Effect of DHA in hippocamapal gene expression of wild type and Alzheimer´s disease mice
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE217430 | GEO | 2023/01/25
REPOSITORIES: GEO
Similar Datasets
Project description:Understanding the mechanisms involved in cognitive resilience in Alzheimer’s disease (AD) represents a promising strategy to identify novel treatments for dementia in AD. Previous findings from our group revealed that the study of aged-Tg2576 cognitive resilient individuals is a suitable tool for this purpose. Here, by performing a transcriptomic analysis of the prefrontal cortex of demented and resilient Tg2576 mice, we have been able to hypothesize that pathways involved in inflammation, amyloid degradation, memory function and neurotransmission may be playing a role on cognitive resilience in AD. Intriguingly, the results obtained in this study are suggestive of a reduction of the influx of peripheral immune cells into the brain on cognitive resilient subjects. Indeed, Cd4 mRNA expression is significantly reduced on Tg2576 mice with cognitive resilience and interestingly, we have found a negative correlation between CD4 mRNA levels in the periphery and the score in the Mini-Mental State Exam of AD patients. All of this, highlights the importance of understanding the role of the immune system on the development of neurodegenerative diseases and points out to the infiltration of CD4+ cells in the brain as a key player of cognitive dysfunction in AD.
2023-09-19 | GSE180968 | GEO
Project description:Olfaction is often deregulated in Alzheimer´s disease (AD) patients, being also impaired in transgenic Tg2576 AD mouse model, which overexpress the Swedish mutated form of human amyloid precursor protein (APP). However, little is known about the molecular mechanisms that accompany the neurodegeneration of olfactory structures in Tg2576 mice. For that, we have applied proteome- and transcriptome-wide approaches to probe molecular disturbances in the olfactory bulb (OB) dissected from aged Tg2576 mice (18 months of age) respect to age matched wild-type (WT) littermates.
2018-02-14 | GSE103835 | GEO
Project description:Extracellular senile plaques of amyloid beta (Abeta) are a pathological hallmark in brain of patients with Alzheimer`s Disease (AD). Abeta is generated by the amyloidogenic processing of the amyloid precursor protein (APP). Concomitant to Abeta load, AD brain is characterized by an increase in protein level and activity of the angiotensin-converting enzyme (ACE). ACE inhibitors are a widely used class of drugs with established benefits for patients with cardiovascular disease. However, the role of ACE and ACE inhibition in the development of Abeta plaques and the process of AD-related neurodegeneration is not clear since ACE was reported to degrade Abeta. To investigate the effect of ACE inhibition on AD-related pathomechanisms, we used Tg2576 mice with neuron-specific expression of APPSwe as AD model. From 12 months of age, substantial Abeta plaque load accumulates in the hippocampus of Tg2576 mice as a brain region, which is highly vulnerable to AD-related neurodegeneration. The effect of central ACE inhibition was studied by treatment of 12 month-old Tg2576 mice for six months with the brain penetrating ACE inhibitor captopril. At an age of 18 months, hippocampal gene expression profiling was performed of captopril-treated Tg2576 mice relative to untreated 18 month-old Tg2576 controls with high Abeta plaque load. As an additional control, we used 12 month-old Tg2576 mice with low Abeta plaque load. Whole genome microarray gene expression profiling revealed gene expression changes induced by the brain-penetrating ACE inhibitor captopril, which could reflect the neuro-regenerative potential of central ACE inhibition. Microarray gene expression profiling was performed of hippocampi isolated from aged, 18 month-old Tg2576 (APPSwe-transgenic) AD mice with high Abeta plaque load relative to age-matched Tg2576 mice, which were treated for 6 months with the centrally active ACE inhibitor captopril. Another study group consisted of 12 month-old Tg2576 mice with low Abeta plaque load. In total, three study groups were analyzed, i.e. (i) 18 month-old untreated Tg2576 mice with high Abeta plaque load, (ii) age-matched Tg2576 mice treated for 6 months with the brain-penetrating ACE inhibitor captopril (20 mg/kg body weight/day in drinking water), and (iii) untreated 12 month-old Tg2576 mice with low Abeta plaque load reflecting the time point when captopril treatment was initiated. Two biological replicates were made of each group, and total hippocampal RNA of four mice was pooled for one gene chip.
2013-05-14 | E-GEOD-46871 | biostudies-arrayexpress
Project description:RNAseq data profiling antimalarial-sensitive P. falciparum piggyBac mutants with and without exposure to low dose of DHA and BTZ.
