Expression data from hippocampus and cortex of 6- and 12-week curcumin-treated 15-month-old rats
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ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE33137 | GEO | 2011/10/22
SECONDARY ACCESSION(S): PRJNA149381
REPOSITORIES: GEO
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Project description:Curcumin has been demonstrated to have many neuroprotective properties, including improvement of cognition in humans and neurogenesis in animals, yet the mechanism of such effects remains unclear. Here, we assessed behavioural performance and hippocampal cell proliferation in aged rats after 6- and 12-week curcumin-fortified diets. Curcumin enhanced non-spatial and spatial memory, as well as dentate gyrate cell proliferation as compared to control diet rats. We also investigated underlying mechanistic pathways that might link curcumin treatment to increased cognition and neurogenesis via microarray analysis of cortical and hippocampal mRNA transcription. We used microarrays to investigate the effects of short-term (6-week) and long-term (12-week) curcumin-supplemented diet on gene expression of hippocampus and cortex in aged rats. The hippocampus and cortex of every three rats from one group were pooled together, respectively and used for RNA extraction and hybridization on Affymetrix microarrays. To ensure the reliability of the data, we conducted hybridization experiments in duplicate microarrays from each RNA sample. The tissues examined by microarray are as follows: the hippocampus and cortex of 6-week curcumin-treated 15-month-old rats, the hippocampus and cortex of 6-week no curcumin-treated 15-month-old rats (control rats), the hippocampus and cortex of 12-week curcumin-treated 15-month-old rats, the hippocampus and cortex of 12-week no curcumin-treated 15-month-old rats (control rats).
2011-10-21 | E-GEOD-33137 | biostudies-arrayexpress
Project description:Objective Obesity is a multidimensional condition that is treatable by the restoration of a lean phenotype; however, some obesity-related outcomes may persist after weight normalization. Among the organs of the human body, the brain possesses a relatively low regenerative capacity and could retain perturbations established as a result of developmental obesity. Calorie restriction (CR) or a restricted ketogenic diet (KD) are successfully used as weight loss approaches, but their impact on obesity-related effects in the brain have not been previously evaluated. Methods We performed a series of experiments in a rat model of developmental obesity induced by a 12-week cafeteria diet, followed by CR to implement weight loss. First, we assessed the impact of obesity on neurogenesis (BrdU incorporation into the hippocampus), cognitive function (water maze), and concomitant changes in hippocampal protein expression (GC/MS-MS, western blot). Next, we repeated these experiments in a rat model of weight loss induced by CR. We also measured mitochondrial enzyme activity in rats after weight loss during the fed or fasting state. By using a modified version of the water maze we evaluated cognitive abilities in rats subjected to weight loss by CR or a restricted KD. Results In this study, obesity affected metabolic processes, upregulated hippocampal NF-κB, and induced proteomic differences which were associated with impaired cognition and neurogenesis. Weight loss improved neurogenesis and enhanced cognition. While the expression pattern of some proteins persisted after weight loss, most of the changes appeared de novo revealing metabolic adjustment by overactivation of citrate synthase and downregulation of ATP synthase. As a consequence of fasting, the activity of these enzymes indicated hippocampal adaptation to negative energy balance during the weight loss phase of CR. Moreover, the effects on cognitive abilities measured after weight loss were negatively correlated with the obesity level and were alleviated by KD, which improved cognition when used as a weight loss approach. Conclusions The study shows that cognition and mitochondrial metabolism in the hippocampus are affected by CR- or KD-induced weight loss.
2021-07-01 | PXD023070 | Pride
Project description:Repeated excessive alcohol consumption increases the risk of developing cognitive decline and dementia. Hazardous drinking among older adults further increases such vulnerabilities. In order to understand the molecular mechanisms underlying alcohol-induced cognitive deficits in older adults, we performed a chronic intermittent ethanol exposure paradigm (ethanol or water gavage every other day 10 times) in 8-week-old young adult and 70-week-old aged rats. While spatial memory retrieval ascertained by probe trials in the Morris water maze was not significantly different between ethanol-treated and water-treated rats in both age groups after the fifth and tenth gavages, behavioral flexibility was impaired in ethanol-treated rats than water-treated rats in the aged group but not in the young adult group. Further proteomic and phosphoproteomic analyses on their hippocampal tissues by tandem mass tag mass spectrometry revealed ethanol-treatment-associated proteomic and phosphoproteomic differences distinct to the aged rats, including the upregulations of Prkcd protein level, several of its phosphosites, and its kinase activity and the same aspects in Camk2a but downregulated, and were enriched in pathways involved in neurotransmission regulation, synaptic plasticity, neuronal apoptosis, and insulin receptor signaling. In conclusion, our behavioral and proteomic results added several candidate proteins and pathways potentially associated with alcohol-induced cognitive decline in aged adults.
