The role of nitric oxide in the pathogenesis of brain lesions during the development of Alzheimer's disease

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

Research output: Contribution to journalReview article

31 Scopus citations

Abstract

Nitric oxide (NO) is a key bioregulatory active molecule in the cardiovascular, immune and nervous systems, synthesized through converting L-arginine to L-citrulline by NO synthase (NOS). Research exploration supports the theory that this molecule appears to be one of the key factors for the disruption of normal brain homeostasis, which causes the development of brain lesions and pathology such as in Allzheimer's disease (AD). Especially the vascular content of NO activity appears to be a major contributor to this pathology before the overexpression of NOS activity in other brain cellular compartments develop. We theorize that pharmacological intervention using NO donors and/or NO suppressors should delay or minimize brain lesion development and further progression of brain pathology and dementia.

Original languageEnglish (US)
Pages (from-to)325-334
Number of pages10
JournalIn Vivo
Volume18
Issue number3
StatePublished - May 1 2004

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Keywords

  • Alzheimer's disease
  • Hypoperfusion
  • Nitric oxide
  • Review
  • Vessel lesion

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Pharmacology

Cite this

Seyidova, D., Aliyev, A., Rzayev, N., Obrenovich, M., Lamb, B. T., Smith, M. A., De La Torre, J. C., Perry, G., & Aliev, G. (2004). The role of nitric oxide in the pathogenesis of brain lesions during the development of Alzheimer's disease. In Vivo, 18(3), 325-334.