Inflammation, genes and zinc in Alzheimer's disease.

Giuseppina Candore, Domenico Lio, Carmela Rita Balistreri, Sonya Vasto, Calogero Caruso, Giuseppina Colonna Romano, Domenico Nuzzo, Danilo Di Bona, Marco Malavolta, Eugenio Mocchegiani, Domenico Nuzzo, Florinda Listi'

Research output: Contribution to journalArticlepeer-review

91 Citations (Scopus)

Abstract

Alzheimer's disease (AD) is a heterogeneous and progressive neurodegenerative diseasewhich in Western society mainly accounts for clinical dementia. AD has been linked toinflammation and metal biological pathway. Neuro-pathological hallmarks are senileplaques, resulting from the accumulation of several proteins and an inflammatory reactionaround deposits of amyloid, a fibrillar protein,Aβ, product of cleavage of amuchlarger protein,the β-amyloid precursor protein (APP) and neurofibrillary tangles. Amyloid deposition, dueto the accumulation of Aβ peptide, is the main pathogenetic mechanism. Inflammationclearly occurs in pathologically vulnerable regions of AD and several inflammatory factorsinfluencing AD development, i.e. environmental factors (pro-inflammatory phenotype) and/or genetic factors (pro-inflammatory genotype) have been described. At the biochemical levelmetals such as zinc are known to accelerate the aggregation of theamyloid peptide and play arole in the control of inflammatory responses. In particular, zinc availability may regulatemRNA cytokine expression, so influencing inflammatory network phenotypic expression.
Original languageEnglish
Pages (from-to)96-105
Number of pages9
JournalBrain Research Reviews
Volume58
Publication statusPublished - 2008

All Science Journal Classification (ASJC) codes

  • General Neuroscience
  • Clinical Neurology

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