Lifeboat Foundation

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.

In my new Newsweek Op-Ed, I tackle a primary issue many people have with trying to stop aging and death via science. Hopefully this philosophical argument will allow more resources & support into the life extension field:

Philosophers often say if humans didn’t die, we’d be bored out of our minds. This idea, called temporal scarcity, argues the finitude of death is what makes life worth living. Transhumanists, whose most urgent goal is to use science to overcome biological death, emphatically disagree.

For decades, the question of temporal scarcity has been debated and analyzed in essays and books. But an original idea transhumanists are putting forth is reinvigorating the debate. It doesn’t discount temporal scarcity in biological humans; it discounts it in what humans will likely become in the future—cyborgs and digitized consciousnesses.

Continue reading “Eliminating Death Doesn’t Mean Life Will Get Boring” »

Summary: Researchers discovered a unique property of psychedelic drugs: their ability to reopen “critical periods” in the brain, times when the brain is highly susceptible to environmental learning signals. These periods, usually associated with skills development like language learning, are reopened by psychedelics for different lengths of time.

This breakthrough in understanding psychedelic drug function may have therapeutic implications for conditions like stroke and deafness. Further, it uncovers novel molecular mechanisms influenced by psychedelics.

Summary: Researchers leveraged a tracking algorithm from video games to study molecules’ behavior within live brain cells.

They adapted the fast and accurate algorithm used to track bullets in combat games for use in super-resolution microscopy. The innovative approach enables scientists to observe how molecules cluster together to perform specific functions in space and time within the brain cells.

The data obtained could shed light on molecular functions’ disruption during aging and disease.

Researchers at Scripps Research have discovered that chronic alcohol consumption can increase sensitivity to pain through two distinct molecular mechanisms: one related to alcohol intake and the other to alcohol withdrawal. This finding, published in the British Journal of Pharmacology, sheds light on the intricate relationship between alcohol and pain.

The researchers sought to better understand the relationship between chronic pain and alcohol use disorder. They wanted to investigate the underlying causes of different types of alcohol-related pain, such as alcoholic neuropathy and allodynia, and how they develop at the spinal cord level. The researchers aimed to examine the role of microglia, immune cells in the central nervous system, in the development of chronic alcohol-induced allodynia and neuropathy.

Alcoholic neuropathy refers to nerve damage caused by long-term excessive alcohol consumption. It is a type of peripheral neuropathy that affects the peripheral nerves, which are responsible for transmitting signals between the brain, spinal cord, and the rest of the body.