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Sökning: L773:1872 6216 OR L773:0047 6374

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11.
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  • Lagunas-Rangel, Francisco Alejandro, et al. (författare)
  • Learning of nature : The curious case of the naked mole rat
  • 2017
  • Ingår i: Mechanisms of Ageing and Development. - : Elsevier BV. - 0047-6374 .- 1872-6216. ; 164, s. 76-81
  • Tidskriftsartikel (refereegranskat)abstract
    • Naked mole rats (NMRs) are the longest-living rodents known, living up to approximately 30 years and showing sustained good health. Nowadays, NMRs are considered excellent models for aging and, additionally, for cancer research, due to the evidence of a remarkable cancer resistance demonstrated through thousands of necropsies performed with very few cases that describe this pathology, which is believed to be a disease that unavoidably accompanies aging. Since some years ago, several studies have tried to explain the possible mechanisms underlying longevity and cancer resistance in NMRs through different perspectives and directions, creating new knowledge that subsequently could be used for cancer prevention and delaying aging in humans. Thus, the purpose of this review is to summarize the recent knowledge on naked mole rats with a particular emphasis on the molecular mechanisms associated with their longevity and cancer resistance.
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16.
  • Lillenes, Meryl S., et al. (författare)
  • Transient OGG1, APE1, PARP1 and Pol beta expression in an Alzheimer's disease mouse model
  • 2013
  • Ingår i: Mechanisms of Ageing and Development. - : Elsevier BV. - 0047-6374 .- 1872-6216. ; 134:10, s. 467-477
  • Tidskriftsartikel (refereegranskat)abstract
    • Alzheimer's disease (AD) is a disease of major public health significance, whose pathogenesis is strongly linked to the presence of fibrillar aggregates of amyloid-beta (A beta) in the aging human brain. We exploited the transgenic (Tg)-ArcSwe mouse model for human AD to explore whether oxidative stress and the capacity to repair oxidative DNA damage via base excision repair (BER) are related to A beta pathology in AD. Tg-ArcSwe mice express variants of A beta, accumulating senile plaques at 4-6 months of age, and develop AD-like neuropathology as adult animals. The relative mRNA levels of genes encoding BER enzymes, including 8-oxoguanine glycosylase (OGG1), AP endonuclease 1 (APE1), polymerase 13 (Pol beta) and poly(ADP-ribose) polymerase 1 (PARP1), were quantified in various brain regions of 6 weeks, 4 months and 12 months old mice. The results show that OGG1 transcriptional expression was higher, and APE1 expression lower, in 4 months old Tg-ArcSwe than in wildtype (wt) mice. Furthermore, Pol beta transcriptional expression was significantly lower in transgenic 12 months old mice than in wt. Transcriptional profiling also showed that BER repair capacity vary during the lifespan in Tg-ArcSwe and wt mice. The BER expression pattern in Tg-ArcSwe mice thus reflects responses to oxidative stress in vulnerable brain structures. 
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  • Onder, Graziano, et al. (författare)
  • Facing multimorbidity in the precision medicine era
  • 2020
  • Ingår i: Mechanisms of Ageing and Development. - : Elsevier BV. - 0047-6374 .- 1872-6216. ; 190
  • Tidskriftsartikel (refereegranskat)abstract
    • The clinical picture of multimorbidity is heterogeneous and it is characterized by great complexity. Precision medicine is an innovative approach to provide personalized care focused on individual characteristics and to deliver the right treatments, at the right time, to the right person. The precision medicine approach, which represents an epochal change in the field of chronic diseases, has been poorly implemented in patients with multimorbidity. Several factors can limit this application. First, the precision medicine approach has been successfully applied in the treatment of mono-factorial diseases while multimorbidity is multifactorial. Second, there is lack of understanding of risk factors in the development and evolution of multimorbidity. Third, precision medicine is mainly focused on understanding genetic aspects of diseases and neglects other characteristics contributing to the definition of individual profiles. Finally, individual pathways may lead to the development of different multimorbidity phenotypes. A possible solution to simplify the application of precision medicine to this condition is to reduce its complexity and to find homogeneous patterns of chronic diseases that may work as targets of preventive and therapeutic strategies. This approach can lead to better understanding how these factors interact at individual level and to define interventions that might target multimorbidity.
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  • Pawelec, G, et al. (författare)
  • The SENIEUR protocol after 16 years.
  • 2001
  • Ingår i: Mechanisms of Ageing and Development. - 0047-6374 .- 1872-6216. ; 122:2, s. 132-134
  • Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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