Prominent decline of newborn cell proliferation, differentiation, and apoptosis in the aging dentate gyrus, in absence of an age-related hypothalamus–pituitary–adrenal axis activation

Heine, Vivi M.; Maslam, Suharti; Joëls, Marian; Lucassen, Paul J.

doi:10.1016/s0197-4580(03)00090-3

Cited by 282 publications

(249 citation statements)

References 92 publications

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“…3C). This observation is consistent with the similarity between age-dependent decreases in BrdU incorporation and cell death reported before in DG [17]. To further confirm these findings, TUNEL staining was performed on brain sections of rats at different ages.…”

Section: Resultssupporting

confidence: 91%

“…Although NPC proliferation in the DG and SVZ is reduced with aging [17,19,23], how programmed cell death of NPCs may be altered during normal brain aging is unknown. Therefore, we investigated the expression of caspase activation products in neuroproliferative zones of the young, young-adult, middle-aged and aged rat brain, as well as the effect of caspase inhibition on neurogenesis.…”

Section: Introductionmentioning

confidence: 99%

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Effect of neural precursor proliferation level on neurogenesis in rat brain during aging and after focal ischemia

Tang

Wang

Xie

et al. 2009

Neurobiology of Aging

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The observed age-related decline in neurogenesis may result from reduced proliferation or increased death rate of neuronal precursor cells (NPCs). We found that caspase-3, but not caspase-6, -7, or -9, was activated in NPCs in neurogenic regions of young, young-adult, middle-aged and aged rat brains. The number of capase-3-immunoreactive cells was highest in young and lowest in aged rats. Surprisingly, intraventricular administration of a caspase-3 inhibitor failed to restore the number of BrdU-positive cells in the aged dentate gyrus, suggesting that the age-related decline in neurogenesis may be attributable primarily to reduced proliferation. Additionally, we also found that NPCs in the subventricular zone of young-adult and aged rat brain were increased after focal cerebral ischemia, suggesting that the increase in neurogenesis induced by ischemia may result from an increase in the rate of NPC proliferation, but not from a decrease in NPC death. Thus, our results suggest that agerelated and injury-induced changes in the rate of neurogenesis are controlled at the level of NPC proliferation. Furthermore, our results may imply that the mechanisms that maintain a stable population of NPCs in the normal adult and in the ischemic brain, which account for the observed age-dependent reduction or injury-induced increases in neurogenesis, impinge on the regulation of cell division at the NPC level.

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Section: Resultssupporting

confidence: 91%

Section: Introductionmentioning

confidence: 99%

Effect of neural precursor proliferation level on neurogenesis in rat brain during aging and after focal ischemia

Tang

Wang

Xie

et al. 2009

Neurobiology of Aging

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“…This finding is surprising in the light of earlier observations in rat models that a dramatic decline in the proliferation of NSCs occurs in the DG between young and old age (Olariu et al 2007;Rao et al 2006), but NSC numbers are preserved in the SGZ during the course of aging (Hattiangady and Shetty 2008). Furthermore, most studies on rodent models point out that proliferation of far fewer NSCs in the aged DG underlies the age-related reduction in net hippocampal neurogenesis (Cameron and McKay 1999;Hattiangady and Shetty 2008;Heine et al 2004;Kuhn et al 1996;McDonald and Wojtowicz 2005;Rao et al 2005;Seki and Arai 1995;Walter et al 2011but see Encinas et al 2011. Consistent with this, other studies have shown that aging in the hippocampus is associated with alterations in NSC proliferation factors such as decreased concentrations of neurotrophic factors that are mitogenic to NSCs Shetty et al 2005;Zeng et al 2011).…”

Section: Discussionmentioning

confidence: 89%

Neural stem cell- and neurogenesis-related gene expression profiles in the young and aged dentate gyrus

Shetty

Hattiangady

Shetty

2013

AGE

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Hippocampal neurogenesis, important for memory and mood function, wanes greatly in old age. Studies in rat models have implied that this decrease is not due to loss of neural stem cells (NSCs) in the subgranular zone of the dentate gyrus (DG) but rather due to an increased quiescence of NSCs. Additional studies have suggested that changes in the microenvironment, particularly declines in the concentrations of neurotrophic factors, underlie this change. In this study, we compared the expression of 84 genes that are important for NSC proliferation and neurogenesis between the DG of young (4 months old) and aged (24 months old) Fischer 344 rats, using a quantitative real-time polymerase chain reaction array. Interestingly, the expression of a vast majority of genes that have been reported previously to positively or negatively regulate NSC proliferation was unaltered with aging. Furthermore, most genes important for cell cycle arrest, regulation of cell differentiation, growth factors and cytokine levels, synaptic functions, apoptosis, cell adhesion and cell signaling, and regulation of transcription displayed stable expression in the DG with aging. The exceptions included increased expression of genes important for NSC proliferation and neurogenesis (Stat3 and Shh), DNA damage response and NFkappaB signaling (Cdk5rap3), neuromodulation (Adora1), and decreased expression of a gene important for neuronal differentiation (HeyL). Thus, age-related decrease in hippocampal neurogenesis is not associated with a decline in the expression of selected genes important for NSC proliferation and neurogenesis in the DG.

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“…Pyknotic cells, identified by darkly stained, round to C-shaped condensed and fragmented chromatin in the Giemsa-stained frozen sections (Amrein et al, 2004a;Heine et al, 2004) was also estimated in this manner. DCX and PSA-NCAM positive cells were counted using the optical fractionator (West et al, 1991).…”

Section: Pyknotic and Immunohistochemically Stained Cellsmentioning

confidence: 99%

A morphologically distinct granule cell type in the dentate gyrus of the red fox correlates with adult hippocampal neurogenesis

Amrein¹,

Slomianka²

2010

Brain Research

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A morphologically distinct granule cell type in the dentate gyrus of the red fox correlates with adult hippocampal neurogenesis Running titleThe dentate gyrus of the red fox Text pages 37Figures 7 Tables 3 Corresponding authorIrmgard In summary, we report a morphologically distinct granule cell type which correlates with adult 3 hippocampal neurogenesis in the fox. Furthermore, the maturation phase of the young neurons may be prolonged as in other long-living species such as primates. SECTIONNervous System Development, Regeneration and Aging

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Prominent decline of newborn cell proliferation, differentiation, and apoptosis in the aging dentate gyrus, in absence of an age-related hypothalamus–pituitary–adrenal axis activation

Cited by 282 publications

References 92 publications

Effect of neural precursor proliferation level on neurogenesis in rat brain during aging and after focal ischemia

Effect of neural precursor proliferation level on neurogenesis in rat brain during aging and after focal ischemia

Neural stem cell- and neurogenesis-related gene expression profiles in the young and aged dentate gyrus

A morphologically distinct granule cell type in the dentate gyrus of the red fox correlates with adult hippocampal neurogenesis

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