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New research on mice has shed light on how high blood pressure causes changes to arteries in the brain, a process that leads to vascular dementia. The research, led by University of Manchester scientists, funded by the British Heart Foundation and published today in the journal Proceedings of the National Academy of Sciences, [1] has uncovered a route to developing the first ever drug treatments for vascular dementia that directly target a cause of the condition.

High blood pressure is the main cause of vascular dementia, a condition characterised by poor blood flow to the brain. The reduced blood supply starves brain cells of nutrients and over time they become damaged and die. Symptoms of vascular dementia include loss of energy, lack of concentration and poor memory.

It’s normal for the brain’s arteries to narrow and widen in response to changes in blood pressure. However, consistently high blood pressure causes arteries to stay narrow and restrict the brain’s blood supply. Until now, it was not known why.

Among humans and many other species, parents have a super sense when it comes to a crying baby. Something in that wordless call communicates distress so clearly that it sparks an instinctive response. And the cries of human, chimp and bonobo babies are so compelling that even other species recognize and react to them, including Nile crocodiles. However, to a croc, a human baby’s screams may sound less like a cry for help—and more like a dinner bell.

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.

A team of New Jersey researchers reviewed the evidence for the impact of robotic exoskeleton devices on recovery of ambulation among individuals with acquired brain injury, laying out a systematic framework for the evaluation of such devices that is needed for rigorous research studies. The open access article, “Lower extremity robotic exoskeleton devices for overground ambulation recovery in acquired brain injury – A review” (doi: 10.3389/fnbot.2023/1014616), was published May 25, 2023 in Frontiers in Neurorobotics.


New Jersey researchers provide framework for evaluating lower extremity robotic exoskeletons and their role in neurorehabilitation following acquired brain injury East Hanover, NJ. August 14, 2023.

About six years ago, scientists discovered a new type of more powerful neural network model known as a transformer. These models can achieve unprecedented performance, such as by generating text from prompts with near-human-like accuracy. A transformer underlies AI systems such as ChatGPT and Bard, for example. While incredibly effective, transformers are also mysterious: Unlike with other -inspired neural network models, it hasn’t been clear how to build them using biological components.

Now, researchers from MIT, the MIT-IBM Watson AI Lab, and Harvard Medical School have produced a hypothesis that may explain how a transformer could be built using biological elements in the brain. They suggest that a biological network composed of neurons and other called astrocytes could perform the same core computation as a transformer.

We often believe computers are more efficient than humans. After all, computers can complete a complex math equation in a moment and can also recall the name of that one actor we keep forgetting. However, human brains can process complicated layers of information quickly, accurately, and with almost no energy input: recognizing a face after only seeing it once or instantly knowing the difference between a mountain and the ocean. These simple human tasks require enormous processing and energy input from computers, and even then, with varying degrees of accuracy.

Creating brain-like computers with minimal energy requirements would revolutionize nearly every aspect of modern life. Funded by the Department of Energy, Quantum Materials for Energy Efficient Neuromorphic Computing (Q-MEEN-C) — a nationwide consortium led by the University of California San Diego — has been at the forefront of this research.

UC San Diego Assistant Professor of Physics Alex Frañó is co-director of Q-MEEN-C and thinks of the center’s work in phases. In the first phase, he worked closely with President Emeritus of University of California and Professor of Physics Robert Dynes, as well as Rutgers Professor of Engineering Shriram Ramanathan. Together, their teams were successful in finding ways to create or mimic the properties of a single brain element (such as a neuron or synapse) in a quantum material.

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.