Modulation of SIRT1 expression in different neurodegenerative models and human pathologies

Pallàs, Mercè; Pizarro, Javier; Gutiérrez‐Cuesta, Javier; Crespo-Biel, Natàlia; Alvira, Daniel; Tajes, Marta; Yeste‐Velasco, Marc; Folch, Jaume; Canudas, Anna Maria; Sureda, Francesc X.; Ferrer, Isidre; Camins, Antoni

doi:10.1016/j.neuroscience.2008.04.065

Cited by 107 publications

(79 citation statements)

References 37 publications

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“…Accordingly, a decrease of SIRT1 expression with age in SAMP8 has been found [97] that correlate with a decrease in tau phosphorylation and with an increase in ADAM10 [58].…”

Section: Sirtuin 1 In Samp8: Biochemical Coincidences In Aging and Admentioning

confidence: 89%

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Senescence-Accelerated Mice P8: A Tool to Study Brain Aging and Alzheimer's Disease in a Mouse Model

Pallàs

2012

ISRN Cell Biology

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The causes of aging remain unknown, but they are probably intimately linked to a multifactorial process that affects cell networks to varying degrees. Although a growing number of aging and Alzheimer's disease (AD) animal models are available, a more comprehensive and physiological mouse model is required. In this context, the senescence-accelerated mouse prone 8 (SAMP8) has a number of advantages, since its rapid physiological senescence means that it has about half the normal lifespan of a rodent. In addition, according to data gathered over the last five years, some of its behavioral traits and histopathology resemble AD human dementia. SAMP8 has remarkable pathological similarities to AD and may prove to be an excellent model for acquiring more in-depth knowledge of the age-related neurodegenerative processes behind brain senescence and AD in particular. We review these facts and particularly the data on parameters related to neurodegeneration. SAMP8 also shows signs of aging in the immune, vascular, and metabolic systems, among others.

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“…Accordingly, a decrease of SIRT1 expression with age in SAMP8 has been found [97] that correlate with a decrease in tau phosphorylation and with an increase in ADAM10 [58].…”

Section: Sirtuin 1 In Samp8: Biochemical Coincidences In Aging and Admentioning

confidence: 89%

“…As mentioned above, alterations in Sirt1 expression have been determined in SAMP8 [97]. Sirt1 has been implicated in several cellular processes and in neurodegenerative disorders [90].…”

Section: Undetermined Pathways In Samp8 That Could Addmentioning

confidence: 93%

Senescence-Accelerated Mice P8: A Tool to Study Brain Aging and Alzheimer's Disease in a Mouse Model

Pallàs

2012

ISRN Cell Biology

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“…RESV also has a neuroprotective effect in dopaminergic neurons in organotypic midbrain slice cultures [39]. However, it remains to be clarified whether these neuroprotective effects in neurons are SIRT1 dependent, since SIRT1 levels decrease during aging and in neurodegenerative disorders such as Alzheimer's disease [40][41][42]. Therefore, the neuroprotective effects of RESV may be due to its antioxidant properties [34].…”

Section: Discussionmentioning

confidence: 99%

Resveratrol Inhibits Proliferation and Promotes Apoptosis of Neuroblastoma Cells: Role of Sirtuin 1

et al. 2010

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Resveratrol prolongs lifespan and prevent cancer formation; however, the mechanisms are not understood. Here we evaluated the cell-cycle inhibition and apoptosis of resveratrol in B65 neuroblastoma cells, and we also studied the effects of resveratrol on the mammalian silent information regulator 2 (SIRT1). Results show that resveratrol reduces cell viability and causes apoptosis at 24 h of treatment. Resveratrol partially blocked cell proliferation, and significantly increased the fraction of cells arrested in the S phase. The role of SIRT1 in cell-cycle effects mediated by resveratrol was studied through changes in the expression of SIRT1 using western blot. Exposure to resveratrol decreased SIRT1 content, concomitant with an increase in the acetylated form of sirtuin substrates p53 and NFκ-β. Treatment of B65 neuroblastoma cells with resveratrol also reduced the content of the phosphorylated form of AKT. Exposure to the SIRT1 inhibitors nicotinamide and sirtinol altered neither cell viability nor the fraction of apoptotic cells. Furthermore, when cells were exposed simultaneously to resveratrol and nicotinamide or sirtinol, no changes were observed in the fraction of apoptotic cells. Our results show that a decrease in SIRT1 content, caused by exposure to resveratrol, does not appear to be involved in cell-cycle arrest or activation of apoptosis.

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“…On the other hand, Sirt1 expression and its activity, and consequentially CCT activity, may be decreased in aging and diseased brains. A significant decrease in Sirt1 level has in fact been shown for brain tissues of HD (Pallà s et al, 2008) and AD (Julien et al, 2009) patients. Restoration or stimulation of Sirt1 level and activity may have therefore slowed neurodegeneration in the various animal models through CCT-mediated reduction of toxic protein aggregates.…”

Section: Cct's Role In the Folding And Clearance Of Polyglutamine Aggmentioning

confidence: 86%

Sirt1’s beneficial roles in neurodegenerative diseases – a chaperonin containing TCP‐1 (CCT) connection?

Gan

Tang

2010

Aging Cell

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SummarySir2 ⁄ Sirt1 and its orthologues are known lifespan extension factors in several aging models from yeast to invertebrates. Sirt1 activation is also known to be beneficial and protective in both invertebrate and mammalian models of neurodegenerative disease. Sirt1's lifespan extension effect, as well as the beneficial outcome of its activation in models of aging-associated diseases, is often attributed to its ability to instill a gene expression profile that is pro-survival and antiaging. A recent report from Nyströ m and colleagues showed that the yeast Sir2p affects the function of the polarisome in segregation and retrograde transport of damaged and aggregated proteins from the bud to the mother cell, thereby ensuring the generation of a 'rejuvenated' daughter cell. Interestingly, the role of Sir2p in this case involves deacetylation and activation of cytoplasmic chaperonin containing TCP-1 (CCT, or TriC), thereby enhancing actin folding and polymerization. In view of a previously documented role of CCT in modulating polyglutamine-containing protein aggregation and toxicity, we hypothesized that CCT deacetylation may also underlie Sirt1's beneficial effects in several neurodegenerative diseases precipitated by toxic aggregates. Other than alterations in gene expression profile, another major way whereby Sirt1 activation may counter neural aging could be to promote neuronal survival via prevention of toxic aggregate formation through CCT.

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Modulation of SIRT1 expression in different neurodegenerative models and human pathologies

Cited by 107 publications

References 37 publications

Senescence-Accelerated Mice P8: A Tool to Study Brain Aging and Alzheimer's Disease in a Mouse Model

Senescence-Accelerated Mice P8: A Tool to Study Brain Aging and Alzheimer's Disease in a Mouse Model

Resveratrol Inhibits Proliferation and Promotes Apoptosis of Neuroblastoma Cells: Role of Sirtuin 1

Sirt1’s beneficial roles in neurodegenerative diseases – a chaperonin containing TCP‐1 (CCT) connection?

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