Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1212/WNL.0000000000009569 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
APOE Christchurch enhances a disease-associated microglial response to plaque but suppresses response to tau pathology.
Mol Neurodegener
January 2025
Department of Neurobiology and Behavior, Charlie Dunlop School of Biological Sciences, University of California, Irvine, CA, 92697-4545, USA.
Background: Apolipoprotein E ε4 (APOE4) is the strongest genetic risk factor for late-onset Alzheimer's disease (LOAD). A recent case report identified a rare variant in APOE, APOE3-R136S (Christchurch), proposed to confer resistance to autosomal dominant Alzheimer's Disease (AD). However, it remains unclear whether and how this variant exerts its protective effects.
View Article and Find Full Text PDFProteins Involved in Endothelial Function and Inflammation Are Implicated in Cerebral Small Vessel Disease.
Stroke
January 2025
Stroke Research Group, Department of Clinical Neurosciences, University of Cambridge, United Kingdom. (Z.S., E.L.H., H.S.M.).
Background: Endothelial dysfunction and inflammation have been implicated in the pathophysiology of cerebral small vessel disease (SVD). However, whether they are causal, and if so which components of the pathways represent potential treatment targets, remains uncertain.
Methods: Two-sample Mendelian randomization (MR) was used to test the association between the circulating abundance of 996 proteins involved in endothelial dysfunction and inflammation and SVD.
Atherosclerosis, a slowly progressing inflammatory disease, is characterized by the presence of monocyte-derived macrophages. Interventions targeting the inflammatory characteristics of atherosclerosis hold promising potential. Although interleukin (IL)-10 is widely acknowledged for its anti-inflammatory effects, systemic administration of IL-10 has limitations due to its short half-life and significant systemic side effects.
View Article and Find Full Text PDFTOMM40 may mediate GFAP, neurofilament light Protein, pTau181, and brain morphometry in aging.
Aging Brain
December 2024
University of Kansas Alzheimer's Disease Research Center, University of Kansas Medical Center, Kansas City, KS, 66160, USA.
A growing amount of data has implicated the gene in the risk for Alzheimer's disease (AD), neurodegeneration, and accelerated aging. No studies have investigated the relationship of rs2075650 ('650 on the structural complexity of the brain or plasma markers of neurodegeneration. We used a comprehensive approach to quantify the impact of '650 on brain morphology and multiple cortical attributes in cognitively unimpaired (CU) individuals.
View Article and Find Full Text PDFThe study on cuproptosis in Alzheimer's disease based on the cuproptosis key gene .
Front Aging Neurosci
December 2024
Department of Neurology, The First Affiliated Hospital of University of Science and Technology of China, Hefei, Anhui, China.
Background: Alzheimer's disease (AD) is a neurodegenerative disorder characterized by memory and cognitive impairments. Previous studies have shown neuronal death in the brains of AD patients, but the role of cuproptosis and its associated genes in AD neurons remains unclear.
Methods: Intersection analysis was conducted using the AD transcriptome dataset GSE63060, neuron dataset GSE147528, and reported cuproptosis-related genes to identify the cuproptosis key gene highly expressed in AD.
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!