Inflammation and oxidative damage in Alzheimer's disease: Friend or foe?

Research output: Contribution to journalArticle

Abstract

The two major neuropathologic hallmarks of AD are extracellular Amyloid beta plaques and intracellular neurofibrillary tangles. A number of additional pathogenic mechanisms have been described, including inflammation and oxidative damage. Regarding inflammation, several cytokines and chemokines have been detected both immunohistochemically and in Cerebrospinal Fluid from patients. Some of them, including Tumor Necrosis Factoralpha, Interferon-gamma-inducible Protein-10, Monocyte Chemotactic Protein-1 and Interleukin-8, are increased in AD and in Mild Cognitive Impairment, considered the prodromal stage of AD, suggesting that these modifications occur very early during the development of the disease, possibly explaining the failure of trials with antiinflammatory agents in patients with severe AD. Further evidence suggests that cytokines and chemokines could play a role in other neurodegenerative disorders. These disorders are considered multifactorial diseases, and genetic factors influence pathological events and contribute to change the disease phenotype from patient to patient. Gene polymorphisms in crucial molecules, including cytokines, chemokines and molecules related to oxidative stress, may act as susceptibility factors, or may operate as regulatory factors, modulating the severity of pathogenic processes.

Original languageEnglish
Pages (from-to)252-266
Number of pages15
JournalFrontiers in Bioscience - Scholar
Volume3 S
Issue number1
Publication statusPublished - Jan 1 2011

Keywords

  • Alzheimer's disease
  • Amyloid beta
  • Inflammation
  • Nitric oxide
  • Oxidative damage
  • Review
  • Tau

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Immunology and Microbiology(all)
  • Medicine(all)

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