 2011. V. 36. P. 1149-1156. http://www.ncbi.nlm.nih.gov/pubmed/21184278
  15. Sensi S.L., Paoletti P., Bush A.I., Sekler I. Zinc in the physiology and pathology of the CNS. // Nat Rev Neurosci. 2009. V. 10. P. 780-792. http://www.ncbi.nlm.nih.gov/pubmed/19826435
  16. Steinert J. R., Chernova T., Forsythe I. D. Nitric oxide signaling in brain function, dysfunction, and dementia. // Neuroscientist. 2010. V. 16. P. 435-452. http://www.ncbi.nlm.nih.gov/pubmed/20817920
  17. Szutowicz A. Aluminum, NO, and nerve growth factor neurotoxicity in cholinergic neurons. // J Neurosci Res. 2001. V. 66. P. 1009-1018. http://www.ncbi.nlm.nih.gov/pubmed/11746431
  18. Fortress A. M., Buhusi M., Helke K. L., Granholm A. C. E. Cholinergic degeneration and alterations in the TrkA and p75NTR balance as a result of pro-NGF injection into aged rats. // J Aging Res. 2011. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3140182/?report=reader
  19. Perez S.E., He B., Muhmmad N., Oh K.J. et al. Cholinotropic basal forebrain system alterationsin 3xTg-AD transgenic mice. // Neurobiol Dis. 2011. V. 41. P. 338-352. http://www.ncbi.nlm.nih.gov/pubmed/20937383
  20. Takeda A. Zinc signaling in the hippocampus and its relation to pathogenesis of depression. // Mol Neurobiol. 2011. V. 44. P. 166-174. http://www.ncbi.nlm.nih.gov/pubmed/21161611
  21. Frederickson C. J., Maret W., Cuajungco M. P. Zinc and excitotoxic brain injury. // Neuroscientist. 2004. V. 10. P. 18-25. http://www.ncbi.nlm.nih.gov/pubmed/14987444
  22. Mocchegiani E., Bertoni-Freddari C., Marcellini F., Malavolta M. Brain, aging and neurodegeneration: role of zinc ion availability. // Progr Neurobiol. 2005. V. 75. P. 367-390. http://www.ncbi.nlm.nih.gov/pubmed/15927345
  23. Hynd M.R., Scott H. L., Dodd P. R. Glutamate-mediated excitotoxicity and neurodegeneration in Alzheimer-s disease. // Neurochem Int. 2004. V. 45. P. 583-595. http://www.ncbi.nlm.nih.gov/pubmed/15234100
  24. Supnet C., Bezprozvanny I. Neuronal calcium signaling, mitochondrial dysfunction, and Alzheimer-s disease. // J Alzheimer-s Dis. 2010. V. 20. P. S487-S498. http://www.ncbi.nlm.nih.gov/pubmed/20413848
  25. Yu J. T., Chang R. C. C., Tan L. Calcium dysregulation in Alzheimer-s disease: from mechanisms to therapeutic opportunities. // Progr Neurobiol. 2009. V. 89. P. 240-255. http://www.ncbi.nlm.nih.gov/pubmed/19664678
  26. Jhala S.S., Hazell A.S. Modeling neurodegenerative disease pathophysiology in thiamine deficiency: consequences of impaired oxidative metabolism. // Neurochem Int. 2011. V. 58. P. 248-260. http://www.ncbi.nlm.nih.gov/pubmed/21130821
  27. Ronowska A., Gul-Hinc S., Bielarczyk H., Pawełczyk T. Effects of zinc on SN56 cholinergic neuroblastoma cells. // J Neurochem. 2007. V. 103. P. 972-983. http://www.ncbi.nlm.nih.gov/pubmed/17662047
  28. Ronowska A., Dyś A., Jankowska-Kulawy A., Klimaszewska-Łata J. et al. Short-term effects of zinc on acetylcholine metabolism and viability of SN56 cholinergic neuroblastom cells. // Neurochem Int. 2010. V. 56. P. 143-151. http://www.ncbi.nlm.nih.gov/pubmed/19781588
  29. Madhavarao N. C., Chinopoulos C., Chandrasekaran K., Namboodiri M. A. A. Characterization of the N-acetylaspartate biosynthetic enzyme from rat brain. // J Neurochem. 2003. V. 86. P. 824-835. http://www.ncbi.nlm.nih.gov/pubmed/12887681
