Impact of age and caloric restriction on neurogenesis in the dentate gyrus of C57BL/6 mice

Bondolfi, Luca; Ermini, Florian; Long, Jefferey M; Ingram, Donald K.; Jucker, Mathias

doi:10.1016/s0197-4580(03)00083-6

Cited by 232 publications

(169 citation statements)

References 44 publications

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“…At LSND, however, these effects were dramatically decreased, indicating that the overall effect of the neurodegeneration on neurogenesis is decreased following neurodegenerative progression. As neurogenesis is down regulated by aging (Amrein, et al, 2004, Bondolfi, et al, 2004, Verret, et al, 2007, it is not clear whether this shift is or is not purely due to the effect of aging on neurogenesis. Second, the effect of neurodegeneration on neurogenesis is neurogenic stage-specific.…”

Section: Discussionmentioning

confidence: 99%

Adult neurogenesis is functionally associated with AD-like neurodegeneration

Chen

Nakajima

Choi

et al. 2008

Neurobiology of Disease

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Alzheimer's disease (AD) is predominantly characterized by progressive neuronal loss in the brain. It has been recently found that adult neurogenesis in the hippocampal dentate gyrus of AD patients is significantly enhanced, while its functional significance is still unknown. By using an AD-like neurodegeneration mouse model, we show here that neurogenesis in the dentate gyrus was neurodegenerative stage-dependent. At early stages of neurodegeneration, neurogenesis was significantly enhanced and newly generated neurons migrated into the local neuronal network. Up to late stages of neurodegeneration, however, the survival of newly generated neurons was impaired so that the enhanced neurogenesis could not be detected any more. Most interestingly, these dynamic changes in neurogenesis were correlated with the severity of neuronal loss in the dentate gyrus, indicating that neurogenesis may work as a self-repairing mechanism to compensate for neurodegeneration. Therefore, to enhance endogenous neurogenesis at early stages of neurodegeneration may be a valuable strategy to delay neurodegenerative progress.

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Section: Discussionmentioning

confidence: 99%

Adult neurogenesis is functionally associated with AD-like neurodegeneration

Chen

Nakajima

Choi

et al. 2008

Neurobiology of Disease

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“…In young adult mice, constitutive deletion of Bmi1 triggers increased glial cell production in vivo (Zencak et al, 2005) and decreased neurogenic capacity of cultured adult NSCs after serial passaging (Bruggeman et al, 2007). This increase in astrocytes phenocopies the increase in astrocyte production known to occur in the brain during aging (Bondolfi et al, 2004), raising the possibility that altered activity of BMI1 during aging contributes to a loss of stem cell multipotency.…”

Section: Chromatin Modifiers In Aging Stem Cellsmentioning

confidence: 94%

“…In the nervous system, the ability of NSCs to produce new neurons (neurogenesis) declines with age (Kuhn et al, 1996;Tropepe et al, 1997;Bondolfi et al, 2004;Enwere et al, 2004;Hattiangady and Shetty, 2008). Instead, aging is accompanied by increased production of astrocytes and elevated expression of astrocytespecific genes in the brain, indicating a loss of multipotentiality of stem/progenitor cells and astroglial lineage skewing (Peinado et al, 1998;Lee et al, 2000;Bondolfi et al, 2004).…”

Section: Defects In Number In Aging Stem Cellsmentioning

confidence: 99%

“…Instead, aging is accompanied by increased production of astrocytes and elevated expression of astrocytespecific genes in the brain, indicating a loss of multipotentiality of stem/progenitor cells and astroglial lineage skewing (Peinado et al, 1998;Lee et al, 2000;Bondolfi et al, 2004). On the basis of findings in the HSC field, it is tempting to speculate that age-dependent changes to the subcomposition of a potentially heterogeneous pool of NSCs (Merkle et al, 2007) may partially account for alterations in NSC differentiation potential.…”

Section: Defects In Number In Aging Stem Cellsmentioning

confidence: 99%

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Epigenetic regulation of aging stem cells

2011

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“…In addition, it has recently been shown that the juvenile and adult brain can generate new neurons through proliferation of progenitor cells, and thus might help to repair brain damage (Arvidsson et al, 2002;Bartley et al, 2005;Daval et al, 2004;Eriksson et al, 1998;Plane et al, 2004;Scheepens et al, 2003;Sun et al, 2005). It has been demonstrated that neurogenesis in the mammalian brain continues throughout life but decreases with age (Bondolfi et al, 2004;Gray et al, 2002;Jin et al, 2004;Kuhn et al, 1996;Sun et al, 2005), and this process was shown to be stimulated by various pathologic conditions (Bartley et al, 2005;Daval et al, 2004;Gray et al, 2002;Sun et al, 2005). Neurogenesis induced by brain ischemia implies that deficient neuronal function might be repaired by replacing lost neurons.…”

Section: Introductionmentioning

confidence: 99%

Less Neurogenesis and Inflammation in the Immature than in the Juvenile Brain after Cerebral Hypoxia-Ischemia

Qiu

Zhu

Wang

et al. 2006

J Cereb Blood Flow Metab

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The effects of hypoxia-ischemia (HI) on proliferation and differentiation in the immature (postnatal day 9) and juvenile (postnatal day 21) mouse hippocampus were investigated by injecting bromodeoxyuridine (50 mg/kg) daily for 7 days after the insult and evaluating the labeling 5 weeks after HI. Phenotypic differentiation was evaluated using NeuN, Iba1, APC, and S100b as markers of neurons, microglia, oligodendrocytes, and astrocytes, respectively. The basal proliferation, in particular neurogenesis, was higher in the immature than in the juvenile hippocampus. Hypoxiaischemia did not increase neurogenesis significantly in the immature dentate gyrus (DG), but it increased several-fold in the juvenile brain, reaching the same level as in the normal, noninjured immature brain. This suggests that the immature hippocampus is already working at the top of its proliferative capacity and that even though basal neurogenesis decreased with age, the injuryinduced generation of new neurons in the juvenile hippocampus could not increase beyond the basal level of the immature brain. Generation of glial cells of all three types after HI was significantly more pronounced in the cornu ammonis of the hippocampus region of the juvenile hippocampus. In the DG, only microglia production was greater in the juvenile brain. Increased microglia proliferation correlated with increased levels of the proinflammatory cytokines MCP-1 and IL-18 3 days after HI, indicating that the inflammatory response is stronger in the juvenile hippocampus. In summary, contrary to what has been generally assumed, our results indicate that the juvenile brain has a greater capacity for neurogenesis after injury than the immature brain.

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Impact of age and caloric restriction on neurogenesis in the dentate gyrus of C57BL/6 mice

Cited by 232 publications

References 44 publications

Adult neurogenesis is functionally associated with AD-like neurodegeneration

Adult neurogenesis is functionally associated with AD-like neurodegeneration

Epigenetic regulation of aging stem cells

Less Neurogenesis and Inflammation in the Immature than in the Juvenile Brain after Cerebral Hypoxia-Ischemia

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