Inflammation, genes and zinc in Alzheimer's disease.

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

Risultato della ricerca: Article

87 Citazioni (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.
Lingua originaleEnglish
pagine (da-a)96-105
Numero di pagine9
RivistaBrain Research Reviews
Volume58
Stato di pubblicazionePublished - 2008

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Zinc
Alzheimer Disease
Inflammation
Amyloid beta-Protein Precursor
Genes
Peptides
Neurofibrillary Tangles
Amyloid Plaques
Staphylococcal Protein A
Amyloid
Dementia
Metals
Genotype
Cytokines
Phenotype
Proteins

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)
  • Clinical Neurology

Cita questo

Inflammation, genes and zinc in Alzheimer's disease. / Balistreri, Carmela Rita; Caruso, Calogero; Candore, Giuseppina; Vasto, Sonya; Colonna Romano, Giuseppina; Lio, Domenico; Nuzzo, Domenico; Di Bona, Danilo; Malavolta, Marco; Mocchegiani, Eugenio; Nuzzo, Domenico; Listi', Florinda.

In: Brain Research Reviews, Vol. 58, 2008, pag. 96-105.

Risultato della ricerca: Article

Balistreri, CR, Caruso, C, Candore, G, Vasto, S, Colonna Romano, G, Lio, D, Nuzzo, D, Di Bona, D, Malavolta, M, Mocchegiani, E, Nuzzo, D & Listi', F 2008, 'Inflammation, genes and zinc in Alzheimer's disease.', Brain Research Reviews, vol. 58, pagg. 96-105.
Balistreri, Carmela Rita ; Caruso, Calogero ; Candore, Giuseppina ; Vasto, Sonya ; Colonna Romano, Giuseppina ; Lio, Domenico ; Nuzzo, Domenico ; Di Bona, Danilo ; Malavolta, Marco ; Mocchegiani, Eugenio ; Nuzzo, Domenico ; Listi', Florinda. / Inflammation, genes and zinc in Alzheimer's disease. In: Brain Research Reviews. 2008 ; Vol. 58. pagg. 96-105.
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AU - Candore, Giuseppina

AU - Vasto, Sonya

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AU - Lio, Domenico

AU - Nuzzo, Domenico

AU - Di Bona, Danilo

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AU - Listi', Florinda

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AB - 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.

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