Intracerebroventricular infusion of insulin-like growth factor-I ameliorates the age-related decline in hippocampal neurogenesis

Lichtenwalner, Robin J.; Forbes, M. Elizabeth; Bennett, Scott; Lynch, Colleen D.; Sonntag, William E.; Riddle, David R.

doi:10.1016/s0306-4522(01)00378-5

Cited by 377 publications

(297 citation statements)

References 69 publications

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“…We examined both the density of proliferating, Ki67 + cells in the SGZ of the rodent hippocampus and, more specifically, the density of immature, DCX + neurons. The density of Ki67 + and DCX + cells was lower in middle aged and older rats than in young adults, as shown previously (15)(16)(17)(18). Recent evidence indicates that the aging-related decrease in neurogenesis results from decreased proliferation, rather than changes in survival or cell cycle length (17,44).…”

Section: Discussionsupporting

confidence: 77%

“…A chronic inflammatory response, identified by increases in ED1 + activated microglia, has been demonstrated repeatedly in the CNS of young animals months after irradiation (8,10,13,14). To date, however, experimental studies of radiation-induced inflammation, brain injury and cognitive dysfunction have been conducted almost exclusively in animals a few weeks to a few months old, young ages that do not reflect important neurobiological changes that occur with normal aging, such as decreased proliferation and neurogenesis (15)(16)(17)(18), increased microglial activation (19,20) and expression of pro-inflammatory cytokines (20)(21)(22). Experimental studies of stroke, traumatic brain injury, exogenous cytokine administration, and axotomy support the hypothesis that aging impacts the intensity and duration of brain inflammation and glial activation following challenges (23)(24)(25)(26)(27)(28).…”

Section: Introductionmentioning

confidence: 99%

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Aging-Dependent Changes in the Radiation Response of the Adult Rat Brain

Schindler¹,

Forbes²,

Robbins³

et al. 2008

International Journal of Radiation Oncology*Biology*Physics

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Purpose-To assess the impact of aging on the radiation response in the adult rat brain.Methods and Materials-Male rats 8, 18, or 28 months of age received a single 10Gy dose of whole brain irradiation (WBI). The hippocampal dentate gyrus (DG) was analyzed one and ten weeks later for sensitive neurobiological markers associated with radiation-induced damage: changes in the density of proliferating cells, immature neurons, total microglia, and activated microglia.Results-A significant reduction in basal levels of proliferating cells and immature neurons and increased microglial activation occurred with normal aging. WBI induced a transient increase in proliferation that was greater in older animals. This proliferation response did not increase the number of immature neurons, which decreased following WBI in young rats but not in old rats. Total microglial number decreased following WBI at all ages but microglial activation increased markedly, particularly in older animals.Conclusions-Age is an important factor to consider when investigating the radiation response of the brain. In contrast to young adults, older rats show no sustained decrease in the number of immature neurons following WBI but have a greater inflammatory response. The latter may play an enhanced role in the development of radiation-induced cognitive dysfunction in older individuals.

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Section: Discussionsupporting

confidence: 77%

Section: Introductionmentioning

confidence: 99%

Aging-Dependent Changes in the Radiation Response of the Adult Rat Brain

Schindler¹,

Forbes²,

Robbins³

et al. 2008

International Journal of Radiation Oncology*Biology*Physics

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“…For example, reducing circulating levels of corticosteroids in adult rats by adrenalectomy has been shown to restore neural progenitor proliferation and neurogenesis (Cameron and McKay, 1999) and increasing the declining levels of insulin growth factor 1 (IGF-1) in aged rodents promotes adult neurogenesis and stem-celldependent muscle regeneration (Lichtenwalner et al, 2001;Musaro et al, 2004). In further support of reversible alterations to stem cell function in some tissues, changes in external stimuli, such as exposure to an enriched social environment (Kempermann et al, 1998b(Kempermann et al, , 2002 or physical exercise (Kronenberg et al, 2006;Lugert et al, 2010), improve age-related declines in NSC proliferation and neurogenesis.…”

Section: Defects In Number In Aging Stem Cellsmentioning

confidence: 99%

Epigenetic regulation of aging stem cells

2011

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“…Aging is associated with elevated basal levels of corticosteroids (Sapolsky, 1992), and removal of corticosteroids by adrenalectomy significantly enhances DGC production in aged rats (Cameron and McKay, 1999;Montaron et al, 1999). Direct infusion of various growth factors, including heparin-binding EGF-like growth factor (HB-EGF), basic fibroblast growth factor (bFGF, also known as FGF-2), and insulin-like growth factor-1 (IGF-1), into the senescent brain reverses the age-related decline in neurogenesis in the dentate gyrus (Lichtenwalner et al, 2001;Jin et al, 2003a).…”

Section: Agementioning

confidence: 99%

Adult Neurogenesis and the Ischemic Forebrain

Lichtenwalner

Parent

2005

J Cereb Blood Flow Metab

262

190

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The recent identification of endogenous neural stem cells and persistent neuronal production in the adult brain suggests a previously unrecognized capacity for self-repair after brain injury. Neurogenesis not only continues in discrete regions of the adult mammalian brain, but new evidence also suggests that neural progenitors form new neurons that integrate into existing circuitry after certain forms of brain injury in the adult. Experimental stroke in adult rodents and primates increases neurogenesis in the persistent forebrain subventricular and hippocampal dentate gyrus germinative zones. Of greater relevance for regenerative potential, ischemic insults stimulate endogenous neural progenitors to migrate to areas of damage and form neurons in otherwise dormant forebrain regions, such as the neostriatum and hippocampal pyramidal cell layer, of the mature brain. This review summarizes the current understanding of adult neurogenesis and its regulation in vivo, and describes evidence for stroke-induced neurogenesis and neuronal replacement in the adult. Current strategies used to modify endogenous neurogenesis after ischemic brain injury also will be discussed, as well as future research directions with potential for achieving regeneration after stroke and other brain insults.

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Intracerebroventricular infusion of insulin-like growth factor-I ameliorates the age-related decline in hippocampal neurogenesis

Cited by 377 publications

References 69 publications

Aging-Dependent Changes in the Radiation Response of the Adult Rat Brain

Aging-Dependent Changes in the Radiation Response of the Adult Rat Brain

Epigenetic regulation of aging stem cells

Adult Neurogenesis and the Ischemic Forebrain

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