Metabolic syndrome (MetS) and cognitive dysfunction pose significant challenges to global health and the economy. Systemic inflammation, endocrine disruption, and autoregulatory impairment drive neurodegeneration and microcirculatory damage in MetS. Due to their unique anatomy and function, astrocytes sense and integrate multiple metabolic signals, including peripheral endocrine hormones and nutrients. Astrocytes and synapses engage in a complex dialogue of energetic and immunological interactions. Astrocytes act as a bridge between MetS and cognitive dysfunction, undergoing diverse activation in response to metabolic dysfunction. This article summarizes the alterations in astrocyte phenotypic characteristics across multiple pathological factors in MetS. It also discusses the clinical value of astrocytes as a critical pathologic diagnostic marker and potential therapeutic target for MetS-associated cognitive dysfunction.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11116704 | PMC |
| http://dx.doi.org/10.3389/fendo.2024.1393253 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
The potential of alphapinene as a therapeutic agent for maternal hypoxia-induced cognitive impairments: a study on HO-1 and Nrf2 gene expression in rats.
Metab Brain Dis
January 2025
Department of Biochemistry and Molecular Biology, Faculty of Veterinary Medicine, Shahid Chamran University of Ahvaz, Ahvaz, Iran.
This research seeks to address the gap in past studies by examining the role of the Nrf2 (nuclear factor erythroid 2-related factor 2) and HO-1 (heme oxygenase-1) signaling pathways in hypoxia and the potential effects of alpha-pinene on these factors. Wistar rats were divided into 7 experimental groups (n = 7): 1) control, 2 and 3) groups receiving alpha-pinene 5 and 10 mg/kg (i.p.
View Article and Find Full Text PDFCross-Sectional Comparison of Structural MRI Markers of Impairment in a Diverse Cohort of Older Adults.
Hum Brain Mapp
February 2025
Department of Neurology, Washington University in St. Louis, St. Louis, Missouri, USA.
Neurodegeneration is presumed to be the pathological process measure most proximal to clinical symptom onset in Alzheimer Disease (AD). Structural MRI is routinely collected in research and clinical trial settings. Several quantitative MRI-based measures of atrophy have been proposed, but their low correspondence with each other has been previously documented.
View Article and Find Full Text PDFNutrition: A non-negligible factor in the pathogenesis and treatment of Alzheimer's disease.
Alzheimers Dement
January 2025
Innovation Center for Neurological Disorders and Department of Neurology, Xuanwu Hospital, Capital Medical University, National Clinical Research Center for Geriatric Diseases, Xicheng District, Beijing, China.
Alzheimer's disease (AD) is a degenerative disease characterized by progressive cognitive dysfunction. The strong link between nutrition and the occurrence and progression of AD pathology has been well documented. Poor nutritional status accelerates AD progress by potentially aggravating amyloid beta (Aβ) and tau deposition, exacerbating oxidative stress response, modulating the microbiota-gut-brain axis, and disrupting blood-brain barrier function.
View Article and Find Full Text PDFBackground: Tau protein accumulation is closely linked to synaptic and neuronal loss in Alzheimer's disease (AD), resulting in progressive cognitive decline. Although tau-PET imaging is a direct biomarker of tau pathology, it is costly, carries radiation risks, and is not widely accessible. Resting-state functional MRI (rs-fMRI) complexity-an entropy-based measure of BOLD signal variation-has been proposed as a non-invasive surrogate biomarker of early neuronal dysfunction associated with tau pathology.
View Article and Find Full Text PDFBackground: Radiation therapy (RT) treats primary and metastatic brain tumors, with about one million Americans surviving beyond six months post-treatment. However, up to 90% of survivors experience RT-induced cognitive impairment. Emerging evidence links cognitive decline to RT-induced endothelial dysfunction in brain microvessels, yet studies of endothelial injury remain limited.
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!