Project description:The Ts1Cje mouse model of Down syndrome (DS) has partial triplication of mouse chromosome 16, of which a large portion is homologous to human chromosome 21. The mouse model shows an impaired neurogenesis in hippocampus at 3-month-old . We analyzed the effect of Ts1Cje trisomic region on global gene expression in the adult brain of Ts1Cje mice at 3-month-old.
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).
Project description:Down syndrome is characterized by a complex phenotype that includes developmental disabilities and congenital anomalies. The molecular origin of these abnormalities is poorly understood. The objective of this study is to analyze whole transcriptome changes in the cortex and hippocampus of the Ts1Cje mouse model of Down syndrome to identify signaling pathways and cellular processes that are consistently perturbed in both brain regions. These pathways will offer a new opportunity for therapeutic interventions to improve cognition in Down syndrome. We refined the translocation breakpoints of MMU12 and MMU16 described previously and established the brain transcriptional map for both monosomic (MMU12) and trisomic (MMU16) regions in Ts1Cje mice. We showed that the hippocampus have more differentially regulated genes, however, the directions of regulation of these genes were generally similar in both brain regions. The secondary genome-wide effect implicated genes known to play major roles in cellular functions that are affected in Down syndrome. Functional analyses highlighted the importance of NFAT signaling, oxidative stress, neuroinflammation, hormone metabolism and olfactory perception via G-protein signaling. This study offers novel targets for therapeutic intervention in Down syndrome. We analyzed the cerebral cortex and hippocampus whole transcriptome from 8-10 weeks old Ts1Cje (n=6) and wild-type (n=5) using Affymetrix mouse gene 1.0 ST array. Data were normalized and analyzed to identify and accurately map genes that are significantly differentially expressed. Functional analyses were performed using GSEA and DAVID to better characterize cellular processes and pathways that are consistently affected in both brain regions.
Project description:The Ts1Cje mouse model of Down syndrome (DS) has partial triplication of mouse chromosome 16, of which a large portion is homologous to human chromosome 21. The mouse model shows an impaired neurogenesis at E14.5. We analyzed the effect of Ts1Cje trisomic region on global gene expression in the embryonic brain of Ts1Cje mice at E14.5.
Project description:The Ts1Cje mouse model of Down syndrome (DS) has partial triplication of mouse chromosome 16 (MMU16), which is partially homologous to human chromosome 21. The mouse model develops various neuropathological features identified in DS individuals. We analysed the effect of partial triplication of the MMU16 segment on global gene expression in the cerebral cortex, cerebellum and hippocampus of Ts1Cje mice at 4 time-points; postnatal day (P)1, P15, P30 and P84. RNA was extracted from thre brain regions (Cerebral cortex, hippocampus and cerebellum) for hybridization to arrays from 3 pairs of Ts1Cje and disomic C57BL/6 littermate control for each timepoints at postnatal (P) day 1, P15, P30 and P84.
Project description:To look for age-related changes in the liver, we used RNAseq gene expression analysis to characterize mRNA expression profile in livers from 1-month vs. 6-month-old mice
Project description:The purpose of this experiment is to examine the cellular and molecular changes in the microglia and other non-neuron cells in the hippocampus of 7 month old Mr1+/+ and Mr1-/- mice.