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Researchers have identified two ion channel switches that regulate the release of dopamine in the brain, a first step that might one day lead to therapeutics for a wide range of diseases and disorders that currently have few solutions.

The switches help regulate learning and motivational state in mice. Humans also have hundreds of these channels, which govern many chemical and hormonal processes that influence behavior and mood. The University of Washington School of Medicine research team hopes to identify drugs to target these channels. Those drug candidates could then be tested in clinical trials.

“The ability to precisely manipulate how dopamine-producing neurons of the brain regulate different behaviors is a major step toward developing better therapies for a range of mental illnesses,” said Larry Zweifel, professor of psychiatry & behavioral sciences at the UW School of Medicine.

The findings were published Aug. 10 in the journal Nature Neuroscience.

“It’s amazing that children with the same symptoms end up with two distinct forms of altered neural networks,” said Dr. Flora Vaccarino, the Harris Professor in the Child Study Center at Yale School of Medicine and co-senior author of the paper.


Two distinct neurodevelopmental abnormalities that arise just weeks after the start of brain development have been associated with the emergence of autism spectrum disorder, according to a new Yale-led study in which researchers developed brain organoids from the stem cells of boys diagnosed with the disorder.

And, researchers say, the specific abnormalities seem to be dictated by the size of the child’s brain, a finding that could help doctors and researchers to diagnosis and treat autism in the future.

A form of gene therapy currently used to treat Parkinson’s disease may dramatically reduce alcohol use among chronic heavy drinkers, researchers at Oregon Health & Science University and institutions across the country have found.

The study in nonhuman primates showed that implanting a specific type of molecule that induces cell growth effectively resets the brain’s dopamine reward pathway in animals predisposed to heavy drinking. The gene therapy procedure involves brain surgery, and may be useful in the most severe cases of alcohol use disorder.


Already used in clinical trials to treat Parkinson’s disease, OHSU researchers found surgical treatment dramatically reduced chronic heavy drinking.

In a groundbreaking study published today in Nature, Australian scientists have resolved a long-standing problem in regenerative medicine. Led by Professor Ryan Lister from the Harry Perkins Institute of Medical Research and The University of Western Australia and Professor Jose M Polo from Monash University and the University of Adelaide, the team developed a new method to reprogram human cells to better mimic embryonic stem cells, with significant implications for biomedical and therapeutic uses.

In a revolutionary advance in the mid-2000s, it was discovered that the non-reproductive adult cells of the body, called ‘somatic’ cells, could be artificially reprogrammed into a state that resembles embryonic stem (ES) cells which have the capacity to then generate any cell of the body.

The ability to artificially reprogram human somatic cells, such as skin cells, into these so-called induced pluripotent stem (iPS) cells provided a way to make an essentially unlimited supply of ES-like cells, with widespread applications in disease modelling, drug screening and cell-based therapies.

A protein involved in wound healing can improve learning and memory in ageing mice1.

Platelet factor 4 (PF4) has long been known for its role in promoting blood clotting and sealing broken blood vessels. Now, researchers are wondering whether this signalling molecule could be used to treat age-related cognitive disorders such as Alzheimer’s disease.

“The therapeutic possibilities are very exciting,” says geneticist and anti-ageing scientist David Sinclair at Harvard University in Boston, Massachusetts, who was not involved in the research. The study was published on 16 August in Nature.

Young blood, old brains.


A platelet factor joins the list of blood components that might have anti-ageing effects.

Free will?

Neuroscientists and psychologists have been trying for decades to better understand how humans make decisions, in the hope to devise more effective interventions to promote healthy and beneficial lifestyle choices. Two brain regions that have been linked to decision-making are the orbitofrontal cortex (OFC) and the anterior cingulate cortex (ACC).

Researchers at University of California, Berkeley (UC Berkeley), have been conducting extensive research focusing on these two areas of the brain and exploring their involvement in . In a recent paper published in Nature Neuroscience, they presented interesting new findings that could shed light on the through which the brain prepares to make choices.

“We previously used neural recordings to determine what was going on during decision-making,” Joni Wallis, one of the researchers who carried out the study, told Medical Xpress. “We showed that OFC neurons represent the value of the options under consideration and flip-flopping them back and forth representing the value of each option in turn, as though the OFC is weighing up the two options. This flip-flopping predicts decision making: the more flip-flopping, the more likely the subject is to make a suboptimal choice or to take a long time over their decision.”

This is a significant development that brings hope to the one billion individuals with obesity worldwide. Researchers led by Director C. Justin LEE from the Center for Cognition and Sociality (CCS) within the Institute for Basic Science (IBS) have discovered new insights into the regulation of fat metabolism. The focus of their study lies within the star-shaped non-neuronal cells in the brain, known as ‘astrocytes’. Furthermore, the group announced successful animal experiments using the newly developed drug ‘KDS2010’, which allowed the mice to successfully achieve weight loss without resorting to dietary restrictions.

