Bulletin of Experimental Biology and Medicine

, Volume 132, Issue 5, pp 1079–1083

Dimebon and Tacrine Inhibit Neurotoxic Action of β-Amyloid in Culture and Block L-type Ca2+ Channels

  • N. N. Lermontova
  • A. E. Redkozubov
  • E. F. Shevtsova
  • T. P. Serkova
  • E. G. Kireeva
  • S. O. Bachurin
Article

DOI: 10.1023/A:1017972709652

Cite this article as:
Lermontova, N.N., Redkozubov, A.E., Shevtsova, E.F. et al. Bulletin of Experimental Biology and Medicine (2001) 132: 1079. doi:10.1023/A:1017972709652

Abstract

Dimebon, a Russian-made drug, inhibited toxic effects of beta -amyloid on cultured neurons. Excessive accumulation of beta-amyloid in the brain is characteristic of Alzheimer dementias. Antialzheimer preparations tacrine and dimebon improve survival of cerebellar granule cells during long-term incubation with Ab25-35, the neurotoxic fragment of beta-amyloid. Both preparations can block potential-dependent Ca2+ entry into neurons by about 20%, which is explained by their selective action on L-type Ca2+ channels. It was assumed that the neuroprotective effect of dimebon and tacrine against Ab25-35 partially depends on inhibition of potential-dependent Ca2+ entry.

dimebon tacrine Ab25-35, cerebellar granule cells L-type Ca2+channels 

Copyright information

© Plenum Publishing Corporation 2001

Authors and Affiliations

  • N. N. Lermontova
    • 1
  • A. E. Redkozubov
    • 1
  • E. F. Shevtsova
    • 1
  • T. P. Serkova
    • 1
  • E. G. Kireeva
    • 1
  • S. O. Bachurin
    • 1
  1. 1.Department of Biological Research, Institute of Physiologically Active SubstancesRussian Academy of SciencesChernogolovka, Moscow Region

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