Inflammation, genes and zinc in Alzheimer's disease

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

Research output: Contribution to journalArticlepeer-review


Alzheimer's disease (AD) is a heterogeneous and progressive neurodegenerative disease which in Western society mainly accounts for clinical dementia. AD has been linked to inflammation and metal biological pathway. Neuro-pathological hallmarks are senile plaques, resulting from the accumulation of several proteins and an inflammatory reaction around deposits of amyloid, a fibrillar protein, Aβ, product of cleavage of a much larger protein, the β-amyloid precursor protein (APP) and neurofibrillary tangles. Amyloid deposition, due to the accumulation of Aβ peptide, is the main pathogenetic mechanism. Inflammation clearly occurs in pathologically vulnerable regions of AD and several inflammatory factors influencing AD development, i.e. environmental factors (pro-inflammatory phenotype) and/or genetic factors (pro-inflammatory genotype) have been described. At the biochemical level metals such as zinc are known to accelerate the aggregation of the amyloid peptide and play a role in the control of inflammatory responses. In particular, zinc availability may regulate mRNA cytokine expression, so influencing inflammatory network phenotypic expression.

Original languageEnglish
Pages (from-to)96-105
Number of pages10
JournalBrain Research Reviews
Issue number1
Publication statusPublished - Jun 2008


  • Alzheimer's disease
  • Immunogenetic
  • Inflammation
  • Zinc

ASJC Scopus subject areas

  • Neuroscience(all)


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