The complex balance between food intake and energy expenditure is overseen by the hypothalamus in the brain. While it has been known that the neurons in the lateral hypothalamus are connected to fat tissue and are involved in fat metabolism, their exact role in fat metabolism regulation has remained a mystery. The researchers discovered a cluster of neurons in the hypothalamus that specifically express the receptor for the inhibitory neurotransmitter ‘GABA (Gamma-Aminobutyric Acid)’. This cluster has been found to be associated with the α5 subunit of the GABAA receptor and was hence named the GABRA5 cluster.

In a diet-induced obese mouse model, the researchers observed significant slowing in the pacemaker firing of the GABRA5 neurons. Researchers continued with the study by attempting to inhibit the activity of these GABRA5 neurons using chemogenetic methods. This in turn caused a reduction in heat production (energy consumption) in the brown fat tissue, leading to fat accumulation and weight gain. On the other hand, when the GABRA5 neurons in the hypothalamus were activated, the mice were able to achieve a successful weight reduction. This suggests that the GABRA5 neurons may act as a switch for weight regulation.

In a study of brains from contact sport players who died before reaching 30, more than 40% had chronic traumatic encephalopathy, oXavier?

The findings confirm that CTE can occur even in young people, but more work is needed to determine how CTE relates to clinical symptoms.

Millions of people worldwide get repetitive head impacts through various activities. These can lead to chronic traumatic encephalopathy (CTE), a progressive neurodegenerative disease that causes brain damage similar to that seen in Alzheimer’s disease. CTE has been reported in people as young as 17. The incidence of CTE in young people, however, is unknown.

An NIH-funded research team, led by Dr. Ann McKee at Boston University and VA Boston Health Care, analyzed 152 brains (141 male and 11 female) that were donated to a brain bank. The brain donors had a history of repetitive head impacts from playing contact sports and were younger than 30 years old when they died. Researchers examined the brains and surveyed the donors’ next of kin about clinical symptoms. Results were published in JAMA Neurology on August 28, 2023.

More than 40% of the donors (63 out of 152) had CTE based on established criteria. Nearly all cases of CTE were mild (stages 1 or 2 out of 4). Donors with CTE tended to be older than those without the disease. The most common cause of death among the donors was suicide, followed by unintentional drug overdose. The causes of death did not differ between those with and without CTE. Most of the donors with CTE were male, but one was female–a collegiate soccer player.

Neural Link’s first-In-human clinical trials.

We are happy to announce that we’ve received approval from the reviewing independent institutional review board and our first hospital site to begin recruitment for our first-in-human clinical trial. The PRIME Study (short for Precise Robotically Implanted Brain-Computer Interface) – a groundbreaking investigational medical device trial for our fully-implantable, wireless brain-computer interface (BCI) – aims to evaluate the safety of our implant (N1) and surgical robot (R1) and assess the initial functionality of our BCI for enabling people with paralysis to control external devices with their thoughts.

During the study, the R1 Robot will be used to surgically place the N1 Implant’s ultra-fine and flexible threads in a region of the brain that controls movement intention. Once in place, the N1 Implant is cosmetically invisible and is intended to record and transmit brain signals wirelessly to an app that decodes movement intention. The initial goal of our BCI is to grant people the ability to control a computer cursor or keyboard using their thoughts alone.

A new review published in The Lancet Neurology by researchers at Mass General Brigham presents findings indicating that cardiovascular disease risk may be increased by traumatic brain injury (TBI). The review presented evidence of the long-term associations between TBI and cardiovascular disease noting that post-injury comorbidities, as well as neuroinflammation, and changes in the brain-gut connection may be culprits in the elevated risk compared to the general population.

“Despite decades of extensive traumatic brain-injury-focused research, surprisingly, there has been minimal progress in mitigating long-term outcomes and mortality following injuries. The cardiovascular effects of TBI may be a missing link in advancing our efforts to improve long-term quality of life and reducing mortality rates in TBI patients,” said first author Saef Izzy, MD, of the Stroke and Cerebrovascular Center of Brigham and Women’s Hospital. “We have the opportunity to identify and improve targeted screening for high-risk populations, build preventative care strategies and improve outcomes for survivors of TBI.”

While past research has exhibited there is a strong link between TBI and neurodegenerative conditions such as Alzheimer’s disease and dementia, decades of research has failed to understand the mechanisms that occur after a TBI that drive these diseases. Izzy and review co-authors now suggest that there may be non-neurological effects of TBI, including cardiovascular, cardiometabolic, and endocrine dysfunction that may act as intermediaries that contribute to neurological disorders that may appear decades later.