2023-03-11 | PXD034443 | Pride
Project description:Positive experiences, such as social interaction, cognitive training and physical exercise, have been shown to ameliorate some of the harms to cognition associated with ageing. Animal models of positive interventions, commonly known as environmental enrichment, strongly influence neuronal morphology and synaptic function and enhance cognitive performance. While the profound structural and functional benefits of enrichment have been appreciated for decades, little is known as to how the environment influences neurons to respond and adapt to these positive sensory experiences. We show that adult and aged male wild-type mice that underwent a 10-week environmental enrichment protocol demonstrated improved performance in a variety of behavioural tasks, including those testing spatial working and spatial reference memory, and an enhancement in hippocampal LTP. Aged animals in particular benefitted from enrichment, performing spatial memory tasks at levels similar to healthy adult mice. Many of these benefits, including in gene expression, were absent in mice with a mutation in an enzyme, MSK1, which is activated by BDNF, a growth factor implicated in rodent and human cognition. We conclude that enrichment is beneficial across the lifespan and that MSK1 is required for the full extent of these experience-induced improvements of cognitive abilities, synaptic plasticity and gene expression.
2023-06-20 | GSE235037 | GEO
Project description:Although aging is a physiological process to which all organisms are subject, the presence of obesity and type 2 diabetes accelerates biological aging. Recent studies have demonstrated the causal relationships between dietary interventions suppressing obesity and type 2 diabetes and delaying the onset of age-related endocrine changes. Curcumin, a natural antioxidant, has putative therapeutic properties such as reinstating insulin sensitivity in obese mice. However, how curcumin contributes to maintaining insulin homeostasis in aged organisms largely remains unclear. Thus, the objective of this study is to examine the pleiotropic effect of dietary curcumin on insulin homeostasis in a diet-induced obese (DIO) aged mouse model. Aged (18-20 months old) male mice given a high-fat high-sugar diet supplemented with curcumin displayed a different metabolic phenotype compared to mice given a high-fat high-sugar diet alone. Furthermore, curcumin supplementation altered hepatic gene expression profiling, especially insulin signaling and senescence pathways. We then mechanistically investigated how curcumin functions to fine-tune insulin sensitivity. We found that curcumin supplementation increased hepatic insulin degrading enzyme (IDE) expression levels and preserved islet integrity, both of which are beneficial during aging. Our findings suggest that the multifaceted therapeutic potential of curcumin can be used as a protective agent for age-induced metabolic diseases.
2021-11-04 | GSE186971 | GEO
Project description:Male Fischer 344 rats aged 4 months (young, n=10), 14 months (mid-aged, n=10), and 24 months (aged, n=10) were trained sequentially on two tasks: Morris Spatial Water Maze (SWM) and Object Memory Task (OMT). The training/testing sequence lasted 7 d, and hippocampal tissue was collected 24 hr later. Training and testing occured on each day except for days 2 and 3 of the 7 d sequence. (01/10/05: Series was updated to correct mislabeling of all sample signal values within the Young Treatment Group)
2007-10-12 | E-GEOD-854 | biostudies-arrayexpress
Project description:This study focused on transcription in the medial PFC (mPFC) as a function of age and cognition. Young and aged F344 rats were characterized on tasks, attentional set shift and spatial memory, which depend on the mPFC and hippocampus, respectively. Differences in transcription associated with age and cognitive function were examined using RNA sequencing to construct transcriptomic profiles for the mPFC, white matter, and region CA1 of the hippocampus. The results indicate regional differences in vulnerability to aging associated with increased expression of immune and defense response genes and a decline in synaptic and neural activity genes. Importantly, we provide evidence for region specific transcription related to behavior. In particular, expression of transcriptional regulators and neural activity-related immediate-early genes (IEGs) are increased in the mPFC of aged animals that exhibit delayed set shift behavior; relative to age-matched animals that exhibit set shift behavior similar to younger animals. The study contains 11 young and 20 aged rats for the mPFC and CA1 samples, which were used to investigate expression patterns associated with aging and behavior. White matter samples were used to investigate an age-related effect with 8 young and 9 aged rats.
