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Mechanism of Sirtuin1-Mediated Deacetylation of p65-Mediated Ferroptosis of Hippocampal Neurons in Cerebral Injury after Cardiopulmonary Resuscitation in Rats.
Neurochem Res
January 2025
Department of Radiology, the Second Affiliated Hospital of Kunming Medical University, No.374 Yunnan-Burma Road, Wuhua District, Kunming, Yunnan, 650101, PR China.
Objective: Post-resuscitation brain injury is a common sequela after cardiac arrest (CA). Increasing sirtuin1 (SIRT1) has been involved in neuroprotection in oxygen-glucose deprivation (OGD) neurons, and we investigated its mechanism in post-cardiopulmonary resuscitation (CPR) rat brain injury by mediating p65 deacetylation modification to mediate hippocampal neuronal ferroptosis.
Methods: Sprague-Dawley rat CA/CPR model was established and treated with Ad-SIRT1 and Ad-GFP adenovirus vectors, or Erastin.
Basic Science and Pathogenesis.
Alzheimers Dement
December 2024
the University of Texas at Austin, Austin, TX, USA.
Background: Imbalanced Fe levels can lead to oxidative stress and initiate ferroptosis, an Fe-dependent cell death that involves lipid peroxidation and can lead to neuron cell loss in neurodegenerative diseases including Alzheimer's disease (AD). While the Fe/Fe ratio has been identified as the primary determining factor for lipid peroxidation, the role of Fe redox equilibrium and dynamic in AD is not well understood, due to limited tools for visualizing Fe and Fe simultaneously. To overcome this limitation, we recently reported DNAzyme-based sensors for simultaneous imaging of Fe and Fe.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
Florey Institute of Neuroscience and Mental Health, University of Melbourne, Parkville, VIC, Australia.
Background: A better understanding of the molecular process that drive Alzheimer's disease(AD) are required to develop effective biomarkers and therapies. This includes determining how essential elements like Fe, Cu and Zn are involved in the disease. In the literature there is debate over the role of iron in AD and there are reports of increased, decreased and unchanged levels of Fe in AD brain.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
University of Newcastle, Callaghan, NSW, Australia.
Background: UK Biobank data show mutations related to the iron disorder hemochromatosis can approximately double the risk of dementia, in particular clinically diagnosed vascular dementia. Insights into the etiology of this dementia may be provided by cerebrovasculopathy in our new "Aβ+Iron" mouse model, which combines hemochromatosis-related mutations and amyloidosis, with increases in soluble Aβ species and plaques. This was created by crossing an established APP/PS1 model of β-amyloidosis with our reported HfexTfr2 model of hemochromatosis-related mutations exhibiting brain iron dyshomeostasis (Heidari Mol.
View Article and Find Full Text PDFProgressive iron overload in middle-aged mice impairs olfactory function, triggers lipid oxidation and induces apoptosis.
Front Pharmacol
December 2024
Laboratory of Experimental Animal Disease Model, College of Veterinary Medicine, Sichuan Agricultural University, Chengdu, China.
Introduction: This study aims to investigate the progressive impact of chronic iron overload on the olfactory bulb, a region significantly affected in early neurodegenerative diseases like Parkinson's and Alzheimer's. The focus is on understanding how iron accumulation leads to oxidative stress, mitochondrial dysfunction, and neuronal damage over time in middle-aged mice.
Method: The mice were continuously administered FC for a duration of 16 weeks, and the olfactory behavior of the mice was observed at intervals of 4 weeks.
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