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Typical western diet exacerbates dystrophic neurite pathology in APP/PS1 and APP/PS1/Tau mouse models by reducing the clustering of microglia around β-amyloid plaques

ABSTRACT: Here, we studied the interaction between dietary (TWD) and genetic factors (APPswe/PS1dE9 and tau P301L mutations) and their effect on memory, brain pathology, global gene expression and on insulin-Akt-GSK3β pathway in brain of mice with four different AD-linked genetic backgrounds: wild-type (AwTw), APPswe/PS1dE9 (A+Tw), P301Ltau (AwT+), and triple transgenic (A+T+).

ORGANISM(S): Mus musculus

PROVIDER: GSE144746 | GEO | 2020/11/24

REPOSITORIES: GEO

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Olfactory bulb proteome characterization in APP/PS1 mice

Project description:Here we used double-transgenic amyloid precursor protein/presenilin 1 (APPswe/PS1dE9) mice and label-free quantitative proteomics to analyze potential early pathological effects on the olfactory bulb (OB) during AD progression.

2016-08-09 | PXD003683 | Pride

miRNA profile in the hippocampus of APP/PS1 transgenic mice

Project description:To explore the miRNAs associated with the memory deficits in Alzheimer's disease, we detected the miRNA profiles in the hippocampus of 6-month-old male APPswe/PS1dE9 (APP/PS1) mice and age-matched wild type C57BL/6 mice.

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APP/PS1 mice characterization and time progression.

Project description:RNA samples from the cerebral cortex of APP/PS1 and WT mouse littermates aged 3, 6 and 12 months were analyzed using the Affymetrix Genechip Mouse Gene 1.1 ST Array. The APP-PS1 transgenic mouse express the human mutated forms APPswe and PS1dE9. This is a good model of familial Alzheimer Disease because it reproduces several features of the disease as β-amyloid deposits throughout the brain and exhibit memory impairment by the end of the sixth month and is a simple model to study the molecular pathways. The aim of this study is to identify dysregulation of inflammation pathways in order to understand shifts of inflammation responses with disease progression.

2014-04-30 | E-MTAB-2121 | biostudies-arrayexpress

Proteome profiling in APP/PS1 mice brain and modulation by tocotrienol-rich fraction

Project description:This study examined the proteome profile in the hippocampus, medial prefrontal cortex, and striatum of APPswe/PS1dE9 transgenic mice (APP/PS1) model of Alzheimer’s disease compared to wild-type mice. The effect of tocotrienol-rich fraction (TRF), a mixture of vitamin E analogs derived from palm oil supplementation on the proteome profile of APP/PS1 mice hippocampus, medial prefrontal cortex, and striatum was also investigated. The analysis was performed using ultrahigh-performance liquid chromatography coupled with Q Exactive HF Orbitrap mass spectrometry. This study was in hoped to understand the mechanisms of Alzheimer’s disease at proteome level, and pre-emptive activity of TRF to combat the disease.

2019-12-06 | PXD011068 | Pride

Early amyloid-induced changes in microglia gene expression in APP/PS1 mice [scRNA-seq]

Project description:Alzheimer’s disease (AD) is a progressive neurodegenerative disease and the most common cause of dementia, characterized by deposition of extracellular amyloid-beta (Aβ) aggregates and intraneuronal hyperphosphorylated Tau. Many AD risk genes, identified in genome-wide association studies (GWAS), are expressed in microglia, the innate immune cells of the central nervous system. Specific subtypes of microglia emerged in relation to AD pathology, such as disease-associated microglia (DAMs), which increased in number with age in amyloid mouse models and in human AD cases. However, the initial transcriptional changes in these microglia in response to amyloid are still unknown. Here, to determine early changes in microglia gene expression, hippocampal microglia from APPswe/PS1dE9 (APP/PS1) mice and wildtype littermates were isolated and analyzed by RNA sequencing (RNA-seq). By bulk RNA-seq, transcriptomic changes were detected in hippocampal microglia from 6-months-old APP/PS1 mice. By performing single cell RNA-seq of CD11c-positive and negative microglia from 6-months-old APP/PS1 mice and analysis of the transcriptional trajectory from homeostatic to CD11c-positive microglia, we identified a set of genes that potentally reflect the initial response of microglia to Aβ.

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Differentiated embryonic neurospheres from familial Alzheimer’s disease model show Innate Immune and Glial Cell Responses

Project description:Proteins involved in the Alzheimer’s disease (AD), such as amyloid precursor protein (APP) and presenilin-1 (PS1), play critical roles in early development of the central nervous system (CNS), as well as in innate immune and glial cell responses. However, it is unknown whether these alterations start on development of the CNS of carriers of APPswe and PS1dE9 mutations , associated with familial AD. Using microarray technology we studied the genome-wide gene expression profiles in the differentiated neural progenitor cells (NPCs) from wild-type (WT) and APPswe/PS1dE9 embryo telencephalon. Differential gene expression analysis indicated the occurrence of strong innate immune and glial cell responses in APPswe/PS1dE9 neurospheres, involving mainly microglial cells, inflammatory mediators and chemokines. APPswe/PS1dE9 cells expressed up to 100-fold more CCL12, CCL5, CCL3, C3, CX3CR1, TLR2 and TNF-alpha, which was confirmed by real time PCR. The expression of activated microglia marker Iba-1 was also 20-fold upregulated in APPswe/PS1dE9 cells. The secretome of APPswe/PSldE9 differentiated NPCs increased the chemoattraction of peripheral blood mononuclear cells (PBMCs) compared to the secretome of WT cells. Taken together, our results demonstrated that neurogenic niche obtained from differentiation of embryonic APPswe/PS1dE9 neurospheres is an excellent model for AD in vitro, since this culture spontaneously presents several alterations observed in the adult-brain with this pathology. Moreover, our data strengthen pathophysiological hypotheses that propose an early neurodevelopmental origin for familial AD.

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Early amyloid-induced changes in microglia gene expression in APP/PS1 mice [bulk RNA-seq]

2024-04-01 | GSE226937 | GEO

Typical western diet exacerbates dystrophic neurite pathology in APP/PS1 and APP/PS1/Tau mouse models by reducing the clustering of microglia around β-amyloid plaques

Project description:Typical western diet exacerbates dystrophic neurite pathology in APP/PS1 and APP/PS1/Tau mouse models by reducing the clustering of microglia around β-amyloid plaques

| PRJNA604773 | ENA

Beneficial effect of an adenosine A2AR antagonist in the APPswe/PS1dE9 mouse model of Alzheimer’s Disease

Project description:Beneficial effect of an adenosine A2AR antagonist in the APPswe/PS1dE9 mouse model of Alzheimer’s Disease

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Acutely isolated murine cortical astrocytes and microglia: Alzheimer's disease vs wildtype

Project description:Isolation of glia from Alzheimer's mice reveals inflammation andÂ 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

2015-11-04 | E-GEOD-74615 | biostudies-arrayexpress

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