Correction: Early age decline in DNA repair capacity in the liver: in depth profile of differential gene expression

Guedj, Avital; Geiger-Maor, Anat; Benyamini, Hadar; Nevo, Yaval; Elgavish, Sharona; Galun, Eithan; Amsalem, Hagai; Rachmilewitz, Jacob

doi:10.18632/aging.101242

Cited by 2 publications

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“…The GT effect has been studied in different animal models of learning impairments. Administration (1 g in 100 mL water for 5 min at 100°C, corresponding to 0.6–1 mg EGCG per day), from gestation to adulthood, corrected the lower BDNF mRNA levels in the hippocampus of mice overexpressing DYRK1A (dual-specificity tyrosine phosphorylation-regulated kinase 1A) but did not affect the performance in memory tasks [ 78 ].…”

Section: Green Tea ( Camellia Sinensis (L) Kunmentioning

confidence: 99%

Botanicals as Modulators of Neuroplasticity: Focus on BDNF

et al. 2017

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The involvement of brain-derived neurotrophic factor (BDNF) in different central nervous system (CNS) diseases suggests that this neurotrophin may represent an interesting and reliable therapeutic target. Accordingly, the search for new compounds, also from natural sources, able to modulate BDNF has been increasingly explored. The present review considers the literature on the effects of botanicals on BDNF. Botanicals considered were Bacopa monnieri (L.) Pennell, Coffea arabica L., Crocus sativus L., Eleutherococcus senticosus Maxim., Camellia sinensis (L.) Kuntze (green tea), Ginkgo biloba L., Hypericum perforatum L., Olea europaea L. (olive oil), Panax ginseng C.A. Meyer, Rhodiola rosea L., Salvia miltiorrhiza Bunge, Vitis vinifera L., Withania somnifera (L.) Dunal, and Perilla frutescens (L.) Britton. The effect of the active principles responsible for the efficacy of the extracts is reviewed and discussed as well. The high number of articles published (more than one hundred manuscripts for 14 botanicals) supports the growing interest in the use of natural products as BDNF modulators. The studies reported strengthen the hypothesis that botanicals may be considered useful modulators of BDNF in CNS diseases, without high side effects. Further clinical studies are mandatory to confirm botanicals as preventive agents or as useful adjuvant to the pharmacological treatment.

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Section: Green Tea ( Camellia Sinensis (L) Kunmentioning

confidence: 99%

Botanicals as Modulators of Neuroplasticity: Focus on BDNF

et al. 2017

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“…Numerous studies have found a significant decline of all four major repair pathways activities: BER ( Intano et al, 2002 , 2003 ; Zhang et al, 2010 ; Løhr et al, 2015 ; Xu et al, 2015 ), NER ( Goukassian et al, 2000 ; Boyle et al, 2005 ; Yamada et al, 2006 ), MMR ( Yehuda et al, 2001 ; Neri et al, 2005 ) and DSBR ( Seluanov et al, 2004 ; Ju et al, 2006 ; Vyjayanti and Rao, 2006 ; Mao et al, 2012 ; Vaidya et al, 2014 ; Li et al, 2016 ; Delabaere et al, 2017 ) with aging. Increasing evidence suggests that deficiencies in BER, NER, and DSBR indeed induce aging-associated phenotypes ( Borgesius et al, 2011 ; Pan et al, 2016 ; Guedj et al, 2017 ). Werner syndrome patients with an inherited defect in BER show features of premature aging ( Pan et al, 2016 ).…”

Section: Introductionmentioning

confidence: 99%

Pathologic Replication-Independent Endogenous DNA Double-Strand Breaks Repair Defect in Chronological Aging Yeast

2018

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Reduction of physiologic replication-independent endogenous DNA double strand breaks (Phy-RIND-EDSBs) in chronological aging yeast increases pathologic RIND-EDSBs (Path-RIND-EDSBs). Path-RIND-EDSBs can occur spontaneously in non-dividing cells without any inductive agents, and they must be repaired immediately otherwise their accumulation can lead to senescence. If yeasts have DSB repair defect, retention of Path-RIND-EDSBs can be found. Previously, we found that Path-RIND-EDSBs are not only produced but also retained in chronological aging yeast. Here, we evaluated if chronological aging yeasts have a DSB repair defect. We found a significant accumulation of Path-RIND-EDSBs around the same level in aging cells and caffeine treated cells and at a much higher level in the DSB repair mutant cells. Especially in the mutant, some unknown sequence was found inserted at the breaks. In addition, % difference of cell viability between HO induced and non-induced cells was significantly greater in aging cells. Our results suggested that RIND-EDSBs repair efficiency declines, but is not absent, in chronological aging yeast which might promote senescence phenotype. When a repair protein is deficient, an alternative pathway might be employed or an end modification process might occur as inserted sequences at the breaks were observed. Restoring repair defects might slow down the deterioration of cells from chronological aging.

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Correction: Early age decline in DNA repair capacity in the liver: in depth profile of differential gene expression

Cited by 2 publications

References 0 publications

Botanicals as Modulators of Neuroplasticity: Focus on BDNF

Botanicals as Modulators of Neuroplasticity: Focus on BDNF

Pathologic Replication-Independent Endogenous DNA Double-Strand Breaks Repair Defect in Chronological Aging Yeast

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