DEA is used in industrial, agricultural, and consumer products.
“We knew that micropollutants can be incorporated into fatty molecules in the body, but we didn’t know how this occurs or what happens next,” Clardy said. “DEA’s metabolism into an immune signal was completely unexpected.”
The team proposes that DEA could be added to the growing list of biomarkers used to detect some cases of major depressive disorder.
Summary: New research reveals that brain cells use a muscle-like signaling mechanism to relay information over long distances. Scientists discovered that dendrites, the branch-like extensions of neurons, contain a structured network of contact sites that amplify calcium signals—similar to how muscles contract. These contact sites regulate calcium release, activating key proteins involved in learning and memory.
This mechanism explains how neurons process information received at specific points and relay it to the cell body. Understanding this process sheds light on synaptic plasticity, which underlies learning and memory formation. The findings could provide new insights into neurodegenerative diseases like Alzheimer’s.
Nerve cells have amazing strategies to save energy and still perform the most important of their tasks. Researchers from the University Hospital Bonn (UKB) and the University of Bonn as well as the University Medical Center Göttingen found that the neuronal energy conservation program determines the location and number of messenger RNA (mRNA) and proteins and differs depending on the length, longevity and other properties of the respective molecule. The work has now been published in Nature Communications.
We have all experienced the need to save energy in recent years. To do this, we all had to come up with strategies to save energy while still meeting our most important needs.
Our nerve cells are facing a similar dilemma: They have to supply their synapses, i.e., their contact points with other neurons, but also organize their protein synthesis in such a way that they don’t produce too much or too little proteins.
Many describe this as the experience of seeing their life ‘flash before their eyes.’
The recording was made when an 87-year-old patient underwent cardiac arrest while being treated for epilepsy.
Doctors had strapped a device on his head to monitor brain activity, but the man died during the process.
Two hundred million years ago, our mammal ancestors developed a new brain feature: the neocortex. This stamp-sized piece of tissue (wrapped around a brain the size of a walnut) is the key to what humanity has become. Now, futurist Ray Kurzweil suggests, we should get ready for the next big leap in brain power, as we tap into the computing power in the cloud.
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Xenon gas inhalation reduced neurodegeneration and boosted protection in preclinical models of Alzheimer’s disease. Most treatments being pursued today to protect against Alzheimer’s disease focus on amyloid plaques and tau tangles that accumulate in the brain, but new research from Mass General Brigham and Washington University School of Medicine in St. Louis points to a novel — and noble — approach: using Xenon gas. The study found that Xenon gas inhalation suppressed neuroinflammation, reduced brain atrophy, and increased protective neuronal states in mouse models of Alzheimer’s disease. Results are published in Science Translational Medicine, and a phase 1 clinical trial of the treatment in healthy volunteers will begin in early 2025.
“It is a very novel discovery showing that simply inhaling an inert gas can have such a profound neuroprotective effect,” said senior and co-corresponding author Oleg Butovsky, PhD, of the Ann Romney Center for Neurologic Diseases at Brigham and Women’s Hospital (BWH), a founding member of the Mass General Brigham healthcare system. “One of the main limitations in the field of Alzheimer’s disease research and treatment is that it is extremely difficult to design medications that can pass the blood-brain barrier — but Xenon gas does. We look forward to seeing this novel approach tested in humans.”
“It is exciting that in both animal models that model different aspects of Alzheimer’s disease, amyloid pathology in one model and tau pathology in another model, that Xenon had protective effects in both situations,” said senior and co-corresponding author David M. Holtzman, MD, from Washington University School of Medicine in St. Louis.
Weill Cornell Medicine investigators have identified in a preclinical model a specific brain circuit whose inhibition appears to reduce anxiety without side effects. Their work suggests a new target for treating anxiety disorders and related conditions and demonstrates a general strategy, based on a method called photopharmacology, for mapping drug effects on the brain.
In their study, published Jan. 28 in Neuron, the researchers examined the effects of experimental drug compounds that activate a type of brain-cell receptor called the metabotropic glutamate receptor 2 (mGluR2). While these receptors are found on neurons within many brain circuits, the team showed that activating them in a specific circuit terminating in an emotion-related brain region called the amygdala reduces signs of anxiety without apparent adverse side effects. Current treatments for anxiety disorders, panic disorder and associated conditions can have unwanted side effects including cognitive impairments.
“Our findings indicate a new and important target for the treatment of anxiety-related disorders and show that our photopharmacology-based approach holds promise more broadly as a way to precisely reverse-engineer how therapeutics work in the brain,” said study senior author Dr. Joshua Levitz, an associate professor of biochemistry at Weill Cornell Medicine.
Researchers at the Ernst Strüngmann Institute in Frankfurt am Main, Germany, led by Wolf Singer, have made a new discovery in understanding fundamental brain processes. For the first time, the team has provided compelling evidence that the brain’s characteristic rhythmic patterns play a crucial role in information processing. While these oscillatory dynamics have long been observed in the brain, their purpose has remained mostly elusive until now.
The study has the potential to transform our understanding of brain activity. Using computer simulations, the researchers show that recurrent networks with oscillating nodes demonstrate better performance compared to non-oscillating networks and replicate many experimentally observed phenomena.
These findings indicate that oscillatory dynamics are not just an epiphenomenon but are essential for efficient computation in the brain. The work is published in the journal Proceedings of the National Academy of Sciences.
Researchers at the Sainsbury Wellcome Center (SWC) at UCL have unveiled the precise brain mechanisms that enable animals to overcome instinctive fears. Published in Science, the study in mice could have implications for developing therapeutics for fear-related disorders such as phobias, anxiety and post-traumatic stress disorder (PTSD).
The research team, led by Dr. Sara Mederos and Professor Sonja Hofer, mapped out how the brain learns to suppress responses to perceived threats that prove harmless over time.
“Humans are born with instinctive fear reactions, such as responses to loud noises or fast-approaching objects,” explains Dr. Mederos, Research Fellow in the Hofer Lab at SWC.
