Lifeboat Foundation

Researchers at the RIKEN Center for Brain Science (CBS) in Japan have discovered a set of related mutations that lead to intracranial aneurysms—weakened blood vessels in the brain that can burst at any time. The mutations all appear to act on the same biological signaling pathway, and the researchers report the first ever pharmaceutical treatment in a mouse model, which works by blocking this signal. The study was published in Science Translational Medicine.

About 5% of the population have unruptured intracranial aneurysms in blood vessels on the surface of the brain. Despite being ballooned arteries with weakened walls, intracranial aneurysms often go undetected—until a rupture leads to deadly bleeding around the brain.

Even when they are detected in advance, the only currently available treatment options involve surgery, which has its own set of risks, especially if the aneurysm is in a sensitive location. Finding other, non-surgical options is thus a high priority, and research into the origin of intracranial aneurysms has led the RIKEN CBS team to one such potential treatment.

Mitochondria that power cellular activity fragment and change shape in breast cancer cells that migrate to the brain, an adaptation that appears necessary for the cells to survive, UT Southwestern Medical Center researchers report in a new study. The findings, published in Nature Cancer, could lead to new ways to prevent brain metastases, or the spread of cells from primary tumors to the brain.

“Through mitochondrial plasticity, these cancer cells undergo metabolic reprogramming that aids their survival in the brain niche that otherwise would not be available to them. Exploiting this vulnerability could offer a way to prevent brain metastases,” said study leader Srinivas Malladi, Ph.D., Assistant Professor of Pathology at UT Southwestern and a member of the Harold C. Simmons Comprehensive Cancer Center.

Metastatic cancer, which is treated as stage IV cancer, is responsible for the majority of cancer deaths.

A team of researchers in the United States and United Kingdom say they have created the world’s first synthetic human embryo-like structures from stem cells, bypassing the need for eggs and sperm.

These embryo-like structures are at the very earliest stages of human development: They don’t have a beating heart or a brain, for example. But scientists say they could one day help advance the understanding of genetic diseases or the causes of miscarriages.

The research raises critical legal and ethical questions, and many countries, including the US, don’t have laws governing the creation or treatment of synthetic embryos.

Scientists have created one of the most detailed 3D images of the synapse, the important juncture where neurons communicate with each other through an exchange of chemical signals. These nanometer-scale models will help scientists better understand and study neurodegenerative diseases such as Huntington’s disease and schizophrenia.

The new study appears in the journal PNAS and was authored by a team led by Steve Goldman, MD, Ph.D., co-director of the Center for Translational Neuromedicine at the University of Rochester and the University of Copenhagen. The findings represent a significant technical achievement that allows researchers to study the different cells that converge at individual synapses at a level of detail not previously achievable.

“It is one thing to understand the structure of the synapse from the literature, but it is another to see the precise geometry of interactions between individual cells with your own eyes,” said Abdellatif Benraiss, Ph.D., a research associate professor in the Center for Translational Neuromedicine and co-author of the study. “The ability to measure these extremely small environments is a young field, and holds the potential to advance our understanding of a number of neurodegenerative and neuropsychiatric diseases in which synaptic function is disturbed.”

People in the earliest stage of Alzheimer’s disease—after brain changes have begun but before cognitive symptoms become apparent—harbor an assortment of bacteria in their intestines that differs from the gut bacteria of healthy people, according to a study by researchers at Washington University School of Medicine in St. Louis.

The findings, published June 14 in Science Translational Medicine, open up the possibility of analyzing the gut bacterial community to identify people at higher risk of developing dementia, and of designing microbiome-altering preventive treatments to stave off cognitive decline.

“We don’t yet know whether the gut is influencing the brain or the brain is influencing the gut, but this association is valuable to know in either case,” said co-corresponding author Gautam Dantas, Ph.D., the Conan Professor of Laboratory and Genomic Medicine. “It could be that the changes in the gut microbiome are just a readout of pathological changes in the brain. The other alternative is that the gut microbiome is contributing to Alzheimer’s disease, in which case altering the gut microbiome with probiotics or fecal transfers might help change the course of the disease.”

The team, led by Professor Magdalena Zernicka-Goetz, developed the embryo model without eggs or sperm, and instead used stem cells – the body’s master cells, which can develop into almost any cell type in the body.

The researchers mimicked natural processes in the lab by guiding the three types of stem cells found in early mammalian development to the point where they start interacting. By inducing the expression of a particular set of genes and establishing a unique environment for their interactions, the researchers were able to get the stem cells to ‘talk’ to each other.

Researchers have created model embryos from mouse stem cells that form a brain, a beating heart, and the foundations of all the other organs of the body.

Summary: Researchers developed one of the most comprehensive 3D models of the synapse, the neuron juncture crucial for intercellular communication. This breakthrough allows an unprecedented view of the complex interactions between individual cells at the synapse, offering fresh insights into neurodegenerative diseases such as Huntington’s disease and schizophrenia.

The team used this novel approach to compare healthy mice brains to those with the Huntington’s mutant gene, revealing structural flaws potentially disrupting cellular communication. The researchers believe this technique could significantly advance our understanding of various neurodegenerative and neuropsychiatric diseases.

The aim of non-pharmacologic interventions for brain health is to preserve cognitive function and safeguard brain structure. This review explores various diets (MeDi, DASH, MIND, ketogenic), exercise approaches (endurance, resistance, yoga, HIIT), and highlights the need for further research to uncover the underlying mechanisms.

As people get older, they tend to have lower levels of anxiety. But why? A new brain imaging study has found that older individuals are faster at recognizing and responding to negative emotions. The findings, published NeuroImage, go against the idea that older adults are less engaged with negative emotions due to cognitive decline or that they are better at regulating negative emotions. Instead, the results suggest that older adults may develop a more automatic way of processing negative emotions.

The study aimed to investigate the relationship between aging, trait anxiety, and changes in cognitive and affective functions. The researchers were motivated by previous findings that older adults tend to have lower susceptibility to anxiety disorders compared to younger and middle-aged adults. However, it was not clear how age-related changes in anxiety symptoms, such as worry and somatic symptoms, were related to changes in cognitive and affective processes.

“We are interested in emotion dysfunction in early dementia, including those people with subjective complaints of memory problem and mild cognitive impairment,” said study author Chiang-shan Ray Li, a professor of psychiatry and neuroscience at Yale University School of Medicine.