Trascriptome data in the brain from Propolis treated-Alzheimer's disease model mice
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE234109 | GEO | 2023/06/09
REPOSITORIES: GEO
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Project description:A hive product propolis has been used for folk medicine for more than 4, 000 years. So far, several line of studies demonstrated that propolis improved glucose metabolism in obese models. In this study, we inverstigated whether propolis modulates stromal cells of mesenteric adipose tissue of ob/ob mice. Male ob/ob mice were inhjected with Brazilian propolis ethanol extract (100mg/kg ip, twice a week) or vehicle for 12 weeks. Subsequently, vasucular stromal fraction was prepared from mesenteric adipose tissue. Total cellular RNA extracted from the fraction was used for microarray analysis. Biological triplicates were subjected.
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Project description:Alzheimer’s disease (AD) is the most common form of adult-onset dementia with severe intellectual deterioration and is characterised by the accumulation of the amyloid-β (Aβ) peptides and the presence of hyperphosphorylated microtubule- associated protein, tau. (-)-Epigallocatechin-3-gallate (EGCG) – a polyphenolic catechin found in green tea leaves, not only acts as a proteasome inhibitor, it is also involved in neuroprotection. A total of 7 RNA samples were analyzed. Cultured murine primary cortical neurons were treated with 1uM EGCG for 24h (n=3) in addition to the vehicle control (n=4).
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Project description:The effect of Brazilian green propolis on regulatory T cells
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Project description:Alzheimer’s disease (AD) is the most common form of adult-onset dementia with severe intellectual deterioration and is characterised by the accumulation of the amyloid-β (Aβ) peptides and the presence of hyperphosphorylated microtubule- associated protein, tau. (-)-Epigallocatechin-3-gallate (EGCG) – a polyphenolic catechin found in green tea leaves, not only acts as a proteasome inhibitor, it is also involved in neuroprotection.
2013-12-31 | GSE22996 | GEO
Project description:Amyloid-beta (Aβ) plays a key role in the pathogenesis of Alzheimer’s disease (AD), but little is known about the proteoforms present in human AD brain. We used high-resolution mass spectrometry to analyze intact, undigested Aβ from purified soluble aggregates and insoluble material in brains of 6 cases with severe dementia and pathologically confirmed AD. The soluble aggregates are especially relevant because they are believed to be the most toxic form of Aβ. We found a diversity of Aβ peptides, with 26 unique proteoforms including various N- and C-terminal truncations. N- and C-terminal truncations comprised 73% and 30%, respectively, of the number of Aβ proteoforms detected. The Aβ proteoforms segregated between the soluble and more insoluble aggregates with N-terminal truncations predominating in the insoluble material and C- terminal truncations segregating into the soluble aggregates. In contrast, canonical Aβ comprised the minority of the number of identified proteoforms (15.3%) and did not distinguish between the soluble and more insoluble aggregates. The relative abundance of many truncated Aβ proteoforms did not correlate with post-mortem interval, suggesting they are not artefacts. This heterogeneity of Aβ proteoforms deepens our understanding of AD and offers many new avenues for investigation into pathological mechanisms of the disease, with implications for therapeutic development.
2017-08-28 | PXD006552 | Pride
Project description:Amyloid-beta (Aβ) plays a key role in the neuropathogenesis of Alzheimer’s disease, but little is known about the proteoforms (i.e., all protein variants of a single gene including post-translational modifications and sequence variants) present in human AD brain. We used high-resolution mass spectrometry to analyze intact, whole Aβ from soluble and insoluble aggregates in brains of 6 cases with severe dementia and pathologically confirmed Alzheimer’s disease. We found an extraordinary diversity of Aβ peptides totaling 91 unique proteoforms including various N- and C-terminal truncations, 17 different types of post-translational modifications (PTMs), and remarkably 5 amino acid variants in the peptide sequence never before described. Ratios of Aβ proteoforms did not distinguish between soluble and insoluble aggregates, but four individual Aβ proteoforms, three in the insoluble and one in the soluble fraction, were markedly increased when compared across aggregates. Such heterogeneity of the Aβ peptide both deepens our understanding of AD, but perhaps also warrants pause and consideration in our investigation into pathological mechanisms of the disease and therapeutic development.
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Project description:To reveal the mechanisms that Ogt controls inflammatory response of astrocytes, we first performed RNA-seq with Ctrl and Ogt cKO astrocytes isolated from the brains of adult mice. Given the inflammation in the brain of Alzheimer’s disease, we next performed RNA-seq with astrocytes isolated from the brains of adult Ctrl and 5X APP Alzheimer’s mice model (AD), and Aβ treated astrocytes, respectively. Taken together, these findings suggest that differentially expressed genes shared between cKO astrocytes, AD astrocytes and Aβ-treated astrocytes are related with inflammation.
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Project description:In neurodegenerative disorders such as Alzheimer’s disease (AD), brain miRNA profiles are altered; thus miRNA dysfunction could be both a cause and a consequence of disease. Our study dissects the complexity of human AD pathology, in the absence of a post mortem delay, and provides the first miRNA profiling analysis addressing the contribution of amyloid-β (Aβ), a known causative factor of AD, to the de-regulation of neuronal miRNA expression. We used murine primary hippocampal neurons to show that Aβ is a powerful regulator of mature miRNA expression and a prominent miRNA down-regulation is evoked in response to Aβ peptides. Our study provides insight into a previously unexplored mechanism of how Aβ may impact the pathology of AD and identification of key miRNAs affected by Aβ will allow further analysis on target genes and biological pathways contributing to AD pathomechanisms.
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Project description:Isolation of glia from Alzheimer's mice reveals inflammation and dysfunction. Reactive astrocytes and microglia are associated with amyloid plaques in Alzheimer's disease (AD). Yet, not much is known about the molecular alterations underlying this reactive phenotype. To get an insight into the molecular changes underlying AD induced astrocyte and microglia reactivity, we performed a transcriptional analysis on acutely isolated astrocytes and microglia from the cortex of aged controls and APPswe/PS1dE9 AD mice. As expected, both cell types acquired a proinflammatory phenotype, which confirms the validity of our approach. Interestingly, we observed that the immune alteration in astrocytes was relatively more pronounced than in microglia. Concurrently, our data reveal that astrocytes display a reduced expression of neuronal support genes and genes involved in neuronal communication. The microglia showed a reduced expression of phagocytosis and/or endocytosis genes. Co-expression analysis of a human AD expression data set and the astrocyte and microglia data sets revealed that the inflammatory changes in astrocytes were remarkably comparable in mouse and human AD, whereas the microglia changes showed less similarity. Based on these findings we argue that chronically proinflammatory astrocyte and microglia phenotypes, showing a reduction of genes involved in neuronal support and neuronal signaling, are likely to contribute to the neuronal dysfunction and cognitive decline in AD. 2 cell types from 2 conditions: cortical microglia and cortical astrocytes from 15-18 month old APPswe/PS1dE9 mice compared to wildtype littermates. Biological replicates: microglia from APPswe/PS1dE9, N=7, microglia from WT, N=7, astrocytes from APPswe/PS1dE9, N=4, microglia from WT, N=4
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