2022-01-31 | GSE188542 | GEO
Project description:Effect of DHA in hippocamapal gene expression of wild type and Alzheimer´s disease mice
| PRJNA899001 | ENA
Project description:This study elucidated the role of DHA-modulated genes in the development and growth of bluefin tuna (Thunnus thynnus) larvae ingesting increasing levels of DHA in their rotifer prey. The effect of feeding low, medium, and high rotifer (Brachionus rotundiformis) DHA levels (2.0, 3.6 and 10.9 mg DHA g-1 DW, respectively) was tested on 2-15 days post hatching (dph) bluefin tuna larvae. Larval DHA content markedly (P < 0.05) increased in a DHA dose-dependent manner (1.5, 3.9, 6.1 mg DHA g-1 DW larva, respectively), that was positively correlated with larval prey consumption, and growth (P < 0.05). Gene ontology enrichment analyses of DEGs demonstrated dietary DHA significantly (P < 0.05) affected different genes and biological processes at different developmental ages. The number of DHA up-regulated DEGs was highest in 10 dph larvae (408), compared to 5 (11) and 15 dph fish (34), and were mainly involved in neural and synaptic development in the brain and spinal cord. In contrast, DHA in older 15 dph larvae elicited fewer DEGs but played critical roles over a wider range of developing organs. The emerging picture underscores the importance of DHA-modulated gene expression as a driving force in bluefin tuna larval development and growth.
2024-10-09 | GSE263473 | GEO
Project description:Extracellular senile plaques of amyloid beta (Abeta) are a pathological hallmark in brain of patients with Alzheimer`s Disease (AD). Abeta is generated by the amyloidogenic processing of the amyloid precursor protein (APP). Concomitant to Abeta load, AD brain is characterized by an increase in protein level and activity of the angiotensin-converting enzyme (ACE). ACE inhibitors are a widely used class of drugs with established benefits for patients with cardiovascular disease. However, the role of ACE and ACE inhibition in the development of Abeta plaques and the process of AD-related neurodegeneration is not clear since ACE was reported to degrade Abeta. To investigate the effect of ACE inhibition on AD-related pathomechanisms, we used Tg2576 mice with neuron-specific expression of APPSwe as AD model. From 12 months of age, substantial Abeta plaque load accumulates in the hippocampus of Tg2576 mice as a brain region, which is highly vulnerable to AD-related neurodegeneration. The effect of central ACE inhibition was studied by treatment of 12 month-old Tg2576 mice for six months with the brain penetrating ACE inhibitor captopril. At an age of 18 months, hippocampal gene expression profiling was performed of captopril-treated Tg2576 mice relative to untreated 18 month-old Tg2576 controls with high Abeta plaque load. As an additional control, we used 12 month-old Tg2576 mice with low Abeta plaque load. Whole genome microarray gene expression profiling revealed gene expression changes induced by the brain-penetrating ACE inhibitor captopril, which could reflect the neuro-regenerative potential of central ACE inhibition.
2013-05-14 | GSE46871 | GEO
Project description:Transcriptional profiling of Human Umbilical Vein Endothelial Cells (HUVEC) comparing untreated control cells with IL-1-treated cells with or without pre-treatment with DHA. Three condition experiment: DHA treated HUVEC cells (25 µmol/L DHA for 48 hours) vs control; IL-1 treated HUVEC cells (5ng/ml for 3 hours) vs control; HUVEC treated with 25 µmol/L DHA for 48 hours and then stimulated with 5 ng/mL IL-1? for 3 hours. For each condition, 3 replicates
2015-05-20 | E-GEOD-57825 | biostudies-arrayexpress
Project description:The omega-3 fatty acid docosahexaenoic acid (DHA) has potent anti-atherogenic properties but its mechanisms of action at the vascular level remain poorly explored. Knowing the broad range of molecular targets of omega-3 fatty acids, microarray analysis was used to open-mindedly evaluate the effects of DHA on aorta gene expression in LDLR-/- mice and better understand its local anti-atherogenic action . Mice were fed an atherogenic diet and received daily oral gavages with oils rich in oleic acid or DHA. Bioinformatics analysis of microarray data first identified inflammation and innate immunity as processes the most affected by DHA supplementation within aorta. More precisely, several down-regulated genes were associated with the inflammatory functions of macrophages (e.g. CCL5, CCR7), cell movement (e.g. ICAM-2, SELP, PECAM-1), and the major histocompatibility complex (e.g. HLA-DQA1, HLA-DRB1). Interestingly, the expression of several genes were identified as specifc biomarkers of macrophage polarization and their changes suggested a preferential orientation towards a M2 reparative phenotype. This observation was supported by the upstream regulator analysis highlighting the involvment of three main regulators of macrophage polarization, namely PPARM-NM-3 (z-score=2.367, p=1.50x10-13), INFM-NM-3 (z-score=-2.797, p=2.81x10-14) and NFM-NM-:B (z-score=2.360, p=6.32x10-9). Moreover, immunohistological analysis of aortic root revealed an increased abundance of Arg1 (+111%, p=0.01), a specific biomarker of M2 macrophage.The present study showed for the first time that DHA supplementation during atherogenesis is associated with protective modulation of inflammation and innate immunity pathways within aorta putatively through the orientation of plaque macrophages towards a M2 reparative phenotype. Mice (LDLR-/-) Aorta samples. 2 groups: Control (K), DHA (C). Biological replicates=8. Dye switch.
2015-01-10 | E-GEOD-59661 | biostudies-arrayexpress
Project description:In this study we explored if colitis induced by dextran sulfate sodium (DSS) in young, presymptomatic/preplaque mice worse and/or anticipate age-dependent cognitive impairment in Tg2576, a widely used mouse model of Alzheimer disease.
2024-05-29 | GSE253108 | GEO