SIRT1 is decreased during relapses in patients with multiple sclerosis

Tegla, Cosmin; Azimzadeh, Philippe; Andrian-Albescu, Maria; Martin, Alvaro; Cudrici, Cornelia; Trippe, Richard; Sugarman, Adam; Chen, Hegang; Boodhoo, Dallas; Vlaicu, Sonia I.; Royal, Walter; Bever, Christopher T.; Rus, Violeta; Rus, Horea

doi:10.1016/j.yexmp.2013.12.010

Cited by 62 publications

(42 citation statements)

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“…Previous findings showed that a reduced concentration of Sirt1 protein is observed in AD patients serum [11]. Since Sirt1 mRNA and protein are expressed in peripheral blood leukocytes [38], it can be assumed that the protein released in serum is produced by blood cells. If this is the case, our findings suggest that the control of Sirt1 protein levels is not exerted through the repression of mRNA expression by promoter hypermethylation.…”

Section: Discussionmentioning

confidence: 98%

Peripheral leukocyte expression of the potential biomarker proteins Bdnf, Sirt1, and Psen1 is not regulated by promoter methylation in Alzheimer's disease patients

Carboni

Lattanzio

Candeletti

et al. 2015

Neuroscience Letters

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Section: Discussionmentioning

confidence: 98%

Peripheral leukocyte expression of the potential biomarker proteins Bdnf, Sirt1, and Psen1 is not regulated by promoter methylation in Alzheimer's disease patients

Carboni

Lattanzio

Candeletti

et al. 2015

Neuroscience Letters

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“…Resveratrol also attenuates early brain injury after subarachnoid hemorrhage through inhibition of NF-kappaB-dependent inflammatory/MMP-9 (Shao et al , 2014). Protection against other neurodegenerative diseases such as Alzheimer’s (Kim et al , 2007a), Parkinson’s (Wu et al , 2011), Huntington’s (Jiang et al , 2012), amyotrophic lateral sclerosis (Kim et al , 2007a), and multiple sclerosis (Tegla et al , 2014) has also been shown with SIRT1.…”

Section: Pharmacologic Therapiesmentioning

confidence: 99%

Mitochondrial function in hypoxic ischemic injury and influence of aging

Ham

Raju

2017

Progress in Neurobiology

282

205

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Mitochondria are a major target in hypoxic/ischemic injury. Mitochondrial impairment increases with age leading to dysregulation of molecular pathways linked to mitochondria. The perturbation of mitochondrial homeostasis and cellular energetics worsens outcome following hypoxic-ischemic insults in elderly individuals. In response to acute injury conditions, cellular machinery relies on rapid adaptations by modulating posttranslational modifications. Therefore, post-translational regulation of molecular mediators such as hypoxia-inducible factor 1α (HIF-1α), peroxisome proliferator-activated receptor γ coactivator α (PGC-1α), c-MYC, SIRT1 and AMPK play a critical role in the control of the glycolytic-mitochondrial energy axis in response to hypoxic-ischemic conditions. The deficiency of oxygen and nutrients leads to decreased energetic reliance on mitochondria, promoting glycolysis. The combination of pseudohypoxia, declining autophagy, and dysregulation of stress responses with aging adds to impaired host response to hypoxic-ischemic injury. Furthermore, intermitochondrial signal propagation and tissue wide oscillations in mitochondrial metabolism in response to oxidative stress are emerging as vital to cellular energetics. Recently reported intercellular transport of mitochondria through tunneling nanotubes also play a role in the response to and treatments for ischemic injury. In this review we attempt to provide an overview of some of the molecular mechanisms and potential therapies involved in the alteration of cellular energetics with aging and injury with a neurobiological perspective.

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“…The mechanism for readily diploidizing of hESCs remains unclear now, but the age-related pathologies might result from cellular stress conditions during high passage [7]. In certain situations, autophagy has often been regarded as a defense mechanism to protect cells under stress conditions [8], but it has been complicated by the identification that whether autophagy or apoptosis mainly occur in diploidizated hESCs at high passage.…”

Section: Introductionmentioning

confidence: 99%