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.
|Numero di pagine||9|
|Rivista||Brain Research Reviews|
|Stato di pubblicazione||Published - 2008|