http://www.cnr.it/ontology/cnr/individuo/prodotto/ID27781

NOS-mediated morphological and molecular modifications in rats infused with Abeta (1-40), as a model of Alzheimer's disease, in response to a new lipophilic molecular combination codrug-1. (Articolo in rivista)

Type

Prodotto della ricerca (Classe)
Articolo in rivista (Classe)

Label

NOS-mediated morphological and molecular modifications in rats infused with Abeta (1-40), as a model of Alzheimer's disease, in response to a new lipophilic molecular combination codrug-1. (Articolo in rivista) (literal)

Anno

2011-01-01T00:00:00+01:00 (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi

10.1016/j.exger.2010.11.001. (literal)

Alternative label

Zara S, Di Stefano A, Nasuti C, Rapino M, Patruno A, Pesce M, Sozio P, Cerasa LS, Cataldi A. (2011)
NOS-mediated morphological and molecular modifications in rats infused with Abeta (1-40), as a model of Alzheimer's disease, in response to a new lipophilic molecular combination codrug-1.
in Experimental gerontology
(literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori

Zara S, Di Stefano A, Nasuti C, Rapino M, Patruno A, Pesce M, Sozio P, Cerasa LS, Cataldi A. (literal)

Pagina inizio

273 (literal)

Pagina fine

281 (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume

46 (literal)

Rivista

Experimental gerontology (Rivista)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#pagineTotali

9 (literal)

Note

ISI Web of Science (WOS) (literal)

Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni

Dipartimento di Scienze del Farmaco, Università G. d'Annunzio, Chieti, Pescara, Italy Dipartimento di Medicina Sperimentale e Sanità Pubblica, Università di Camerino, Camerino (MC), Italy Istituto di Genetica Molecolare del CNR, Unità di Chieti, Italy Dipartimento di Scienze del Movimento Umano, Università G. d'Annunzio, Chieti, Pescara, Italy Dipartimento di Medicina e Scienze dell'Invecchiamento, Cattedra di Anatomia Umana, Università G. d'Annunzio, Chieti, Pescara, Italy (literal)

Titolo

NOS-mediated morphological and molecular modifications in rats infused with Abeta (1-40), as a model of Alzheimer's disease, in response to a new lipophilic molecular combination codrug-1. (literal)

Abstract

Alzheimer's disease is a neurodegenerative pathology due to the presence of beta-amyloid plaques at brain level and hippocampus level and associated with the loss of memory speech and learning. At the basis of these effects lie molecular mechanisms which include nitric oxide metabolic pathway, whose involvement in the occurrence of morphological modifications related to such neurodegenerative process is suggested. Current evidences show that the non-steroidal anti-inflammatory drug ibuprofen posses a protective effect against the development of the disease, substantially delaying its onset; furthermore (R)-alpha-lipoic acid seems to have an antioxidant ameliorating effect on disease progression. Starting from these data, a new lipophilic codrug 1, obtained by joining an antioxidant molecule with an NSAID, has been previously synthesized. Our aim has been to investigate the possible therapeutical effects of codrug 1, compared to ibuprofen, on the molecular events at the basis of behavioural and morphological modifications occurring in Abeta (1-40) infused rat brains. Ibuprofen and codrug 1 seem to protect the subject against memory performance impairment and against behavioural detriment, induced by administration of Abeta (1-40) peptide. Such evidences are supported by morphological and biochemical findings showing Abeta (1-40) to determine cell disorganization, increased number of beta-amyloid plaques and capillary vessels dilatation in parallel to increased total and specific NOS activity and to apoptosis occurrence, partly prevented by ibuprofen, more broadly by codrug 1. Such results underline the involvement of nitric oxide metabolic pathway in the events related to the onset of this pathology and suggest codrug 1 as a useful tool to protect the brain against cognitive and behavioural dysfunction, by reducing ²-amyloid plaques formation and by inhibiting NOS signalling pathway and apoptosis occurrence. (literal)

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