Lifeboat Foundation

Modified protein-design tool could make it easier to tackle challenging drug targets — but AI antibodies are still a long way from reaching the clinic.

Giving cells an appetite for cancer could enhance treatments.

By Kate Graham-Shaw

🦠💊🌍 https://www.news-medical.net/news/20240321/Rising-antimicrob…action.asp

Review delves into the rising challenge of antimicrobial resistance in sexually transmitted infections, underscoring the need for innovative treatments and the critical role of global surveillance in managing diseases like gonorrhea and syphilis.

Researchers from the Broad Institute of MIT and Harvard, along with colleagues from Harvard Medical School and McLean Hospital, have identified remarkably consistent alterations in gene expression within the brains of individuals with schizophrenia and older adults. This discovery points to a shared biological foundation underlying the cognitive difficulties frequently observed in patients with schizophrenia and in aging populations.

In a study published in Nature, the team describes how they analyzed gene expression in more than a million individual cells from postmortem brain tissue from 191 people. They found that in individuals with schizophrenia and in older adults without schizophrenia, two brain cell types called astrocytes and neurons reduced their expression of genes that support the junctions between neurons called synapses, compared to healthy or younger people. They also discovered tightly synchronized gene expression changes in the two cell types: when neurons decreased the expression of certain genes related to synapses, astrocytes similarly changed expression of a distinct set of genes that support synapses.

The team called this coordinated set of changes the Synaptic Neuron and Astrocyte Program (SNAP). Even in healthy, young people, the expression of the SNAP genes always increased or decreased in a coordinated way in their neurons and astrocytes.

Study finds language-processing difficulties are an indicator — more so than memory loss — of amnestic mild cognitive impairment.

Individuals with mild cognitive impairment, especially of the “amnestic subtype” (aMCI), are at increased risk for dementia due to Alzheimer’s disease relative to cognitively healthy older adults. Now, a study co-authored by researchers from MIT, Cornell University, and Massachusetts General Hospital has identified a key deficit in people with aMCI, which relates to producing complex language.

This deficit is independent of the memory deficit that characterizes this group and may provide an additional “cognitive biomarker” to aid in early detection — the time when treatments, as they continue to be developed, are likely to be most effective.

Results of DNA studies also seem to confirm the idea that optimism is an effective tool for slowing down cellular aging, of which telomere shortening is a biomarker. (Telomeres are the protective caps at the end of our chromosomes.) This research is still in progress, but the early results are informative. In 2012, Elizabeth Blackburn, who three years earlier shared a Nobel Prize for her work in discovering the enzyme that replenishes the telomere, and Elissa Epel at the University of California at San Francisco, in collaboration with other institutions, identified a correlation between pessimism and accelerated telomere shortening in a group of postmenopausal women. A pessimistic attitude, they found, may indeed be associated with shorter telomeres. Studies are moving toward larger sample sizes, but it already seems apparent that optimism and pessimism play a significant role in our health as well as in the rate of cellular senescence. More recently, in 2021, Harvard University scientists, in collaboration with Boston University and the Ospedale Maggiore in Milan, Italy, observed the telomeres of 490 elderly men in the Normative Health Study on U.S. veterans. Subjects with strongly pessimistic attitudes were associated with shorter telomeres — a further encouraging finding in the study of those mechanisms that make optimism and pessimism biologically relevant.

Optimism is thought to be genetically determined for only 25 percent of the population. For the rest, it’s the result of our social relationships or deliberate efforts to learn more positive thinking. In an interview with Jane Brody for the New York Times, Rozanski explained that “our way of thinking is habitual, unaware, so the first step is to learn to control ourselves when negative thoughts assail us and commit ourselves to change the way we look at things. We must recognize that our way of thinking is not necessarily the only way of looking at a situation. This thought alone can lower the toxic effect of negativity.” For Rozanski, optimism, like a muscle, can be trained to become stronger through positivity and gratitude, in order to replace an irrational negative thought with a positive and more reasonable one.

While the exact mechanisms remain under investigation, a growing body of research suggests that optimism plays a significant role in promoting both physical and mental well-being. Cultivating a positive outlook, then, can be a powerful tool for fostering resilience, managing stress, and potentially even enhancing longevity. By adopting practices that nurture optimism, we can empower ourselves to navigate life’s challenges with greater strength and live healthier, happier lives.

A novel approach in the field of Alzheimer’s research is emerging that could potentially transform how we tackle this debilitating disease. Recent studies have revealed a paradigm shift in understanding Alzheimer’s pathology, emphasizing the importance of targeting the early-stage aggregation of the pathogenic amyloid beta (A-beta) protein, specifically focusing on its soluble oligomeric form.

Over the past three decades, conventional treatments for Alzheimer’s have largely been ineffective, primarily due to their focus on combating the fibrillar form of A-beta. However, emerging research suggests that it is the soluble oligomeric form of A-beta that poses the greatest threat to neuronal health, leading to cognitive decline and neurotoxicity.

A recent breakthrough in Alzheimer’s treatment has come from the development of an antibody capable of recognizing both oligomeric and fibrillar forms of A-beta, offering newfound hope to the field. This innovative therapy has demonstrated promising results in delaying disease progression by up to 36% in individuals with early-to-mild cognitive impairment.

Researchers report that lipid droplets in brain cells may be a more significant factor in the development of Alzheimer’s disease than previously thought.

Human brains preserve in diverse environments for at least 12 000 years—new research in Proceedings B this week: https://royalsocietypublishing.org/doi/10.1098/rspb.2023.

Soft tissue preservation in the geological record is relatively rare, and when an archaeologist digs a human skull out of the…

The brain is thought to be among the first human organs to decompose after death. The discovery of brains preserved in the archaeological record is therefore regarded as unusual. Although mechanisms such as dehydration, freezing, saponification, and tanning are known to allow for the preservation of the brain on short time scales in association with other soft tissues (≲4000 years), discoveries of older brains, especially in the absence of other soft tissues, are rare. Here, we collated an archive of more than 4,400 human brains preserved in the archaeological record across approximately 12 000 years, more than 1,300 of which constitute the only soft tissue preserved amongst otherwise skeletonized remains. We found that brains of this type persist on time scales exceeding those preserved by other means, which suggests an unknown mechanism may be responsible for preservation particular to the central nervous system. The untapped archive of preserved ancient brains represents an opportunity for bioarchaeological studies of human evolution, health and disease.

Continue reading “Human brains preserve in diverse environments for at least 12 000 years” »