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Benefits of diazoxide/dibenozylmethane (DZ/DIB) co-treatment on hippocampal gene expression in Female Fisher transgenic 344-AD rats.

ABSTRACT: Benefits of diazoxide/dibenozylmethane (DZ/DIB) co-treatment on hippocampal gene expression in Female Fisher transgenic 344-AD rats.

PROVIDER: PRJNA1030916 | ENA |

REPOSITORIES: ENA

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Benefits of diazoxide/dibenozylmethane (DZ/DIB) co-treatment on hippocampal gene expression in Female Fisher transgenic 344-AD rats.

Project description:Alzheimer’s disease (AD) is the major cause of dementia prevalent in older adults and with a high incidence in females; thus, Identification of early biomarkers is important for preventive interventions. To show potential early biomarkers, we carried out RNA-Sequencing analysis for 4-month(pre-pathology) TgF344-AD rats, a transgenic Alzheimer’s model that exhibits age-dependent AD progression. Our study showed two potential early biomarker genes (early growth response 2 (EGR2) and histone H2AA (HISIT1H2AA)) for AD, in the hippocampus of 4-month TgF344-AD females compared to wild-type littermates. Furthermore, due to the multifactorial cause for AD, we tested the therapeutic benefit of a multi-target approach using a co-treatment with diazoxide (DZ), a potassium channel activator, and dibenzoylmethane (DIB), which inhibits eIF2α-P activity, on TgF344-AD female. Our results strongly support the DZ/DIB-treatment as potential strategy to mitigate AD pathology due to its multi-target approach.

2023-11-22 | GSE245979 | GEO

Effects of BT-11 treatment on hippocampal gene expression in Female Fisher transgenic 344-AD rats. [Female RNAseq]

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Effects of BT-11 treatment on hippocampal gene expression in Male Fisher transgenic 344-AD rats. [Male RNAseq]

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Effects of ibudilast treatment on hippocampal gene expression in Male Fisher transgenic 344-AD rats.

Project description:5 month old Male Fisher transgenic 344-AD (Tg-AD) rats expressing humanSwedishamyloid precursor protein (APPsw) and Δ exon 9 presenelin-1 (PS1ΔE9) were treated with Ibudilast (cat. no. HY-B0763, MCE) at 10 mg/kg body weight administered in rodent chow. Following 6 months of Ibudilast treatment, rats (11 months of age) were tested for cognitive behaviour prior to sacrificing. Hippocampal Brain region were dissected and RNA sequencing (RNAseq) analyses was done on the Isolated sample. Taken together we showed that Ibudilast treatment: (i) reduces inflammation by decreasing the levels of the pro inflammatory cytokine IL6, interferon receptor 1, the macrophage migration inhibitory factor (MIF), microglial associated proteins such as transmembrane protein 119 (TMEM119), arachidonate 5-lipoxygenase activating protein (Alox5ap), toll like receptor 7 (TLR7), lysosomal protein transmembrane 5 (LAPTM5) and triggering receptor expressed on myeloid cells 2 (TREM2); (ii) increases expression of synaptic proteins such as synaptotagmin 2 (SYT2), which regulates vesicular transport, syntaxins (STX), which participates in neurotransmitter release, and cadherin (CDH1), which maintains synapse structure; and (iii) reduces the expression of the neurotrophic factor BDNF by 2-fold in both male and female treated rats.

2023-10-17 | GSE245214 | GEO

Effects of ibudilast treatment on hippocampal gene expression in Female Fisher transgenic 344-AD rats.

Project description:5 month old Female Fisher transgenic 344-AD (Tg-AD) rats expressing humanSwedishamyloid precursor protein (APPsw) and Δ exon 9 presenelin-1 (PS1ΔE9) were treated with Ibudilast (cat. no. HY-B0763, MCE) at 10 mg/kg body weight administered in rodent chow. Following 6 months of Ibudilast treatment, rats (11 months of age) were tested for cognitive behaviour prior to sacrificing. Hippocampal Brain region were dissected and RNA sequencing (RNAseq) analyses was done on the Isolated sample. Taken together we showed that Ibudilast treatment: (i) reduces inflammation by decreasing the levels of the pro inflammatory cytokine IL6, interferon receptor 1, the macrophage migration inhibitory factor (MIF), microglial associated proteins such as transmembrane protein 119 (TMEM119), arachidonate 5-lipoxygenase activating protein (Alox5ap), toll like receptor 7 (TLR7), lysosomal protein transmembrane 5 (LAPTM5) and triggering receptor expressed on myeloid cells 2 (TREM2); (ii) increases expression of synaptic proteins such as synaptotagmin 2 (SYT2), which regulates vesicular transport, syntaxins (STX), which participates in neurotransmitter release, and cadherin (CDH1), which maintains synapse structure; and (iii) reduces the expression of the neurotrophic factor BDNF by 2-fold in both male and female treated rats.

2023-10-17 | GSE245623 | GEO

Effects of ibudilast treatment on hippocampal gene expression in Male Fisher transgenic 344-AD rats.

Project description:Effects of ibudilast treatment on hippocampal gene expression in Male Fisher transgenic 344-AD rats.

| PRJNA1027378 | ENA

Effects of ibudilast treatment on hippocampal gene expression in Female Fisher transgenic 344-AD rats.

Project description:Effects of ibudilast treatment on hippocampal gene expression in Female Fisher transgenic 344-AD rats.

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Effects of BT-11 treatment on hippocampal gene expression in Male Fisher transgenic 344-AD rats. [Male RNAseq]

Project description:Effects of BT-11 treatment on hippocampal gene expression in Male Fisher transgenic 344-AD rats. [Male RNAseq]

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Effects of BT-11 treatment on hippocampal gene expression in Female Fisher transgenic 344-AD rats. [Female RNAseq]

Project description:Effects of BT-11 treatment on hippocampal gene expression in Female Fisher transgenic 344-AD rats. [Female RNAseq]

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Persistence of furan-induced epigenetic aberrations in the livers of Fisher 344 rats

Project description:Furan is a heterocyclic organic compound produced in the chemical manufacturing industry and also found in a broad range of food products, including infant formulas and baby foods. Previous reports have indicated that the adverse biological effects of furan, including its liver tumorigenicity, may be associated with epigenetic abnormalities. In the present study we investigated the persistence of epigenetic alterations in rat liver. Male Fisher 344 (F344) rats were treated by gavage 5 days per week with 8 mg furan/kg body weight (bw)/day for 90 days. After the last treatment, rats were divided randomly into four groups; one group of rats was sacrificed 24 hours after the last treatment, while other groups were maintained without further furan treatment for an additional 90, 180, or 360 days. Treatment with furan for 90 days resulted in alterations in histone lysine methylation and acetylation, oxidative damage to DNA, and changes in the gene expression in the livers. A majority of these furan-induced molecular changes was transient and disappeared after the cessation of furan treatment. In contrast, histone H3 lysine 9, H3 lysine 27, and H3 lysine 56 showed a sustained and time-depended decrease in acetylation, which was associated with formation of heterochromatin and altered gene expression. These results indicate that furan-induced adverse effects may be mechanistically related to sustained changes in histone lysine acetylation that compromise the ability of cells to maintain and control properly the expression of genetic information.

2014-12-02 | GSE63740 | GEO

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