CNF1 Increases Brain Energy Level, Counteracts Neuroinflammatory Markers and Rescues Cognitive Deficits in a Murine Model of Alzheimer's Disease (Articolo in rivista)

Type

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

Label

• CNF1 Increases Brain Energy Level, Counteracts Neuroinflammatory Markers and Rescues Cognitive Deficits in a Murine Model of Alzheimer's Disease (Articolo in rivista) (literal)

Anno

• 2013-01-01T00:00:00+01:00 (literal)

Alternative label

• Loizzo Stefano1; Rimondini Roberto2; Travaglione Sara1; Fabbri Alessia1; Guidotti Marco3; Ferri Alberto4; Campana Gabriele5; Fiorentini Carla1 (2013)
  CNF1 Increases Brain Energy Level, Counteracts Neuroinflammatory Markers and Rescues Cognitive Deficits in a Murine Model of Alzheimer's Disease
  in PloS one
  (literal)

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

• Loizzo Stefano1; Rimondini Roberto2; Travaglione Sara1; Fabbri Alessia1; Guidotti Marco3; Ferri Alberto4; Campana Gabriele5; Fiorentini Carla1 (literal)

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

• 8 (literal)

Rivista

• PloS one (Rivista)

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

• 5 (literal)

Note

• PubMed (literal)

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

• 1 Department of Therapeutic Research and Medicines Evaluation, Istituto Superiore di Sanità, Rome, Italy. 2 Medical and Surgical Sciences Department - DIMEC - University of Bologna, Bologna, Italy. 3 Department of Veterinary Public Health and Food Safety, Istituto Superiore di Sanità, Rome, Italy. 4 Institute of Cellular Biology and Neurobiology, CNR, Rome, Italy. 5 Pharmacy and Biotechnology Department - FaBiT - University of Bologna, Bologna, Italy. (literal)

Titolo

• CNF1 Increases Brain Energy Level, Counteracts Neuroinflammatory Markers and Rescues Cognitive Deficits in a Murine Model of Alzheimer's Disease (literal)

Abstract

• Overexpression of pro-inflammatory cytokines and cellular energy failure are associated with neuroinflammatory disorders, such as Alzheimer's disease. Transgenic mice homozygous for human ApoE4 gene, a well known AD and atherosclerosis animal model, show decreased levels of ATP, increased inflammatory cytokines level and accumulation of beta amyloid in the brain. All these findings are considered responsible for triggering cognitive decline. We have demonstrated that a single administration of the bacterial E. coli protein toxin CNF1 to aged apoE4 mice, beside inducing a strong amelioration of both spatial and emotional memory deficits, favored the cell energy restore through an increment of ATP content. This was accompanied by a modulation of cerebral Rho and Rac1 activity. Furthermore, CNF1 decreased the levels of beta amyloid accumulation and interleukin-1? expression in the hippocampus. Altogether, these data suggest that the pharmacological modulation of Rho GTPases by CNF1 can improve memory performances in an animal model of Alzheimer's disease via a control of neuroinflammation and a rescue of systemic energy homeostasis. (literal)

Prodotto di

• ex SV.P16.003.002 / Studio dei meccanismi molecolari di processi neurodegenerativi (SV.P16.003.005) (Modulo)

Autore CNR

• ALBERTO FERRI (Unità di personale interno)

Incoming links:

Autore CNR di

• ALBERTO FERRI (Unità di personale interno)

Prodotto

• ex SV.P16.003.002 / Studio dei meccanismi molecolari di processi neurodegenerativi (SV.P16.003.005) (Modulo)

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

• PloS one (Rivista)