86 Citazioni (Scopus)

Abstract

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 amuchlarger 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 theamyloid 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.
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
Genes
Peptides
Neurofibrillary Tangles
Proteins
Amyloid beta-Peptides
Amyloid Plaques
Amyloid
Dementia
Metals
Genotype
Cytokines
Phenotype

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)
  • Clinical Neurology

Cita questo

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title = "Inflammation, genes and zinc in Alzheimer's disease.",
abstract = "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 amuchlarger 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 theamyloid 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.",
author = "Calogero Caruso and {Colonna Romano}, Giuseppina and Giuseppina Candore and Domenico Lio and Florinda Listi' and Balistreri, {Carmela Rita} and Domenico Nuzzo and Sonya Vasto and {Di Bona}, Danilo and Marco Malavolta and Eugenio Mocchegiani and Domenico Nuzzo",
year = "2008",
language = "English",
volume = "58",
pages = "96--105",
journal = "Brain Research Reviews",
issn = "0165-0173",
publisher = "Elsevier",

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TY - JOUR

T1 - Inflammation, genes and zinc in Alzheimer's disease.

AU - Caruso, Calogero

AU - Colonna Romano, Giuseppina

AU - Candore, Giuseppina

AU - Lio, Domenico

AU - Listi', Florinda

AU - Balistreri, Carmela Rita

AU - Nuzzo, Domenico

AU - Vasto, Sonya

AU - Di Bona, Danilo

AU - Malavolta, Marco

AU - Mocchegiani, Eugenio

AU - Nuzzo, Domenico

PY - 2008

Y1 - 2008

N2 - 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 amuchlarger 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 theamyloid 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.

AB - 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 amuchlarger 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 theamyloid 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.

UR - http://hdl.handle.net/10447/46636

M3 - Article

VL - 58

SP - 96

EP - 105

JO - Brain Research Reviews

JF - Brain Research Reviews

SN - 0165-0173

ER -