  30. Deutsch J., Rapoport S. I., Rosenberger T. A. Valproyl-CoA and estrified valproic acid are not found in brains of rats treated with valproic acid, but the brain concentrations of CoA and acetyl-CoA are altered. // Neurochem Res. 2003. V. 28. P. 861-866. http://www.ncbi.nlm.nih.gov/pubmed/12718439
  31. Bossy-Wetzel E., Talantova M. V., Lee W. D., Scholzke M.N. et al. Crosstalk between nitric oxide and zinc pathways to neuronal cell death involving mitochondrial dysfunction and p38-activated K+ channels // Neuron. 2004. V. 41. P. 351-365. http://www.ncbi.nlm.nih.gov/pubmed/14766175
  32. Bielarczyk H., Gul S., Ronowska A., Bizon-Zygmańska D. et al. RS-α-lipoic amid protects cholinergic cells against sodium nitroprusside and amyloid-βneurotoxicity through restoration of acetyl-CoA level. // J Neurochem. 2006. V. 98. P. 1242-1251. http://www.ncbi.nlm.nih.gov/pubmed/16787407
  33. Bielarczyk H., Tomaszewicz M., Madziar B., Ćwikowska J. et al. Relationships between cholinergic phenotype and acetyl-CoA level in hybrid Marine neuroblastoma cells of sep tal origin // J Neurosci Res. 2003. V. 73. P. 717-721. http://www.ncbi.nlm.nih.gov/pubmed/12929139
  34. Bielarczyk H., Jankowska A., Madziar B., Matecki A. et al. Differential toxicity of nitric oxide, aluminum and amyloid-beta peptide in SN56 cholinergic cells from mouse septum // Neurochem Int. 2003. V. 42. P. 323-331. http://www.ncbi.nlm.nih.gov/pubmed/12470706
  35. Kassiotis G, Kollias G. Uncoupling the proinflammatory from the immunosuppressive properties of tumor necrosis factor (TNF) at the p55 TNF receptor level: implications for pathogenesis and therapy of autoimmune demyelination. // Journal of Experimental Medicine. 2001. V. 193(4). P. 427-434. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2195909/
  36. Lin J, Ziring D, Desai S, et al.TNFα blockade in human diseases: an overview of efficacy and safety. // Clinical Immunology. 2008. V. 126(1). P. 13-30. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2291511/
  37. The Lenercept Multiple Sclerosis Study Group and The University of British Columbia MS/MRI Analysis Group. TNF neutralization in MS: results of a randomized, placebo-controlled multicenter study. // Neurology. 1999. V. 53(3). P. 457-465.
  38. Robinson W. H., Genovese M. C., Moreland L. W. Demyelinating and neurologic events reported in association with tumor necrosis factor alpha antagonism: by what mechanisms could tumor necrosis factor alpha antagonists improve rheumatoid arthritis but exacerbate multiple sclerosis - // Arthritis & Rheumatism. 2001. V. 44(9). P. 1977-1983.
  39. Ransohoff R. M., Perry V. H. Microglial physiology: unique stimuli, specialized responses. // Annu Rev Immunol. 2009. V. 27. P. 119-145.
  40. Block M. L., Zecca L., Hong J. S. Microglia-mediated neurotoxicity: uncovering the molecular mechanisms. // Nat Rev Neurosci. 2007. V. 8. P. 57-69.
  41. Bernstein H. G., Steiner J., Bogerts B. Glial cells in schizophrenia: pathophysiological significance and possible consequences for therapy. // Expert Rev Neurother. 2009. V. 9. P. 1059-1071.
  42. Monji A., Kato T., Kanba S. Cytokines and schizophrenia: Microglia hypothesis of schizophrenia. // Psychiatry Clin Neurosci. 2009. V. 63. P. 257-265.