2016-05-17 | E-GEOD-75772 | biostudies-arrayexpress
Project description:Although immediate early genes (IEGs) such as Bdnf, Arc and Egr1, have been implicated in plasticity, the larger pathways related to memory and memory disorders are not well understood. Here, we combined statistical Affymetrix microarray and behavioral analyses to identify key genes and pathways associated with aging-related cognitive impairment. Aged rats were separated into cognitively unimpaired (AU) or impaired (AI) groups, based on their Morris water maze performance relative to young-adult (Y) animals. Hippocampal gene expression was assessed in Y, AU and AI on the fifth (last) day of maze training or 21 days posttraining, and in non-trained aged and young animals (eight groups, overall n = 78, one chip/animal). ANOVA, linear contrasts, and overrepresentation analyses identified genes and pathways that differed from Y generally with aging (in both AU and AI) or selectively with cognitive status (only in AI or AU). Plasticity pathways, including insulin/cAMP/IEG signaling, and glycogenolytic and lipogenic pathways, were selectively downregulated (5 days) in AI, whereas Notch2 (regulating oligodendrocyte differentiation) and myelination pathways were upregulated (particularly at 21 days). Downregulation with general aging occurred in signal transduction and axonal growth/transport pathways, whereas upegulation occurred in immune/inflammatory, lipid metabolism/transport (e.g., Lxr-Srebf1), and lysosomal pathways. In AU, receptor/signal transduction genes were selectively upregulated, suggesting possible compensatory mechanisms. Immunohistochemistry confirmed and extended results to the protein level. Thus, this study identified novel cognition-linked processes, suggesting a new model in which energy-intensive, plasticity/lipogenic processes and energy-generating pathways necessary for learning are coordinately downregulated during training, while myelinogenic programs that impair cognition are concurrently activated. Experiment Overall Design: Aged rats were separated into cognitively unimpaired (AU) or impaired (AI) groups, based on their Morris water maze performance relative to young-adult (Y) animals (NT, 5D, and 21D, N=10/group). Hippocampal gene expression was assessed in Y, AU and AI on the fifth (last) day of maze training or 21 days posttraining, and in non-trained aged and young animals (eight groups, overall n = 78, one chip/animal)
2007-11-29 | E-GEOD-5666 | biostudies-arrayexpress
Project description:Adult male rats of the PD/Cub (PD hereafter) strains were fed a laboratory chow diet (STD, ssniff RZ, ssniff Spezialdiäten GmbH, Soest, Germany). At the age of 12 months, rats within each strain were randomly divided into two groups. The control group was fed a high-sucrose diet (HSD, sucrose 70 cal%) while the experimental group was fed a HSD fortified with quercetin (10 g/kg food, Sigma-Aldrich).
2022-09-15 | E-MTAB-11061 | biostudies-arrayexpress
Project description:Aging is associated with low-grade chronic systemic inflammation. Elevated peripheral serum cytokines and chemokines contribute to age-related diseases and correlate with cognitive decline. This study compared the effects of repeated lipopolysaccharide (LPS) treatment in young rats to age-related changes in hippocampal-dependent cognition, synaptic transmission, and transcription. Young (5-7 months) Fischer 344 X Brown Norway hybrid rats were injected intraperitoneally once a week for 6-7 weeks with either LPS (1 mg/kg) or vehicle. Older (14-16 months) rats received a similar injection schedule of vehicle. Older-vehicle animals and young-LPS rats exhibited impaired retention of spatial memory. Examination of the transcriptome of the CA1 and the dentate gyrus indicated that older-vehicle and young-LPS animals exhibited an increase in immune response genes. In contrast to aging, young-LPS animals exhibited an increased expression of genes related to the synapse. Even though young-LPS animals increased the expression of synaptic genes, LPS treatment reduced hippocampal CA3-CA1 total synaptic response and N-methyl-D-aspartate receptor (NMDAR)-mediated component of the synaptic response. Interestingly, the decrease in NMDAR function was not redox-sensitive. This study demonstrates that repeated exposure to LPS has long-term effects on hippocampal synaptic transmission and memory; however, young animals exhibited transcriptional recovery after LPS treatment. Recovery likely results from the acute nature of repeated LPS injections, relative to chronic systemic inflammation observed during aging.
2020-11-30 | GSE140685 | GEO