Expression profiles of ncRNA and mRNA in C57 and AD model mice(APP/PS1 and P301S) at the age of 3, 6 and 12 months respectively
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE242902 | GEO | 2024/05/01
REPOSITORIES: GEO
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Project description:Expression profiles of ncRNA and mRNA in C57 and AD model mice(APP/PS1 and P301S) at the age of 3, 6 and 12 months respectively
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Project description:Amyloid beta (Aβ) monomers aggregate to form fibrils and amyloid plaques, which is one of the important mechanisms in the pathogenesis of Alzheimer's disease (AD). Since the Aβ1-42 aggregation has prominent role in plaque formation, which eventually lead to the patient's brain lesions and cognitive impairment, an increasing number of studies have been devoted to reduce Aβ aggregation process to slow down AD progression. Since the diphenylalanine (FF) sequence is critical for amyloid aggregation, and it has been shown that magnetic fields can affect the alignment of peptide assembly due to the diamagnetic anisotropy of aromatic rings, here we used a moderate-intensity rotating magnetic field (RMF) to explore its effect on Aβ aggregation and AD pathogenesis. Our data showed that RMF can directly inhibit Aβ amyloid fibril formation and reduce Aβ-induced cytotoxicity on neural cells in vitro. Using the AD mouse model APP/PS1, we found that the RMF can restore their motor ability to the healthy control level. Their cognitive impairments, including exploration ability, spatial and non-spatial memory abilities, were also significantly alleviated. Tissue examinations reveal that RMF has reduced amyloid plaque accumulation, attenuated microglial activation ,and reduced oxidative stress in the APP/PS1 mouse brain. Therefore, our data demonstrate the great potential of RMF to be developed as a non-invasive, high-penetration physical approach to be applied in the treatment of AD.
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Project description:The imbalance between production and clearance of amyloid-beta (Aβ) is a key step in the onset and development of Alzheimer's disease (AD). Therefore, reducing Aβ accumulation in the brain is a promising therapeutic strategy for AD. The recently discovered glymphatic system and meningeal lymphatic vasculature have been shown to be critical for the elimination of interstitial waste products, especially Aβ, from the brain. In the present study, ligation of deep cervical lymph nodes was performed to block drainage of this system and explore the consequences on Aβ-related pathophysiology. Five-month-old APP/PS1 mice and their wild-type littermates received deep cervical lymphatic node ligation. One month later, behavioral testing and pathological analysis were conducted. Results demonstrated that ligation of dcLNs exacerbated AD-like phenotypes of APP/PS1 mice, showing more severe brain Aβ accumulation, neuroinflammation, synaptic protein loss, impaired polarization of aquaporin-4 and deficits in cognitive and exploratory behaviors. These results suggest that brain lymphatic clearance malfunction is one of the deteriorating factors in the progression of AD, and restoring its function is a potential therapeutic target against AD.
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Project description:NSAIDs (non-steroidal anti-inflammatory drugs) inhibit cyclooxygenase (COX) enzymes and prevent Alzheimer's disease (AD) at preclinical stages in cognitively normal aging populations. We modeled NSAID prevention of memory impairment in AD model mice to identify novel targets of NSAID action. We found that the widely-used NSAID ibuprofen prevented early hippocampus-dependent memory deficits in APP-PS1 mice. We therefore analyzed gene expression in the hippocampus of these mice. We treated male APPSwe-PS1deltaE9 mice (strain originally provided by Dr. David Borchelt and fully back-crossed to a C57BL/6J background) and their wild-type littermates with ibuprofen in chow from 3 to 6 months of age, after which we sacrificed the mice and dissected one hippocampus from each mouse for RNA isolation and microarray analysis. In each genotype-treatment group, we analyzed samples from 5 mice. Note: In our initial analysis, we found that sample GSM1644138, Hippocampus_WT_Con_rep5, was an outlier in overall gene expression. We therefore removed this sample before performing the analysis published in PMID 27190010.
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Project description:NSAIDs (non-steroidal anti-inflammatory drugs) inhibit cyclooxygenase (COX) enzymes and prevent Alzheimer’s disease (AD) at preclinical stages in cognitively normal aging populations. We modeled NSAID prevention of memory impairment in AD model mice to identify novel targets of NSAID action. We found that the widely-used NSAID ibuprofen prevented early hippocampus-dependent memory deficits in APP-PS1 mice. We therefore analyzed gene expression in the hippocampus of these mice.
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Project description:Alzheimer's disease (AD) is the largest unmet medical complication. The devastation caused by the disease can be assumed from the disease symptoms like speech impairment, loss of self-awareness, acute memory loss etc. The individuals suffering from AD completely depend on caregivers and have to bear the high cost of treatment which increases the socio-economic burden on the society. Recent studies have shown that radiation exposure can have therapeutic effects when given in suitable amount for a specific time period. Therefore, we investigated the role of gamma irradiation in AD pathogenesis. The effect of radiation on amelioration of disease progression was studied in AD transgenic mice model (APP/PS1). Our in-vivo studies using APP/PS1 mice demonstrated that a single dose of 4.0 Gy gamma irradiation improves AD associated behavioral impairment. Radiation exposure also increased the level of anti-oxidant enzymes and reduced the astrocyte activation in the brain of APP/PS1 mice. A significant reduction was observed in AD associated proteins (APP, pTau, BACE) and neurofibrillary tangle formations (NFTs). Exposure to a single dose of 4 Gy gamma radiation also increased glucose metabolic functionality in AD transgenic mouse model. The kinases involved in insulin signaling such as GSK, ERK and JNK were also found to be modulated. However, an increased level of GSK3? (ser 9) was observed, which could be responsible for downregulating ERK and JNK phosphorylation. This resulted in a decrease in neurofibrillary tangle formations and amyloid deposition. The reduced hyperphosphorylation of Tau can be attributed to the increased level of GSK3? (ser 9) downregulating ERK and JNK phosphorylation. Thus, a single dose of 4 Gy gamma irradiation was found to have therapeutic benefits in treating AD via potentiating insulin signaling in APP/PS1 transgenic mice.
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Project description:NLRC3 inhibits inflammatory responses. Neuroinflammation induces and accelerates the onset of Alzheimer's disease (AD). This study is aimed at investigating whether NLRC3 plays a role in neuroinflammation, Aβ accumulation, and neuroprotection in AD mice. 12-month-old APP/PS1 transgenic and C57 mice were used for studies in vivo. In vitro, organotypic hippocampal slices were cultured. We found that the expression of NLRC3 was downregulated in the brain tissues of APP/PS1 mice. Mice in the APP/PS1 group had a significant attenuation of learning and memory ability compared to the control group, and the ability was improved in APP/PS1 + LV-NLRC3 mice. The expressions of 6E10, GFAP, Iba1, and PI3K in the hippocampus and brains of APP/PS1 mice were significantly higher than those of the control group, while the expressions of NeuN were lower than that of the control group. With the overexpression of NLRC3 in the APP/PS1 + LV-NLRC3 group, the expressions of 6e10, GFAP, Iba1, and PI3K were significantly lower, while the expression of NeuN was significantly higher compared to the APP/PS1 group. NLRC3 colocalized with NeuN. PI3K activation with 740YP increased the expression of GFAP and Iba-1 in the hippocampus with the exogenous NLRC3 protein. We conclude that NLRC3 may play an important role in the development and progression of AD. Downregulation of NLRC3 can lead to the activation of PI3K, resulting in abnormal plaque deposition, glial cell activation, and neuron loss during AD. NLRC3 delays the progression of AD in APP/PS1 mice via inhibiting PI3K activation.
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