AI Article Synopsis
- Alzheimer's disease (AD) is primarily characterized by the buildup of amyloid β (Aβ) in the brain, which is linked to dementia.
- MicroRNAs (miRNAs) play a critical role in regulating genes that affect Aβ metabolism, and their expression levels change during AD progression, making them potential diagnostic markers.
- The study used a mouse model to identify altered miRNA levels, discovering nine common miRNAs between sibling pairs, which appear to influence genes in the PI3K/Akt signaling pathway, shedding light on Aβ-induced neuronal dysfunction in AD.
Article Abstract
Alzheimer's disease (AD) is the most common cause of dementia. One of the pathological hallmarks of AD is amyloid β (Aβ) deposition. MicroRNAs (miRNAs) are small non-coding RNAs whose expression levels change significantly during neuronal pathogenesis and may be used as diagnostic markers. Some miRNAs are important in AD development by targeting genes responsible for Aβ metabolism. However, a systematic assessment of the miRNA expression profile induced by Aβ-mediated neuronal pathogenesis is still lacking. In the present study, we examined miRNA expression profile by using the APPswe/PS1ΔE9 mouse model of AD. Two sibling pairs of mice were examined, showing 30 and 24 miRNAs with significantly altered expression levels from each paired control, respectively. Nine known miRNAs were common in both groups. Prediction of putative target genes and functional annotation implied that these altered miRNAs affect many target genes mainly involved in PI3K/Akt signaling pathway. This study provides a general profile of miRNAs regulated by Aβ-associated signal pathways, which is helpful to understand the mechanism of Aβ-induced neuronal dysfunction in AD development.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4141691 | PMC |
| http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0101725 | PLOS |
Publication Analysis
Top Keywords
Similar Publications
SENP1 inhibits aerobic glycolysis in Aβ-incubated astrocytes by promoting PUM2 deSUMOylation.
Cell Biol Toxicol
January 2025
Department of Neurology, The Fourth Affiliated Hospital of China Medical University, Shenyang, China.
Alzheimer's disease (AD), the most prevalent form of dementia in the elderly, involves critical changes such as reduced aerobic glycolysis in astrocytes and increased neuronal apoptosis, both of which are significant in the disease's pathology. In our study, astrocytes treated with amyloid β1-42 (Aβ) to simulate AD conditions exhibited upregulated expressions of small ubiquitin-like modifier (SUMO)-specific protease 1 (SENP1) and Pumilio RNA Binding Family Member 2 (PUM2), alongside decreased levels of Nuclear factor erythroid 2-related factor 2 (NRF2). SENP1 is notably the most upregulated SUMOylation enzyme in Aβ-exposed astrocytes.
View Article and Find Full Text PDFFecal microbiota transplantation attenuates Alzheimer's disease symptoms in APP/PS1 transgenic mice via inhibition of the TLR4-MyD88-NF-κB signaling pathway-mediated inflammation.
Behav Brain Funct
January 2025
Wenzhou Key Laboratory of Sanitary Microbiology; School of Laboratory Medicine and Life Sciences; Key Laboratory of Laboratory Medicine, Ministry of Education, Wenzhou Medical University, Wenzhou, Zhejiang Province, China.
Alzheimer's disease (AD) is a prevalent and progressive neurodegenerative disorder that is the leading cause of dementia. The underlying mechanisms of AD have not yet been completely explored. Neuroinflammation, an inflammatory response mediated by certain mediators, has been exhibited to play a crucial role in the pathogenesis of AD.
View Article and Find Full Text PDFAccumulated BCAAs and BCKAs contribute to the HFD-induced deterioration of Alzheimer's disease via a dysfunctional TREM2-related reduction in microglial β-amyloid clearance.
J Neuroinflammation
December 2024
Department of Nutrition and Food Hygiene, Hubei Key Laboratory of Food Nutrition and Safety, MOE Key Laboratory of Environment and Health, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, 430030, People's Republic of China.
A high-fat diet (HFD) induces obesity and insulin resistance, which may exacerbate amyloid-β peptide (Aβ) pathology during Alzheimer's disease (AD) progression. Branched-chain amino acids (BCAAs) accumulate in obese or insulin-resistant patients and animal models. However, roles of accumulated BCAAs and their metabolites, branched-chain keto acids (BCKAs), in the HFD-induced deterioration of AD and the underlying mechanisms remains largely unclear.
View Article and Find Full Text PDFIntegrated network pharmacology and brain metabolomics to analyze the mechanism of Dihuang Yinzi intervention in Alzheimer's disease.
Heliyon
March 2024
School of Basic Medicine, Heilongjiang University Of Chinese Medicine, Harbin, 150040, China.
Ethnopharmacological Relevance: Alzheimer's disease (AD) is an incurable neurodegenerative disease that has become one of the most important diseases threatening global public health security. Dihuang Yinzi (DHYZ) is a traditional Chinese medicine that has been widely used for the treatment of AD and has significant therapeutic effects, but its specific mechanism of action is still unclear.The aim of the study is to investigate the specific mechanism of DHYZ in treating AD based on brain metabolomics and network pharmacology.
View Article and Find Full Text PDFRetraction Note: nAChRs gene expression and neuroinflammation in APPswe/PS1dE9 transgenic mouse.
Sci Rep
November 2024
Department of Medical, Oral and Biotechnological Sciences, University "G. D'Annunzio", Via dei Vestini 31, 66100, Chieti, Italy.
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!