Age‐related increases in glial fibrillary acidic protein do not show proportionate changes in transcription rates or DNA methylation in the cerebral cortex and hippocampus of male rats

Laping, Nicholas J.; Teter, Bruce; Anderson, Clarke P.; Osterburg, Heinz H.; O’Callaghan, James P.; Johnson, Steven A.; Finch, Caleb E.

doi:10.1002/jnr.490390612

Cited by 16 publications

(5 citation statements)

References 50 publications

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“…For each probeset, SAM generates a d-statistic and p-value used to determine if a significant group difference is evident. Increased GFAP mRNA in the entire hippocampus is observed in our study population and widely reported elsewhere (Nichols et al, 1993; Laping et al, 1994; Sugaya et al, 1996; Smith et al, 2001). SAM analysis of the current microarray data revealed increased expression of this gene in aged subjects in all three subregional comparisons, consistent with the published data (Fig 1B).…”

Section: Resultssupporting

confidence: 90%

Prominent hippocampal CA3 gene expression profile in neurocognitive aging

Haberman

Colantuoni

Stocker

et al. 2011

Neurobiology of Aging

124

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Research in aging laboratory animals has characterized physiological and cellular alterations in medial temporal lobe structures, particularly the hippocampus, that are central to age-related memory deficits. The current study compares molecular alterations across hippocampal subregions in a rat model that closely mirrors individual differences in neurocognitive features of aging humans, including both impaired memory and preserved function. Using mRNA profiling of the CA1, CA3 and dentate gyrus subregions, we have distinguished between genes and pathways related to chronological age and those associated with impaired or preserved cognitive outcomes in healthy aged Long Evans rats. The CA3 profile exhibited the most prominent gene expression differences related to cognitive status and of the three subregions, best distinguished preserved from impaired function among the aged animals. Within this profile differential expression of synaptic plasticity and neurodegenerative disease-related genes suggests recruitment of adaptive mechanisms to maintain function and structural integrity in aged unimpaired rats that does not occur in aged impaired animals.

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Section: Resultssupporting

confidence: 90%

Prominent hippocampal CA3 gene expression profile in neurocognitive aging

Haberman

Colantuoni

Stocker

et al. 2011

Neurobiology of Aging

124

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show abstract

“…With regard to astrocytes, the morphological alterations associated with aging are described as astrogliosis, a term that covers a rise in the expression of the astrocytic intermediate filament glial fibrillary acidic protein (GFAP). GFAP is a marker of astrogliosis that is elevated with age in mammals and is increased under inflammatory conditions [51]. Here, we investigated the effects of a short-term dietary supplementation with LCω3 PUFAs on CD11b, GFAP, IL-1β, IL-6 and TNFα mRNA expression in the hippocampus of aged mice.…”

Section: Resultsmentioning

confidence: 99%

Short-Term Long Chain Omega3 Diet Protects from Neuroinflammatory Processes and Memory Impairment in Aged Mice

et al. 2012

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Regular consumption of food enriched in omega3 polyunsaturated fatty acids (ω3 PUFAs) has been shown to reduce risk of cognitive decline in elderly, and possibly development of Alzheimer's disease. Docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) are the most likely active components of ω3-rich PUFAs diets in the brain. We therefore hypothesized that exposing mice to a DHA and EPA enriched diet may reduce neuroinflammation and protect against memory impairment in aged mice. For this purpose, mice were exposed to a control diet throughout life and were further submitted to a diet enriched in EPA and DHA during 2 additional months. Cytokine expression together with a thorough analysis of astrocytes morphology assessed by a 3D reconstruction was measured in the hippocampus of young (3-month-old) and aged (22-month-old) mice. In addition, the effects of EPA and DHA on spatial memory and associated Fos activation in the hippocampus were assessed. We showed that a 2-month EPA/DHA treatment increased these long-chain ω3 PUFAs in the brain, prevented cytokines expression and astrocytes morphology changes in the hippocampus and restored spatial memory deficits and Fos-associated activation in the hippocampus of aged mice. Collectively, these data indicated that diet-induced accumulation of EPA and DHA in the brain protects against neuroinflammation and cognitive impairment linked to aging, further reinforcing the idea that increased EPA and DHA intake may provide protection to the brain of aged subjects.

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“…However, the link between gene expression, aging, and cognitive decline is not a simple function of altered promoter methylation. Promoter methylation status does not underlie increased expression of the astrocyte marker of aging, glial fibrillary acidic protein ( gfap ) (Laping and others 1994). Furthermore, promoter methylation is not well correlated with behavioral impairment of older animals (Haberman and others 2012) and despite basal changes, the methylation status of some genes remain responsive to behavioral testing (Penner and others 2011; Penner and others 2016).…”

Section: Localization Of Altered Dna Methylationmentioning

confidence: 99%

Aging in the Brain: New Roles of Epigenetics in Cognitive Decline

Barter

Foster

2018

Neuroscientist

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Gene expression in the aging brain depends on transcription signals generated by senescent physiology, interacting with genetic and epigenetic programs. In turn, environmental factors influence epigenetic mechanisms, such that an epigenetic-environmental link may contribute to the accumulation of cellular damage, susceptibility or resilience to stressors, and variability in the trajectory of age-related cognitive decline. Epigenetic mechanisms, DNA methylation and histone modifications, alter chromatin structure and the accessibility of DNA. Furthermore, small non-coding RNA, termed microRNA (miRNA) bind to messenger RNA (mRNA) to regulate translation. In this review, we examine key questions concerning epigenetic mechanisms in regulating the expression of genes associated with brain aging and age-related cognitive decline. In addition, we highlight the interaction of epigenetics with senescent physiology and environmental factors in regulating transcription.

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Age‐related increases in glial fibrillary acidic protein do not show proportionate changes in transcription rates or DNA methylation in the cerebral cortex and hippocampus of male rats

Cited by 16 publications

References 50 publications

Prominent hippocampal CA3 gene expression profile in neurocognitive aging

Prominent hippocampal CA3 gene expression profile in neurocognitive aging

Short-Term Long Chain Omega3 Diet Protects from Neuroinflammatory Processes and Memory Impairment in Aged Mice

Aging in the Brain: New Roles of Epigenetics in Cognitive Decline

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