Publications by authors named "M Traglia"
Article Synopsis
- COVID-19 is linked to serious thrombotic events and neurological symptoms that can persist in long COVID patients, but the mechanisms behind these complications are not well understood and treatment options are limited.
- *Fibrinogen, a key component of blood clots, is found in high amounts in the lungs and brains of COVID-19 patients, where it correlates with the severity of the disease and can predict cognitive issues afterward.
- *Research shows that fibrin interacts with the SARS-CoV-2 spike protein, causing inflammatory blood clots that contribute to complications like inflammation and nerve damage, suggesting that therapies targeting fibrin may be beneficial for treating both acute and long COVID cases.*
Article Synopsis
- * The research showed that individuals with high polygenic risk scores have significantly higher blood pressure (almost 17 mmHg more) and over seven times the risk of developing hypertension compared to those with low scores.
- * Incorporating these genetic risk scores into hypertension prediction models improved their accuracy, and excitingly, similar genetic associations were found in a large African-American sample, underscoring the potential of these findings for precision health initiatives.
Article Synopsis
- Oxygen deprivation and excess are both toxic, making the body's adaptation to oxygen levels crucial for survival.
- The study investigates protein turnover rates in mouse heart, lung, and brain under different oxygen levels, finding that the lung shows the most significant response.
- It highlights that certain extracellular matrix proteins stabilize in the lung during both low (hypoxia) and high (hyperoxia) oxygen, while a component of the electron transport chain becomes unstable in high oxygen, implicating MYBBP1A as a regulator in this context.
Apolipoprotein E4 (APOE4) is the strongest genetic risk factor for late-onset Alzheimer's disease (LOAD), leading to earlier age of clinical onset and exacerbating pathologies. There is a critical need to identify protective targets. Recently, a rare APOE variant, APOE3-R136S (Christchurch), was found to protect against early-onset AD in a PSEN1-E280A carrier.
View Article and Find Full Text PDFApolipoprotein E4 (APOE4) is an important driver of Tau pathology, gliosis, and degeneration in Alzheimer's disease (AD). Still, the mechanisms underlying these APOE4-driven pathological effects remain elusive. Here, we report in a tauopathy mouse model that APOE4 promoted the nucleocytoplasmic translocation and release of high-mobility group box 1 (HMGB1) from hippocampal neurons, which correlated with the severity of hippocampal microgliosis and degeneration.
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