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Central Administration of Amyloid β-Peptide (25–35) and Individual Features of Cognitive Behavior in Rats

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The individual characteristics of cognitive behavior induced by intracerebroventricular administration of aggregated amyloid β-peptide (25–35) (Aβ25–35) were studied. A new approach to evaluating individual features of the actions of Aβ25–35 was used. Navigational training was performed in a single brief session using random target positions, and training sessions were repeated a few days later. These experiments produced the first indication that cognitive behavior was undamaged in 50% of the rats at the early stage of Aβ25–35 exposure. The activities of the antioxidant enzymes superoxide dismutase and catalase in the cortex and hippocampus were significantly decreased in animals with and without cognitive impairments. We suggest that phenotypic characteristics may underlie the individual features of the animals’ responses to Aβ. At the early stage, aggregated Aβ may induce a compensatory reaction which prevents impairment of cognitive processes.

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References

  1. A. P. Grigorenko and E. I. Rogaev, “Molecular basis of Alzheimer’s disease,” Mol. Biol., 41, 331–345 (2007).

    Article  CAS  Google Scholar 

  2. S. V. Seredenin and E. A. Val’dman, “Genetic and biochemical approaches to the individual sensitivity to drugs,” Eksper. Klin. Farmakol., 66, 57–59 (2003).

    CAS  Google Scholar 

  3. C. Beauchamp and I. Gridovich, “Superoxide dismutase: improved assays and an assay applicable to acrylamide gels,” Anal. Biochem., 44, 276–281 (1971).

    Article  CAS  PubMed  Google Scholar 

  4. R. Cacabelos, “Pharmacogenomics in Alzheimer’s disease,” Meth. Mol. Biol., 448, 213–357 (2008).

    Article  CAS  Google Scholar 

  5. F. Cetin and S. Dincer, “The effect of intrahippocampal beta amyloid (1–42) peptide injection on oxidant and antioxidant status in rat brain,” Ann. N.Y. Acad. sci., 1100, 510–517 (2007).

    Article  CAS  PubMed  Google Scholar 

  6. B. Klementiev, T. Novikova, V. Novitskaya, P. S. Walmod, O. Dmytriyeva, B. Pakkenberg,V. Verezin, and E. Bock, “A neural cell adhesion molecule-derived peptide reduces neuropathological signs and cognitive impairment induced by Abeta(25–35),” Neurosci., 145, 209–224 (2007).

    Article  CAS  Google Scholar 

  7. E. Kosenko,Y. Kaminsky, I. G. Stavroskaya, and V. Felipo, “Alteration of mitochondrial calcium homeostasis by ammonia-induced activation of NMDA receptors in rat brain in vivo,” Brain Res., 880, 139–146 (2000).

    Article  CAS  PubMed  Google Scholar 

  8. M. A. Lovall, W. D. Ehmann, S. M. Butler, and W. R. Markesbery, “Elevated thiobarbituric acid-reactive substances and antioxidant enzyme activity in the brain in Alzheimer’s disease,” Neurology, 45, 1594–1601 (1995).

    Google Scholar 

  9. M. A. Lovell and W. R. Markesbery, “Oxidative DNA damage in mild cognitive impairment and late-stage Alzheimer’s disease,” Nucl. Acids Res., 35, 7497–7504 (2007).

    Article  CAS  PubMed  Google Scholar 

  10. E. A. Mugantseva, E. G. Makarova, and I. Ya. Podolski, “Investigation of neurotoxicity induced by beta-amyloid in rats,” in: Abstracts of International Interdisciplinary Congress “Neuroscience for Medicine and Psychology,” Sudak, Crimea, Ukraine (2007), pp. 164–154.

  11. G. Paxinos and C. Watson, The Rat Brain in Stereotaxic Coordinates, Academic Press, Sydney (1982).

    Google Scholar 

  12. I. Ya. Podolski, Z. A. Podlubnaya, E. A. Kosenko, E. A. Mugantseva, E. G. Makarova, L. G. Marsagishvili, M. D. Shpagina,Yu. G. Kaminsky, G. V. Andrievsky, and V. K. Klochkov, “Fullerene effects on amyloid β-peptide fibrillization in vitro and performance of the cognitive task,” J. Nanosci. Nanotechnol., 7, 1479–1485 (2007).

    Article  CAS  PubMed  Google Scholar 

  13. D. J. Selkoe, “Soluble oligomers of the amyloid beta-protein impair synaptic plasticity and behavior,” Behav. Brain Res., 192, 106–113 (2008).

    Article  CAS  PubMed  Google Scholar 

  14. M. Y. Stepanichev, M. V. Onufriev, O. S. Mitrokhina,Y. V. Moiseeva, N. A. Lazareva, I. V. Victorov, and N. V. Gluyaeva, “Neurochemical, behavioral, and neuromorphological effects of central administration of beta-amyloid peptide (25–35) in rat,” Neirokhimiya, 17, 278–293 (2000).

    CAS  Google Scholar 

  15. J. L. Yang, L. Weissman, V. A. Bohr, and M. P. Mattson, “Mitochondrial DNA damage and repair in neurodegenerative disorders,” DNA Repair, 8, 1110–1120 (2008).

    Article  Google Scholar 

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Correspondence to I. Ya. Podolskii.

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Translated from Zhurnal Vysshei Nervnoi Deyatel’nosti imeni I. P. Pavlova, Vol. 59, No. 5, pp. 616–621, September–October, 2009.

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Mugantseva, E.A., Podolskii, I.Y. Central Administration of Amyloid β-Peptide (25–35) and Individual Features of Cognitive Behavior in Rats. Neurosci Behav Physi 40, 964–968 (2010). https://doi.org/10.1007/s11055-010-9353-x

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  • DOI: https://doi.org/10.1007/s11055-010-9353-x

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