In this large cohort study, carotid plaque status at baseline was independently associated with in cognitive function decline, especially in nonverbal memory and executive functioning over 8-year follow-up period in the general population.
This website uses a security service to protect against malicious bots. This page is displayed while the website verifies you are not a bot.
The brain is equally divided into grey and white matter. Grey matter contains the brain’s processing hubs, linked by an information highway — the white matter. Although white matter damage is a defining feature of multiple sclerosis and is also seen in neurodegeneration including Alzheimer’s and Parkinson’s disease, the consequences of white matter damage are not well understood.
The team created localised damage to myelin – the main component of white matter – in a well-defined brain circuit and followed what happened over time. They found that small, localised myelin damage triggered a striking response in a connected, remote grey matter region. Neuronal activity fell, microglia – the brain’s immune cells – became activated, and connections between neurons were lost.
Crucially, these changes were not permanent. After myelin was regenerated, neuronal activity recovered, connections between neurons returned, and the inflammatory response subsided.
The study also challenges a common assumption about brain inflammation. Grey matter inflammation is traditionally viewed as harmful. But here, the team found that this transient response was part of the repair process itself. When they prevented grey matter inflammation, myelin regeneration was impaired.
Conversely, when the team blocked myelin regeneration, the grey matter response did not resolve and instead became chronic. This suggests that failed myelin regeneration may help drive the persistent low-grade inflammation seen in neurodegenerative disease. ScienceMission sciencenewshighlights.
Damage to white matter in the brain can trigger features associated with neurodegenerative disease, The researchers have discovered in a new study published in the journal Nature.
NASA-funded scientists have discovered that life on Earth over 3 billion years ago relied on the metal molybdenum, which was incredibly scarce in the environment at the time. The study, published in Nature Communications on Tuesday, is the first to show that molybdenum was used by ancient life this far back in our planet’s history.
On Earth today, molybdenum helps speed up vital biochemical reactions in cells. The metal is a component of essential enzymes that drive several major biological reactions in organisms. This is not only important for the individual organisms, but also biogeochemical cycles, such as the nitrogen cycle, which affect our entire planet. Without molybdenum, those important reactions could still happen in nature, but they would be too slow to sustain life.
“Molybdenum sits at the catalytic center of enzymes that run major carbon, nitrogen, and sulfur reactions,” explained Betül Kaçar, head of the Kaçar Lab at the University of Wisconsin-Madison and senior author on the study. Kaçar leads MUSE, a NASA Interdisciplinary Consortia for Astrobiology Research (ICAR) at UW-Madison.
Noradrenergic innervation and β-cell dedifferentiation in diabetes.
Dedifferentiation, a survival mechanism whereby mature β-cells revert to a nonfunctional state under metabolic stress, represents a fundamental driver of β-cell failure in type 2 diabetes.
Dedifferentiation is reversible, primarily through dietary intervention or bariatric surgery, and redifferentiation may promote type 2 diabetes remission.
Noradrenergic fiber density is increased in diabetic pancreases and correlates with β-cell dedifferentiation, suggesting that altered signaling may trigger the process.
A link between diet, redifferentiation, reduction of noradrenergic fibers, and type 2 diabetes remission has been hypothesized.
The review proposes that targeting pancreatic noradrenergic innervation could be a novel therapeutic strategy to reverse β-cell dedifferentiation, restore insulin function, and achieve type 2 diabetes remission. sciencenewshighlights ScienceMission https://sciencemission.com/noradrenergic-innervation–in-diabetes
University of Birmingham research published today has shown a new low-temperature method for producing hydrogen that is suitable for both centralized hydrogen production, and also local generation using waste heat from large-scale industrial plants.
Hydrogen is the most abundant element in the universe and is a clean and environmentally friendly energy carrier. Unlike fossil fuels, which produce harmful emissions and carbon dioxide, it produces only heat and water on combustion and can also power fuel cells that produce electricity. But while hydrogen is carbon-free at the point of use, 95% of current production relies on fossil fuels.
Thermochemical splitting, where a catalyst splits water into hydrogen and oxygen, is emerging as a promising method for hydrogen production. However, current catalysts split water at 700‑1000oC and need temperatures between 1,300 and 1500oC to regenerate between cycles of water-splitting.
JUST PUBLISHED:Click here to read the latest free, Open Access article from BMEF.
The transcription factor Nrf2 orchestrates cellular defenses against redox imbalance and lipid peroxidation, partly through regulating the expression of 2 key gatekeepers of ferroptosis: SLC7A11 and GPX4 [44]. As such, the Keap1/Nrf2 pathway is recognized as a master regulator of ferroptosis in osteoblasts [45]. Under stress conditions, Nrf2 dissociates from the Keap1–Nrf2 complex, translocates into the nucleus, and initiates the transcription of genes containing antioxidant response elements [46]. Previous studies have reported that Nrf2 activation protects osteoblasts from ferroptosis in bone tissue and alleviates osteoporosis [28,47]. Consistently, we observed that under iron overload conditions, baicalein restored nuclear Nrf2 levels and the expression of downstream targets GPX4 and SLC7A11. Both genetic and pharmacological inhibition of Nrf2 abolished the cytoprotective and pro-osteogenic effects of baicalein. These findings suggest that baicalein prevents ferroptosis in osteoblasts via activation of the Nrf2/GPX4 pathway.
Clinically, iron overload conditions, such as transfusion-induced iron overload in thalassemia and hereditary hemochromatosis, are strongly associated with low bone mass and increased fracture risk [48,49]. Current treatment options (e.g., iron chelators, phlebotomy, and anti-resorptive agents) fail to simultaneously address iron overload and bone damage. Baicalein has undergone human safety and pharmacokinetic studies, which indicate no significant side effects even at high doses [50,51]. Our study demonstrates that baicalein not only prevents bone loss by protecting osteoblasts from ferroptosis but also effectively reduces systemic iron storage. Although beyond the scope of this work, baicalein’s known anti-osteoclastogenic effects may synergistically contribute to its overall bone-protective actions in iron overload conditions. These findings suggest that baicalein is a promising therapeutic agent for iron overload-related bone disorders. Although clinical trials are warranted, the dose of baicalein used in our study was extrapolated from clinically tolerated doses in humans, thereby supporting the potential feasibility of its clinical application.
In summary, this study provides the first definitive evidence that baicalein effectively inhibits iron overload-induced ferroptosis in osteoblasts by activating the Nrf2/GPX4 signaling pathway, thereby promoting bone formation and preventing bone loss. Our findings not only elucidate the mechanism by which baicalein functions as a novel ferroptosis inhibitor in bone protection but also highlight its role as a “dual-function” therapeutic strategy—combining iron chelation and anti-bone-loss capacities. Given its favorable safety profile and existing human pharmacokinetic data, our results provide strong preclinical evidence supporting the clinical translation of baicalein for the treatment of iron overload-related bone diseases. Targeting the ferroptosis pathway, particularly via Nrf2/GPX4 activation by baicalein, represents a highly promising novel strategy for preventing and treating iron overload-induced bone loss.