  43. Dong Y., Benveniste E. N. Immune function of astrocytes. // Glia. 2001. V. 36. P. 180-190. http://www.ncbi.nlm.nih.gov/pubmed/11596126
  44. Donato R. Intracellular and extracellular roles of S100 proteins. // Microsc Res Tech. 2003. V. 60. P. 540-551. http://www.ncbi.nlm.nih.gov/pubmed/12645002
  45. Heizmann C. W., Ackermann G. E., Galichet A. Pathologies involving the S100 proteins and RAGE. // Subcell Biochem. 2007. V. 45. P. 93-138. http://www.ncbi.nlm.nih.gov/pubmed/18193636
  46. Rothermundt M., Ponath G., Glaser T., Hetzel G. S100B serum levels and long-term improvement of negative symptoms in patients with schizophrenia. // Neuropsychopharmacology. 2004. V. 29. P. 1004-1011. http://www.ncbi.nlm.nih.gov/pubmed/14997170
  47. Adami C., Sorci G., Blasi E. et al. S100B Expression in and effects on microglia // Glia. 2001. V. 33. P. 131-142.
  48. Sorci G., Bianchi R., Riuzzi F., Tubaro C. et al. S100B protein, a damage-associated molecular pattern protein in the brain and heart, and beyond. // Cardiovasc Psychiatry Neurol. 2010. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2933911/
  49. Steiner J., Bogerts B., Schroeter M. L., Bernstein H.G. S100B protein in neurodegenerative disorders. // Clin Chem Lab Med. 2011. V. 49. P. 409-424.
  50. Steiner J., Myint A.M., Schiltz K., Westphal S. et al. S100B serum levels in schizophrenia are presumably related to visceral obesity and insulin resistance. // Cardiovasc Psychiatry Neurol. 2010. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2902008/
  51. Steiner J., Bernstein H. G., Bielau H., Berndt A. et al. Evidence for a wide extra-astrocytic distribution of S100B in human brain. // BMC Neurosci. 2007. V. 8. P. 2. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1769505/
  52. Gomazkov O. A. «Nejjropeptidy i rostovye faktory mozga» Informacionno-spravochnoe izdanie. Moskva, 2002. 240 s.
  53. Ferrari G., Toffano G., Skaper S.D. Epidermal growth factor exerts neuronotrophic effects on dopaminergic and GABAergic CNS neurons: comparison with basic fibroblast growth factor. // J Neurosci Res. 1991. V. 30. P. 493-497. http://www.ncbi.nlm.nih.gov/pubmed/1800771
  54. Li Y., Liu L., Barger S.W., Griffin W.S. Interleukin-1 mediates pathological effects of microglia on tau phosphorylation and on synaptophysin synthesis in cortical neurons through a p38-MAPK pathway. // J Neurosci. 2003. V. 23. P. 1605-1611. http://www.ncbi.nlm.nih.gov/pubmed/12629164
  55. Namba H., Nagano T., Iwakura Y., Xiong H. et al. Transforming growth factor alpha attenuates the functional expression of AMPA receptors in cortical GABAergic neurons. // Mol Cell Neurosci. 2006. V. 31. P. 628-641. http://www.ncbi.nlm.nih.gov/pubmed/16443372
  56. Namba H., Takei N., Nawa H. Transforming growth factor-alpha changes firing properties of developing neocortical GABAergic neurons by down-regulation of voltage-gated potassium currents. // Neuroscience. 2003. V. 122. P. 637-646. http://www.ncbi.nlm.nih.gov/pubmed/14622907
  57. Qin L., Wu X., Block M.L., Liu Y. et al. Systemic LPS causes chronic neuroinflammation and progressive neurodegeneration. // Glia. 2007. V. 55. P. 453-462. http://www.ncbi.nlm.nih.gov/pubmed/17203472
  58. Kronfol Z., Remick D. G. Cytokines and the brain: implications for clinical psychiatry. // Am J Psychiatry. 2000. V. 157. P. 683-694. http://www.ncbi.nlm.nih.gov/pubmed/10784457
  59. Raison C. L., Miller A. H. Is depression an inflammatory disorder? // Curr Psychiatry Rep. 2011. V. 13. P. 467-475. http://www.ncbi.nlm.nih.gov/pubmed/21927805
  60. Benilova I., Karran E., De Strooper B. The toxic Aβoligomer and Alzheimer-s disease: an emperor in need of clothes. // Nat Neurosci. 2012. V. 15. P. 1-9. http://www.ncbi.nlm.nih.gov/pubmed/22286176
  61. Klunk W.E. Amyloid imaging as a biomarker for cerebral β-amyloidosis and risk prediction for Alzheimer dementia. // Neurobiol Aging. 2011. V. 32. P. S20-S36. http://www.ncbi.nlm.nih.gov/pubmed/22078170
  62. Robakis N. K. Mechanisms of AD neurodegeneration may be independent of Aβand its derivatives. // Neurobiol Aging. 2011. V. 32. P. 372-379. http://www.ncbi.nlm.nih.gov/pubmed/20594619