Senescence-associated beta-galactosidase activity expression in aging hippocampal neurons

Geng, Yiqun; Guan, Jitian; Xu, Xiaoling; Fu, Yucai

doi:10.1016/j.bbrc.2010.05.011

Cited by 111 publications

(82 citation statements)

References 16 publications

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“…Consistent with the previous findings, SA‐beta‐GAL‐positive cells were observed in the hippocampal CA3 region (Geng, Guan, Xu & Fu, 2010). R1‐C mice showed a few SA‐beta‐GAL‐positive cells, whereas the R1‐T and P8‐C groups had more cells showing prominent SA‐beta‐GAL staining.…”

Section: Resultssupporting

confidence: 92%

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Trimethylamine‐N‐oxide promotes brain aging and cognitive impairment in mice

et al. 2018

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SummaryGut microbiota can influence the aging process and may modulate aging‐related changes in cognitive function. Trimethylamine‐N‐oxide (TMAO), a metabolite of intestinal flora, has been shown to be closely associated with cardiovascular disease and other diseases. However, the relationship between TMAO and aging, especially brain aging, has not been fully elucidated. To explore the relationship between TMAO and brain aging, we analysed the plasma levels of TMAO in both humans and mice and administered exogenous TMAO to 24‐week‐old senescence‐accelerated prone mouse strain 8 (SAMP8) and age‐matched senescence‐accelerated mouse resistant 1 (SAMR1) mice for 16 weeks. We found that the plasma levels of TMAO increased in both the elderly and the aged mice. Compared with SAMR1‐control mice, SAMP8‐control mice exhibited a brain aging phenotype characterized by more senescent cells in the hippocampal CA3 region and cognitive dysfunction. Surprisingly, TMAO treatment increased the number of senescent cells, which were primarily neurons, and enhanced the mitochondrial impairments and superoxide production. Moreover, we observed that TMAO treatment increased synaptic damage and reduced the expression levels of synaptic plasticity‐related proteins by inhibiting the mTOR signalling pathway, which induces and aggravates aging‐related cognitive dysfunction in SAMR1 and SAMP8 mice, respectively. Our findings suggested that TMAO could induce brain aging and age‐related cognitive dysfunction in SAMR1 mice and aggravate the cerebral aging process of SAMP8 mice, which might provide new insight into the effects of intestinal microbiota on the brain aging process and help to delay senescence by regulating intestinal flora metabolites.

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Section: Resultssupporting

confidence: 92%

“…Detailed methods are provided in the Data S1 (Geng et al., 2010; Lin, Hong, Zou & Chen, 2015; Zhang et al., 2014). …”

Section: Methodsmentioning

confidence: 99%

Trimethylamine‐N‐oxide promotes brain aging and cognitive impairment in mice

et al. 2018

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“…However, we did not observed any significant changes in the number of rpS3-immunoreactive polymorphic cells in the dentate gyrus. Another study examined age-related changes in senescence-associated beta-galactosidase (SA-beta-GAL), a widely used marker for cellular senescence, and showed that SA-beta-GAL-positive cells were not observed in the aged rat dentate gyrus [6,19]. Therefore, these and our result might indicate that senescence in the dentate gyrus is different compared to that in the hippocampus proper.…”

contrasting

confidence: 41%

Ribosomal Protein S3 Immunoreactivity in the Young, Adult and Aged Gerbil Hippocampus

Lee

Yoo

Choi

et al. 2011

The Journal of Veterinary Medical Science

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ABSTRACT. Ribosomal protein S3 (rpS3) is well known to participate in DNA repair mechanisms. In the present study, we compared rpS3 immunoreactivity and its protein levels in the hippocampus among young, adult and aged gerbils. In the postnatal month (PM) 3 group as the young, rpS3 immunoreaction was observed in pyramidal and non-pyramidal cells of the hippocampus proper and in granule and polymorphic cells of the dentate gyrus. In the PM 12 group as adult and 24 group as the aged, rpS immunoreactivity in the hippocampus was decreased compared to the PM 3 group. Western blot analysis showed that rpS3 levels were decreased with time; lowest at PM 24. These results indicate that rpS3 immunoreactivity and protein levels were markedly decreased in the aged gerbil hippocampus.

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“…Damaged and dying cells were detected using β-galactosidase staining (Geng et al, 2010). After 7 days in culture, the morphological development of the neurons was complete and was similar to that of fully developed mice in vivo.…”

Section: Loss Of Brg1 Might Results In Neuronal Degeneration Associatementioning

confidence: 98%

Central nervous system-specific knockout of Brg1 causes growth retardation and neuronal degeneration

Deng

Rao

et al. 2015

Brain Research

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Senescence-associated beta-galactosidase activity expression in aging hippocampal neurons

Cited by 111 publications

References 16 publications

Trimethylamine‐N‐oxide promotes brain aging and cognitive impairment in mice

Trimethylamine‐N‐oxide promotes brain aging and cognitive impairment in mice

Ribosomal Protein S3 Immunoreactivity in the Young, Adult and Aged Gerbil Hippocampus

Central nervous system-specific knockout of Brg1 causes growth retardation and neuronal degeneration

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