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Metoprolol succinate, a commonly prescribed beta blocker for heart failure, can cause underrecognized central nervous system (CNS) effects such as hallucinations, delirium, and sleep disturbances. The likelihood of these effects depends on the drug's lipophilicity. We report a heart failure patient who developed new-onset visual hallucinations after starting metoprolol succinate. Once the association between beta blockers induced hallucinations was recognized, metoprolol was discontinued leading to resolution of symptoms. This case highlights the importance of recognizing this potential adverse effect of beta blocker induced hallucinations, as well as understanding the differences among agents within this drug class.
This project tested a hypothesis for a novel cause of bipolar disorder involving changes in levels of brain cholesterol. Mice were treated daily for 7 days with a vehicle (as a control) or a combination of 2 drugs at two different doses. These treatments were hypothesized to reduce brain cholesterol. At the end of the treatment, mice were tested for signs of depression using the spontaneous activity test, change in body weight and the forced swim test. Final results indicated that the only significant effect of either treatment with either dose was that drug-treated mice gained less weight than controls.
Oxidative stress plays a crucial role in Alzheimer’s disease (AD) pathology. This study explores the potential of targeting the Keap1-Nrf2 pathway as a therapeutic approach. Keap1 negatively regulates Nrf2, a key antioxidant defense mechanism. Using molecular modeling and virtual screening, we identified and modified compounds such as Andrographolide, Farrerol, and Curcumin analogs to enhance their binding affinity to Keap1. By disrupting Keap1-Nrf2 interaction, these compounds could activate Nrf2, reducing oxidative damage and neuroinflammation. Our findings highlight promising drug candidates for AD treatment, with improved binding affinity and potential blood-brain barrier penetration.
