Lifeboat Foundation

Psychoses like schizophrenia cost billions of dollars annually and derail the lives of people struggling with the disease. Now Monash University researchers have modeled how the effects of psychosis spread through the brain, allowing them to isolate areas where these changes may originate from and which could be targeted by therapies designed to reduce the disease’s progression.

Scientists have revealed the molecular structure of a type of receptor that’s crucial to brain development and function.

Known as Type A GABA receptors, these receptors are already targeted by pharmaceutical anesthetics, sedatives and antidepressants because of their important role in brain function. The discovery, published today in the journal Nature, reveals the dominant assemblies and states of the GABA receptor, a finding that could enable the development of new compounds that more specifically target a range of medical disorders.

“It is the main player that balances excitation and inhibition in the brain,” said lead author Chang Sun, Ph.D., a postdoctoral researcher in the Vollum Institute at Oregon Health & Science University. “It affects all aspects of brain function, from motor function, to memory and learning, and also emotion and anxiety.”

New research from the University of Missouri School of Medicine suggests there may be another way to treat cigarette cravings. Researchers found that theta-burst transcranial magnetic stimulation (TBS)—strong, rapidly fluctuating magnetic field pulses that can affect brain activity—can lead to improved self-control, reduced cravings and as a result, less smoking.

People with nicotine dependence tend to have significant structural and functional differences in the brain, compared to healthy non-smokers. Smoking cigarettes has been shown to be associated with less gray matter, which means they have less neurons and other cells in the brain.

Research suggests these differences may affect inhibitory control (IC), which is our control over automatic urges and response to stimuli—what enables humans to stop an impulsive reaction to something.

The opioid epidemic in the United States has exacted an incalculable toll on individuals and communities, creating an urgent need for alternative painkillers. The search for non-opioid treatments is crucial, not only to mitigate the risks of addiction and overdose, but also to develop pain management tools that remain effective without inducing tolerance and other challenging side effects in patients.

New research from the University of Chicago identified an alternative signaling pathway in the brain of mice that relieves pain, even in animals that have developed tolerance to opioids.

The study, titled “A Cholinergic Circuit That Relieves Pain, Despite Opioid Tolerance” and published in Neuron, also showed that pain relief through this route did not induce tolerance, did not create withdrawals symptoms after treatment was stopped, and did not activate reward systems, limiting risk for addiction and making it a viable path to developing effective, non-opioid pain relief.

You’re looking at a truck. You’re with a young child and he follows your gaze. He’s interested in the object you’re looking at without you pointing at it. This is called joint attention and it is one of the primary ways children learn to connect words with objects and acquire language.

Lack of joint attention is a core feature of autism. Until now, it was thought that stimulating joint attention in people with autism would help them express themselves verbally. But a meta-analysis of 71 studies on autism challenges this assumption and suggests that people with autism spectrum disorders may acquire language differently.

The study—by Laurent Mottron, a professor in the Department of Psychiatry and Addiction at Université de Montréal and a psychiatrist at the Hôpital en santé mentale Rivière-des-Prairies of the CIUSSS du Nord-de-l’Île-de-Montréal; Mikhail Kissine, a professor of linguistics at Université Libre de Bruxelles; and Ariane St-Denis, a medical student at McGill University—is published in Neuroscience & Biobehavioral Reviews.

“We’re all familiar with the Freudian idea that if we suppress our feelings or thoughts, then these thoughts remain in our unconscious, influencing our behaviour and wellbeing perniciously,” said Anderson. “The whole point of psychotherapy is to dredge up these thoughts so one can deal with them and rob them of their power.” It had become dogma in clinical psychology that efforts to banish thoughts or memories of a particular subject were counterproductive and made people think more about them, he said. “We challenge the view that thought suppression worsens mental illness.” https://www.ft.com/content/5495b3ee-6c08-4d89-a614-c0acb83aa9a6

The commonly-held belief that attempting to suppress negative thoughts is bad for our mental health could be wrong, a new study from scientists at the University of Cambridge suggests.

Elon Musk’s brain-implant startup, Neuralink, said it has received approval from an independent review board to begin recruiting patients for its first human trial. The company is seeking people with paralysis to test its experimental device in a six-year study.

Microglial cells are the maintenance workers of the central nervous system (CNS), protecting against pathogens and pruning damaged neurons to help the brain maintain homeostasis. Considered immune cells, microglia work to protect the brain from before it is fully formed through its lifetime, but they aren’t infallible. The cells can be primed early on to respond in certain ways, making the microglia’s clean-up efforts less efficient. As other cells age, they can complicate microglial function, making them less effective.

But the underlying mechanism of how microglial cells age and how their aging directly affects the brain is poorly understood—meaning that attempts to prevent or treat brain dysfunction may not be as effective as they could be, according to a multi-institutional collaboration led by Bo Peng and Yanxia Rao, both professors at Fudan University.

The team investigated how microglial cells change as they age in both male and female mice across their lifespans, finding what the researchers called “unexpected sex differences.” They also established a model to study aged microglial cells in a non-aged brain, revealing that aged-like microglia contribute to cognitive decline even in young mice. The researchers published their findings in Nature Aging.

Scientists established an epigenetic mouse model for glioma, providing insight into how epigenetics can initiate cancer.