ASA Monitor October 2023, Vol. 87, 12–13.
New synthetic antibiotic compound
Gram-negative bacteria such as Salmonella and E. coli are responsible for many harmful infections such as UTIs, pneumonia, and bloodstream infections. Unfortunately, gram-negative bacteria are resistant to most available antibiotic drugs and continue to grow increasingly resistant to available treatments. A decades-long project at Duke University is combatting gram-negative bacteria with a newly developed compound called LPC-233. The compound works by inhibiting the bacteria’s ability to form its outer lipid layer, which is crucial to its survival. Thus far, it has been tested on 285 bacteria strains, including many highly resistant to current treatments, and has destroyed all of their outer membranes. Pei Zhou, a professor of biochemistry at the Duke School of Medicine, emphasized how fast the treatment works. “LPC-233 can reduce bacterial viability by 100,000-fold within four hours,” Zhou said. The search for this compound was started by the late Duke Biochemistry Chair Christian Raetz in the 1980s. Raetz identified an enzyme called LpxC as a pathway for the development of the outer membrane lipid in gram-negative bacteria. Raetz devoted much of his career to targeting the enzyme pathway and recruited Zhou to help him in 2001. Early versions of the compound could not move on to human trials because of cardiovascular toxicity.
Source: asamonitor.pub/3DOX2HZ
Stem cell transplants offer promise in treating Alzheimer’s
Nearly 6 million Americans struggle with Alzheimer’s, and that number is projected to more than double by 2060. Alzheimer’s is the most common form of dementia and treatment options are few. Currently, treatment options solely manage and attempt to delay symptoms. However, scientists at the University of California, San Diego, have recently shown that stem cell transplants could be a promising option in the future. The researchers transplanted hematopoietic stem and progenitor cells into mice that had a mouse-model of Alzheimer’s disease. The result was mice that showed preserved levels of memory and cognition. Neuroinflammation was also reduced in the mice that received the stem cell treatments. Neuroinflammation is a major indicator and cause of Alzheimer’s disease, which is what this treatment ultimately targets. In Alzheimer’s, microglia, an immune cell in the brain, releases several inflammatories. Under normal conditions, it will also help the brain reach an equilibrium afterward by clearing out β-amyloid plaques. However, Alzheimer’s impairs the microglia’s ability to equilibrate, leaving microglia in prolonged states of inflammation. The scientists were able to improve microglia health by transplanting hematopoietic stem and progenitor cells. In mice, this treatment was effective at stopping mice from progressing any further into Alzheimer’s but was not able to reverse any symptoms. Options like this offer promise, but highlight the need to spot and treat Alzheimer’s as early as possible.
Source: asamonitor.pub/4556rXW
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