Tocotrienol-rich fraction (TRF) is a mixture of vitamin E analogs derived from palm oil. We previously demonstrated that supplementation with TRF improved cognitive function and modulated amyloid pathology in AβPP/PS1 mice brains. The current study was designed to examine proteomic profiles underlying the therapeutic effect of TRF in the brain. Proteomic analyses were performed on samples of hippocampus, medial prefrontal cortex (mPFC), and striatum using liquid chromatography coupled to Q Exactive HF Orbitrap mass spectrometry. From these analyses, we profiled a total of 5,847 proteins of which 155 proteins were differentially expressed between AβPP/PS1 and wild-type mice. TRF supplementation of these mice altered the expression of 255 proteins in the hippocampus, mPFC, and striatum. TRF also negatively modulated the expression of amyloid beta A4 protein and receptor-type tyrosine-protein phosphatase alpha protein in the hippocampus. The expression of proteins in metabolic pathways, oxidative phosphorylation, and those involved in Alzheimer's disease were altered in the brains of AβPP/PS1 mice that received TRF supplementation.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6839455PMC
http://dx.doi.org/10.3233/JAD-181171DOI Listing

Publication Analysis

Top Keywords

aβpp/ps1 mice
12
hippocampus medial
8
medial prefrontal
8
prefrontal cortex
8
palm oil
8
tocotrienol-rich fraction
8
mpfc striatum
8
trf supplementation
8
trf
6
mice
5

Similar Publications

Background: Fluoroethylnormemantine (FENM), a new Memantine (MEM) derivative, prevented amyloid-β[25-35] peptide (Aβ)-induced neurotoxicity in mice, a pharmacological model of Alzheimer's disease (AD) with high predictive value for drug discovery. Here, as drug infusion is likely to better reflect drug bioavailability due to the interspecies pharmacokinetics variation, we analyzed the efficacy of FENM after chronic subcutaneous (SC) infusion, in comparison with IP injections in two AD mouse models, Aβ-injected mice and the transgenic APP/PSEN1 (APP/PS1) line.

Methods: In Aβ-treated mice, FENM was infused at 0.

View Article and Find Full Text PDF

The etiology and pathogenesis of Alzheimer's disease (AD) are complex, and currently, no comprehensive treatment measures exist. In this study, we initially utilized ultra-high-performance liquid chromatography with quadrupole orbitrap mass spectrometry (UHPLC-QE-MS) to profile the bioactive constituents of SZLOL present in the bloodstream. Subsequent Y-maze experimental data demonstrated that SZLOL could ameliorate short-term memory deficits in APP/PS1 mice.

View Article and Find Full Text PDF

Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by cognitive impairment and distinct neuropathological features, including amyloid-β plaques, neurofibrillary tangles, and reactive astrogliosis. Developing effective diagnostic, preventative, and therapeutic strategies for AD necessitates the establishment of animal models that accurately recapitulate the pathophysiological processes of the disease. Existing transgenic mouse models have significantly contributed to understanding AD pathology but often fail to replicate the complexity of human AD.

View Article and Find Full Text PDF

Pseudogene Lamr1-ps1 Aggravates Early Spatial Learning Memory Deficits in Alzheimer's Disease Model Mice.

Neurosci Bull

January 2025

Department of Pathophysiology, School of Basic Medicine and Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.

Alzheimer's disease (AD), a neurodegenerative disorder with complex etiologies, manifests through a cascade of pathological changes before clinical symptoms become apparent. Among these early changes, alterations in the expression of non-coding RNAs (ncRNAs) have emerged as pivotal events. In this study, we focused on the aberrant expression of ncRNAs and revealed that Lamr1-ps1, a pseudogene of the laminin receptor, significantly exacerbates early spatial learning and memory deficits in APP/PS1 mice.

View Article and Find Full Text PDF

Dietary Methionine Restriction Alleviates Cognitive Impairment in Alzheimer's Disease Mice via Sex-Dependent Modulation on Gut Microbiota and Tryptophan Metabolism: A Multiomics Analysis.

J Agric Food Chem

January 2025

Laboratory of Functional Chemistry and Nutrition of Food, College of Food Science and Engineering, Northwest A&F University, Yangling, Shaanxi 712100, China.

Plant-based foods with low methionine contents have gained increasing interest for their potential health benefits, including neuroprotective effects. Methionine restriction (MR) linked to a plant-based diet has been shown to mitigate neurodegenerative diseases such as Alzheimer's disease (AD) through mechanisms that involve the gut microbiota. In this study, a 16-week MR diet (0.

View Article and Find Full Text PDF

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!