Apoptotic proteins in the course of aging of central nervous system in the rat

Dorszewska, Jolanta; Adamczewska-Goncerzewicz, Z; Szczech, J

doi:10.1016/j.resp.2003.10.009

Cited by 22 publications

(14 citation statements)

References 49 publications

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“…Our findings substantiate this concept, showing increased levels of proteins involved in apoptosis activation and execution in control aged animals when compared to adults, in accordance to previous reports (Adams et al 1996;Taglialatela et al 1996;Anglade et al 1997;Dorszewska et al 2004;Mansour et al 2008).…”

Section: Discussionsupporting

confidence: 94%

Neonatal Iron Treatment Increases Apoptotic Markers in Hippocampal and Cortical Areas of Adult Rats

et al. 2010

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Oxidative stress, cellular damage, and neuronal apoptosis are believed to underlie the progressive cognitive decline that accompanies natural aging and to be exacerbated in neurodegenerative diseases. Over the years, we have consistently demonstrated that iron neonatal treatment induces oxidative stress and memory deficits in adult rats, but the mechanisms underlying these effects remained undefined. The purpose of this study was to examine whether neonatal iron overload was associated with apoptotic cell death in adult and old rats. We analyzed Par-4 and caspase-3 immunoreactivity in specific brain areas including the hippocampus CA1, CA3 and dentate gyrus (DG), the adjacent cortex and the striatum in adult (3 months-old) and aged (24 months-old) rats from control (vehicle-treated) and neonatally iron-treated groups. Neonatal iron treatment consisted of a daily oral administration of 10 mg/kg of Fe(+2), for three consecutive days, from post-natal 12-14. Control aged animals showed increased levels of both markers when compared to untreated adult animals. When adults were compared, iron-treated animals presented significantly higher Par-4 and caspase-3 immunoreactivities in CA1, CA3 and cortex. In the DG, this effect was statistically significant only for Par-4. Interestingly, when control and iron-treated aged animals were compared, a significant decrease in both apoptotic markers was observed in the later groups in the same areas. These results may be interpreted as an acceleration of aging progressive damages caused by iron overload and may contribute to a better understanding of the damaging potential of iron accumulation to brain function and the resulting increased susceptibility to neurodegeneration.

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Section: Discussionsupporting

confidence: 94%

Neonatal Iron Treatment Increases Apoptotic Markers in Hippocampal and Cortical Areas of Adult Rats

et al. 2010

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“…7C). This is in agreement with previous work reporting an increase in TUNEL‐positive cells in the striatum (Zhang et al, 1995), cerebellum, and cortex (Dorszewska et al, 2004) of aged animals. Furthermore, the expressions of Bcl‐2 and Bax proteins were evaluated to correlate better with TUNEL observation.…”

Section: Discussionsupporting

confidence: 93%

Alterations in calcium signaling and a decrease in Bcl‐2 expression: Possible correlation with apoptosis in aged striatum

Ureshino

Bertoncini

Fernandes

et al. 2009

J of Neuroscience Research

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Aging is a multifaceted process associated with various functional and structural deficits that might be evolved in degenerative diseases. It has been shown that neurodegenerative disorders are associated with alterations in Ca(2+) homeostasis. Thus, in the present work, we have investigated Ca(2+) signaling and apoptosis in aged striatum. Our results show that glutamate and NMDA evoke a greater Ca(2+) rise in striatum slices from aged animals. However, this difference is not present when glutamate is tested in the absence of external Ca(2+). Immunostaining of glutamate receptors shows that only NMDA receptors (NR1) are increased in the striatum of aged rats. Increases in mitochondrial Ca(2+) content and in the reactive oxygen species levels were also observed in aged animals, which could be associated with tissue vulnerability. In addition, a decrease in the Bcl-2 protein expression and an enhancement in apoptosis were also present in aged striatum. Together the results indicate that, in aged animals, alterations in Ca(2+) handling coupled to an increase in ROS accumulation and a decrease in the prosurvival protein Bcl-2 may contribute to apoptosis induction and cell death in rat striatum.

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“…This is similar to studies on brain volume in mice (Carroll et al, 2011). Although many report neuronal loss in the cerebral cortex, striatum, and in the hippocampus, and an increase in TUNNEL positive cells in the parietal lobe, in the corpus collosum, in the medulla oblongata and in the cerebellum, the neuronal loss may be compensated by an increase in neuroglial cells causing an increase in brain weight with aging (Cerbai et al, 2012;Dorszewska et al, 2004;Zhang et al, 1995). Some studies have reported decreasing human brain weight after the third decade of life, or the sixth decade of life (Dekaban, 1978;McNelly, 1977, 1981;Sawabe et al, 2006).…”

Section: Discussionsupporting

confidence: 85%

Characterization of age-associated changes in peripheral organ and brain region weights in C57BL/6 mice

Lessard‐Beaudoin

Laroche

Demers

et al. 2015

Experimental Gerontology

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Apoptotic proteins in the course of aging of central nervous system in the rat

Cited by 22 publications

References 49 publications

Neonatal Iron Treatment Increases Apoptotic Markers in Hippocampal and Cortical Areas of Adult Rats

Neonatal Iron Treatment Increases Apoptotic Markers in Hippocampal and Cortical Areas of Adult Rats

Alterations in calcium signaling and a decrease in Bcl‐2 expression: Possible correlation with apoptosis in aged striatum

Characterization of age-associated changes in peripheral organ and brain region weights in C57BL/6 mice

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