Is nitric oxide a key target in the pathogenesis of brain lesions during the development of Alzheimer's disease?

Ali Aliyev, Dilara Seyidova, Nizami Rzayev, Mark E. Obrenovich, Bruce T. Lamb, Shu G. Chen, Mark A. Smith, George Perry, Jack C. De La Torre, Gjumrakch Aliev

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28 Scopus citations

Abstract

Nitric oxide (NO) is a short-life key bioregulatory active molecule in the cardiovascular, immune and nervous systems. NO is synthesized by converting L-arginine to L-citrulline by enzymes called NO synthase (NOS). The growing body of evidence strongly supports the theory that this molecule appears to be one of the key targets for the disruption of normal brain homeostasis, which causes the development of brain lesions and pathology such as in Alzheimer's disease (AD) or other related dementia. The vascular content of NO activity appears especially to be a main contributor to this pathology before the over-expression of other NOS isoforms activity in a different brain cellular compartment. We speculate that pharmacological intervention using NO donors and/or NO suppressors will be able to delay or minimize the development of brain pathology and further progression of mental retardation.

Original languageEnglish (US)
Pages (from-to)547-553
Number of pages7
JournalNeurological Research
Volume26
Issue number5
DOIs
StatePublished - Jul 1 2004

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Keywords

  • Brain hypoperfusion
  • Dementia
  • Nitric oxide, Alzheimer's disease
  • Oxidative stress

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology

Cite this

Aliyev, A., Seyidova, D., Rzayev, N., Obrenovich, M. E., Lamb, B. T., Chen, S. G., Smith, M. A., Perry, G., De La Torre, J. C., & Aliev, G. (2004). Is nitric oxide a key target in the pathogenesis of brain lesions during the development of Alzheimer's disease? Neurological Research, 26(5), 547-553. https://doi.org/10.1179/01610425017613