Se-methylselenocysteine (SMC) is a major selenocompound in selenium (Se) enriched plants and has been found to ameliorate neuropathology and cognitive deficits in triple-transgenic mice model of Alzheimer's disease (3 × Tg-AD mice). To explore the underlying molecular mechanisms, the present study is designed to elucidate the protein changes in the cortex of SMC-treated 3 × Tg-AD mice. After SMC supplementation, proteomic analysis revealed that 181, 271, and 41 proteins were identified as differentially expressed proteins (DEPs) between 3 × Tg-AD mice vs wild type (AD/WT group), SMC-treated AD mice vs AD (AD + SMC/AD), and AD + SMC/WT group, respectively. Among these, 138 proteins in the diseased group were reversed by SMC treatment. The DEPs in AD/WT group and AD + SMC/AD group were mainly related to metabolism, synapses, and antioxidant proteins, while their levels were decreased in AD mice but up-regulated after treating with SMC. In addition, we found reduced ATP levels and destroyed synaptic structures in the AD mice brains, which were significantly ameliorated upon SMC treatment. Our study suggests that energy metabolism disorders, abnormal amino acid metabolism, synaptic dysfunction, and oxidative stress may be the key pathogenic phenomena of AD. SMC reversed the expression of proteins associated with them, which might be the main mechanism of its intervention in AD.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1021/acschemneuro.0c00549 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
The total withanolides from the leaves of Datura stramonium L. Improves Alzheimer's disease pathology by restraining neuroinflammation through NLRP3/IL-1β/IL1R1/TOM 1 pathway.
Int Immunopharmacol
January 2025
Key Laboratory of Basic and Application Research of Beiyao (Heilongjiang University of Chinese Medicine), Ministry of Education, China; Traditional Chinese Medicine (TCM) Biological Genetics (Heilongjiang Province Double First-class Construction Interdiscipline, China. Electronic address:
Alzheimer's disease (AD) is a neurodegenerative disorder characterized by the deposition of beta-amyloid (Aβ) peptides. Microglia-mediated neuroinflammation is one of the primary contributors to the pathogenesis of AD. Withanolides, the main constituents in the leaves of Datura stramonium L.
View Article and Find Full Text PDFPedunculoside alleviates cognitive deficits and neuronal cell apoptosis by activating the AMPK signaling cascade.
Chin Med
November 2024
Zhejiang TCM Key Laboratory of Pharmacology and Translational Research of Natural Products, School of Pharmaceutical Sciences, Hangzhou Medical College, Hangzhou, 310014, Zhejiang, China.
Background: Mitochondrial dysfunction emerges as an early pathological hallmark of Alzheimer's disease (AD). The reduction in mitochondrial membrane potential and the elevation of reactive oxygen species (ROS) production are pivotal in the initiation of neuronal cell apoptosis. Pedunculoside(Ped), a novel triterpene saponin derived from the dried barks of Ilex rotunda Thunb, exhibits a potent anti-inflammatory effect.
View Article and Find Full Text PDFDifferential involvement of central and peripheral catecholamines between Alzheimer's disease and vascular dementia.
Heliyon
October 2024
Department of Laboratory Medicine, Zhongnan Hospital of Wuhan University, Donghu Road 169, Wuhan, 430071, Hubei, China.
Article Synopsis
- The study investigates the role of catecholamines (like dopamine and norepinephrine) in the development of Alzheimer's disease (AD) and vascular dementia (VaD) by analyzing their levels in animal models.
- Using specific mouse and rat models, researchers measured catecholamine concentrations in both blood and different brain areas to understand their distribution and expression during these neurodegenerative processes.
- Findings reveal that while catecholamines like dopamine are significant in AD, VaD is more associated with changes in the central noradrenergic system and increased serum catecholamines, suggesting different treatment approaches may be needed for each condition.
Akt-activated GSK3β inhibitory peptide effectively blocks tau hyperphosphorylation.
Arch Pharm Res
November 2024
Department of Pharmacy, College of Pharmacy and Research Institute for Drug Development, Pusan National University, Busan, 46241, Republic of Korea.
Article Synopsis
- Tau hyperphosphorylation and accumulation in neurofibrillary tangles are linked to cognitive decline in Alzheimer's disease, with GSK3β overexpression playing a key role.
- A new GSK3β inhibitory peptide (GIP) was developed, combining motifs from LRP6 and a sequence targeting Akt, effectively blocking tau phosphorylation and reducing cell death.
- In vivo tests on a mouse model showed that GIP reduced tau phosphorylation in the hippocampus, improved memory, and did not affect Aβ plaque levels or neuroinflammation, suggesting a new approach for treating Alzheimer's.
Ovariectomy exacerbates the disturbance of excitation- inhibition balance in the brain of APP/PS-1/tau mice.
Front Mol Neurosci
August 2024
School of Pharmaceutical Sciences and Institute of Materia Medica, Shandong First Medical University and Shandong Academy of Medical Sciences, Jinan, Shandong, China.
Introduction: The prevalence of Alzheimer's disease (AD) is significantly gender-differentiated, with the number of female AD patients far exceeding that of males, accounting for two-thirds of the total prevalence. Although postmenopausal AD mice have been shown to have more prominent pathologic features and memory impairments than normal AD mice, the relevant molecular mechanisms leading to these outcomes have not been well elucidated. In the present study, we used the disturbance of excitation-inhibition balance in the postmenopausal brain as an entry point to explore the link between estrogen deficiency, disorders of the glutamatergic-GABAergic nervous system, and memory impairment.
View Article and Find Full Text PDFWant 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!