http://www.cnr.it/ontology/cnr/individuo/prodotto/ID180427
Inflammation, genes and zinc in Alzheimer's disease. (Articolo in rivista)
- Type
- Label
- Inflammation, genes and zinc in Alzheimer's disease. (Articolo in rivista) (literal)
- Anno
- 2008-01-01T00:00:00+01:00 (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
- 10.1016/j.brainresrev.2007.12.001 (literal)
- Alternative label
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
- Vasto S; Candore G; Listì F; Balistreri CR; Colonna-Romano G; Malavolta M; Lio D; Nuzzo D; Mocchegiani E; Di Bona D; Caruso C (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
- Rivista
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
- Titolo
- Inflammation, genes and zinc in Alzheimer's disease. (literal)
- 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,A?, product of cleavage of amuchlarger protein,
the ?-amyloid precursor protein (APP) and neurofibrillary tangles. Amyloid deposition, due
to the accumulation of A? 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. (literal)
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- Autore CNR
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