Alzheimer's disease (AD) is a complex disorder that affects the central nervous system causing a severe neurodegeneration. This pathology affects an increasing number of people worldwide due to the overall aging of the human population. In recent years SUMO protein modification has emerged as a possible cellular mechanism involved in AD. Some of the proteins engaged in the physiopathological process of AD, like BACE1, GSK3-β tau, AβPP, and JNK, are in fact subject to protein SUMO modifications or interactions. Here, we have investigated the SUMO/deSUMOylation balance and SUMO-related proteins during the onset and progression of the pathology in the Tg2576 mouse model of AD. We examined four age-stages (1.5, 3, 6, 17 months old) and observed shows an increase in SUMO-1 protein conjugation at 3 and 6 months in transgenic mice with respect to WT in both cortex and hippocampus. Interestingly this is paralleled by increased expression levels of Ubc9 and SENP1 in both brain regions. At 6 months of age also the SUMO-1 mRNA resulted augmented. SUMO-2-ylation was surprisingly decreased in old transgenic mice and was unaltered in the other time windows. The fact that alterations in SUMO/deSUMOylation equilibrium occur from the early phases of AD suggests that global posttranslational modifications may play an important role in the mechanisms underlying disease pathogenesis, thus providing potential targets for pharmacological interventions.

Age-related changes of protein SUMOylation balance in the AβPP Tg2576 mouse model of Alzheimer's disease / Nistico', ROBERT GIOVANNI; Caterina, Ferraina; Marconi, Veronica; Fabio, Blandini; Lucia, Negri; Jan, Egebjerg; Marco, Feligioni. - In: FRONTIERS IN PHARMACOLOGY. - ISSN 1663-9812. - 5:(2014), pp. 63-63. [10.3389/fphar.2014.00063]

Age-related changes of protein SUMOylation balance in the AβPP Tg2576 mouse model of Alzheimer's disease.

NISTICO', ROBERT GIOVANNI;MARCONI, VERONICA;
2014

Abstract

Alzheimer's disease (AD) is a complex disorder that affects the central nervous system causing a severe neurodegeneration. This pathology affects an increasing number of people worldwide due to the overall aging of the human population. In recent years SUMO protein modification has emerged as a possible cellular mechanism involved in AD. Some of the proteins engaged in the physiopathological process of AD, like BACE1, GSK3-β tau, AβPP, and JNK, are in fact subject to protein SUMO modifications or interactions. Here, we have investigated the SUMO/deSUMOylation balance and SUMO-related proteins during the onset and progression of the pathology in the Tg2576 mouse model of AD. We examined four age-stages (1.5, 3, 6, 17 months old) and observed shows an increase in SUMO-1 protein conjugation at 3 and 6 months in transgenic mice with respect to WT in both cortex and hippocampus. Interestingly this is paralleled by increased expression levels of Ubc9 and SENP1 in both brain regions. At 6 months of age also the SUMO-1 mRNA resulted augmented. SUMO-2-ylation was surprisingly decreased in old transgenic mice and was unaltered in the other time windows. The fact that alterations in SUMO/deSUMOylation equilibrium occur from the early phases of AD suggests that global posttranslational modifications may play an important role in the mechanisms underlying disease pathogenesis, thus providing potential targets for pharmacological interventions.
2014
tg2576; sumoylation; senp1; ubc9; alzheimer's disease; neurodegeneration; sumo-2/3; sumo-1
01 Pubblicazione su rivista::01a Articolo in rivista
Age-related changes of protein SUMOylation balance in the AβPP Tg2576 mouse model of Alzheimer's disease / Nistico', ROBERT GIOVANNI; Caterina, Ferraina; Marconi, Veronica; Fabio, Blandini; Lucia, Negri; Jan, Egebjerg; Marco, Feligioni. - In: FRONTIERS IN PHARMACOLOGY. - ISSN 1663-9812. - 5:(2014), pp. 63-63. [10.3389/fphar.2014.00063]
File allegati a questo prodotto
Non ci sono file associati a questo prodotto.

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11573/560719
 Attenzione

Attenzione! I dati visualizzati non sono stati sottoposti a validazione da parte dell'ateneo

Citazioni
  • ???jsp.display-item.citation.pmc??? 23
  • Scopus 56
  • ???jsp.display-item.citation.isi??? 52
social impact