ABeta vaccination has been shown to decrease amyloid plaques in patients with Alzheimer’s disease but has proven to be ineffective in improving cognition. One possible explanation could be that vaccination increases neuroinflammation or worsens tau pathology. In our experiment, we injected the hippocampi of amyloid overproducing transgenic (APP) mice with a virus containing full-length human tau protein. Then mice were injected with either anti-beta-amyloid (ABeta) vaccine or adjuvant as controls. We found that ABeta vaccination did not decrease levels of ABeta or amyloid plaques but did have a protective effect against tau pathology and preserve synapse integrity.
John Canfield, Sefa Arlier, Ezinne Mong, John Lockhart, Jeffrey VanWye, Ozlem Guzeloglu-Kayisli, Frederick Schatz, Charles J. Lockwood, John Tsibris, Umit A. Kayisli, Hana Totary-Jain
Preeclampsia (PE) is a major complication of pregnancy consisting of maternal hypertension and proteinuria, and is the second most common cause of maternal mortality. In PE, shallow trophoblast invasion results in poor placental perfusion, leading to the placenta being exposed to increasingly hypoxic conditions. Here we show that an RNA binding protein, LIN28B, is highly expressed in the placenta, and is downregulated in the placenta of PE pregnancies. Furthermore, LIN28B mRNA and protein levels are decreased by hypoxia. The reduced levels of LIN28B inhibits markers of trophoblast invasion and induces markers of inflammation.
Authors: Jeremy D. Baker, Lindsey B. Shelton, Dali Zheng, Chad A. Dickey, John Koren III, Laura J. Blair
Prolines are amino acids crucial to the structure of many proteins. Prolyl-isomerases (PPIases) regulate proline conformation and in-turn help proteins fold naturally. Most neurodegenerative diseases are associated with pathologically misfolded protein aggregates. Here we show that PPIases regulate aggregation of the protein tau, a protein that aggregates and causes the tangles seen in Alzheimer's disease.
Background: Atherosclerotic cardiovascular disease (ASCVD) remains the number one cause of mortality in the United States. Despite the ability to slow or prevent the development of ACSVD through early detection and intervention, many providers lack knowledge and adherence to clinical practice guidelines (CPG) that utilize a screening tool to provide a numeric risk score. Patients frequently have a vague concept of what their personal ASCVD risk is and how that risk can be addressed. In 2013, the American College of Cardiology (ACC) and the American Heart Association (AHA) jointly published cholesterol guidelines which hinge upon the use of the ACC/AHA ASCVD risk analysis tool to provide a numeric risk score for the initiation of clinician-patient risk discussion (CPRD). Methods: A quality improvement project was implemented in an industrial and corporate worksite wellness clinic system to improve Advanced Practice Registered Nurse (APRN) awareness and utilization of current ASCVD screening guidelines before and after provider-specific education. Patient perceptions before and after risk score analysis were also evaluated. Results: The educational intervention improved APRN guideline utilization and documentation of an ASCVD risk score. The percentage of patient encounters with documented risk scores increased from 1% to 35%. Patient perception of risk was overestimated by 93% of patients and only 23% estimated their risk correctly within 10 points. A significant positive correlation was seen between actual risk score and post-CPRD patient estimate. Conclusion: Increasing APRN awareness and utilization of the AHA/ACC ASCVD risk analysis tool can promote primary prevention of ASCVD. Incorporating the same risk tool within a CPRD can improve the accuracy of patient’s perception of ASCVD risk.
