Publications by authors named "W Balduini"
Article Synopsis
- Mitochondrial dysfunction plays a critical role in diseases like neurodegeneration, especially during events like oxygen-glucose deprivation followed by reoxygenation.
- In a study on HT22 cells, melatonin was found to protect mitochondria from damage and oxidative stress caused by this OGD/R condition, maintaining important enzymatic functions.
- Melatonin not only lowered inflammatory markers related to mitochondrial damage but also enhanced the release of fibroblast growth factor-21, suggesting its potential as a protective agent in ischemic brain injury.
The Notch1 signaling pathway plays a crucial role in the development of the central nervous system, governing pivotal functional activities in the brain, such as neurogenesis. Sirt3 is instrumental in managing mitochondrial homeostasis and is essential to cell survival. Dysregulation of these signaling pathways is implicated in the pathogenesis of a wide range of diseases, including neurodegenerative disorders such as stroke.
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- Therapeutic hypothermia (TH) is now a standard treatment to reduce brain damage in newborns with hypoxic-ischaemic encephalopathy (HIE), but many still face high rates of death and disabilities.
- CHF6467 is a modified form of nerve growth factor (NGF) that does not cause pain and has shown protective effects on neurons in rodent models when used with hypothermia.
- This study suggests that combining intranasal administration of CHF6467 with TH significantly reduces brain damage and improves motor and memory function in neonatal HIE, making it a promising treatment option.
Mitochondria functionally degrade as neurons age. Degenerative changes cause inefficient oxidative phosphorylation (OXPHOS) and elevated electron leakage from the electron transport chain (ETC) promoting increased intramitochondrial generation of damaging reactive oxygen and reactive nitrogen species (ROS and RNS). The associated progressive accumulation of molecular damage causes an increasingly rapid decline in mitochondrial physiology contributing to aging.
View Article and Find Full Text PDFPromoting neural cell proliferation may represent an important strategy for enhancing brain repair after developmental brain injury. The present study aimed to assess the effects of melatonin on cell proliferation after an ischemic injury in the developing hippocampus, focusing on cell cycle dynamics. After in vivo neonatal hypoxia-ischemia (HI), hippocampal cell cycle dynamics were assessed by flow cytometry, together with histological evaluation of dentate gyrus cellularity and proliferation.
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