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Category: neuroscience

New mechanism explains how spinal stimulation improves arm movement after stroke

Researchers in the Neuromechatronics Lab at Carnegie Mellon University have already proven that spinal cord stimulation can help people regain movement after stroke, but until now they didn’t quite know how.

In a new study, published today in Cell Reports Medicine, a research team led by Doug Weber, professor of mechanical engineering and neuroscience, and Ph.D. candidate Luigi Borda report that epidural spinal cord stimulation works by restoring inhibitory spinal circuits. These circuits enable the nervous system to coordinate opposing muscles, such as the biceps and triceps, which must work together to bend and straighten the elbow. After a stroke, those neural control circuits are disrupted. The new study found that spinal cord stimulation helps restore that balance, allowing stroke survivors to move their arms more smoothly, quickly and efficiently.

“This discovery allows us to move beyond simply strengthening weak muscles; we can now fine-tune stimulation to release the ‘brakes’ on overactive muscles, providing a more effective and personalized path to recovery,” said Weber.

Sugarcoated nanoparticles show promise for treating most aggressive form of brain cancer

Sugar-coated nanoparticles show promise against glioblastoma.

Researchers have developed mannose-coated lipid nanoparticles capable of crossing the blood-brain barrier and delivering therapeutic PTEN mRNA directly to glioblastoma cells, one of the deadliest forms of brain cancer.

Glioblastoma cells have an exceptionally high demand for glucose. By coating the nanoparticles with a sugar molecule called mannose, the researchers took advantage of this metabolic feature, allowing the particles to enter the brain more efficiently and accumulate within tumors.

Once inside the cancer cells, the nanoparticles restored production of PTEN, a critical tumor-suppressor protein that is frequently lost or dysfunctional in glioblastoma. In mouse models, this approach significantly slowed tumor growth, increased median survival by approximately 50%, and showed no measurable toxicity in major organs.

Although these findings are still preclinical and have not yet been tested in humans, they represent an exciting advance in overcoming one of neuro-oncology’s greatest challenges: safely delivering targeted therapies across the blood-brain barrier.

PORTLAND, Ore. – Researchers at Oregon State University have potentially found a new way to treat the most aggressive form of brain cancer, glioblastoma, whose two-year survival rate is less than 30%.

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Finding the RNA aptamer in the haystack that could improve treatment for Parkinson’s

Synucleinopathies are a group of neurodegenerative disorders that include serious conditions such as Parkinson’s disease and dementia with Lewy bodies. There are currently no cures for these disorders, and treatment is limited to mitigating symptoms. Recently, antibody-based therapies have attracted considerable attention, but alternative approaches are still necessary.

Therapy development for synucleinopathies tends to target the alpha-synuclein protein, αSyn, the abnormal aggregation of which is a hallmark of these diseases. However, targeting this protein using conventional drug discovery strategies is stymied by the molecule’s lack of a stable three-dimensional structure, which promotes aggregation.

Interested in understanding how abnormal protein aggregation drives neurodegeneration, a team of researchers at Kyoto University had an idea that was both scientifically intriguing and therapeutically promising: Could RNA aptamers—often described as “chemical antibodies”—directly recognize αSyn’s disordered regions and suppress pathological aggregation?

Gene therapy restores key fragile X traits in preclinical study

A gene therapy designed to replace the missing protein that causes fragile X syndrome restored several disease-relevant traits in a mouse model, according to a new study published in Gene Therapy.

Fragile X syndrome is the most common inherited form of intellectual disability and a leading single-gene condition associated with autism. There is no cure, and current care focuses on managing symptoms such as anxiety, sensory sensitivity, hyperactivity, developmental seizures and learning challenges.

The study, led by investigators at Cincinnati Children’s and collaborators at Forge Biologics, tested adeno-associated viral vectors carrying human FMR1, the gene silenced in fragile X syndrome. After testing several candidates, the team found an approach that produced the FMRP protein in key brain regions and improved multiple phenotypes in Fmr1 knockout mice.

Dendrites may be key to learning and memory, study suggests

Branchlike structures called dendrites that extend from neurons appear to make their own computations independent of the cell body, helping individual brain cells store memories of the past, respond to the present and anticipate the future, a study led by UT Southwestern Medical Center researchers suggests.

The findings, published in Science, represent a paradigm shift in current models of how learning and memory take place.

“This shifts our entire perspective. Rather than acting as simple switches, neurons behave more like sophisticated processors with internal divisions of labor, dramatically increasing the brain’s computational capacity,” said Attila Losonczy, M.D., Ph.D., professor at the Peter O’Donnell Jr. Brain Institute of Neuroscience and director of the Program in Memory Longevity (PML) at UT Southwestern.

Human-machine learning boosts noninvasive brain-computer control in untrained users

Implantable devices in the brain have been used for about 30 years to assist people with disabilities in completing motor tasks. However, the devices are simply not accessible to the vast majority of people who need help. Despite decades of work in this field, fewer than 100 people worldwide have benefited from the technology. The costs are prohibitive, and the brain surgeries are inherently risky.

That’s why Carnegie Mellon researchers, including Bin He, professor of biomedical engineering, electrical and computer engineering, and the Neuroscience Institute, have long been working on noninvasive brain-computer interfaces (BCIs) to develop technology that is less expensive, safer and more accessible to a wider population. Over the past 10 to 15 years, they have used noninvasive BCIs to fly a drone, control a robotic arm, maintain continuous control of a robotic arm and, most recently, complete fine motor tasks at the finger level. Yet the accuracy and level of control using noninvasive technology remain challenging.

Before babies can hear, their brains are already wiring for sound

Long before a baby’s ears are functional, the brain is already building the circuitry needed for hearing, according to new research from Johns Hopkins University. Published in the journal Science Advances, the study in mice identifies a previously unknown neural “shortcut” that organizes the auditory system before birth, offering new insight into how the auditory system prepares to process sound and eventually learn language.

While it’s well-known that sound travels from the ear to the auditory cortex, the brain’s hub for hearing, Johns Hopkins researchers discovered a new neural circuit that bypasses the ear entirely. Their findings show that the frontal cortex—the region involved in vocalization—sends signals directly to the auditory cortex, allowing the developing brain to activate hearing-related circuits before external sounds can be heard.

“Our results provide the first direct functional evidence of this biological shortcut that doesn’t go through hearing,” says senior author Patrick Kanold, a professor of biomedical engineering and neuroscience at Johns Hopkins. “It’s a novel brain activity source that can shape the earliest development in mammals, like interpreting information and discerning complex sounds.”

Breakdown of immune cells’ interaction is key driver in aging, study finds

We may age at different rates, but none of us escapes aging. A study in mice and human cells by Stanford Medicine researchers pins much of the blame on a particular type of immune cell’s increasing inability, with advancing age, to gobble up another immune cell type.

So-called tissue-resident macrophages appear to be central coordinators of age-related organ decline. Blocking a single receptor on these cells preserved the youthfulness of multiple organs in mice, including the brain, heart, skeletal and heart muscle, liver, spleen, bone marrow, kidney and colon. The receptor binds specifically to a hormone known to cause inflammation and pain in humans as well as mice.

In mice, selectively disabling this receptor exclusively on tissue-resident macrophages prevented chronic inflammation-driven disorders of aging, including frailty, excessive fat accumulation and heart trouble. It also substantially slowed cognitive decline, said Katrin Andreasson, MD, the Edward F. and Irene Thiel Pimley professor of neurology and neurological sciences.

Can magnetic fields help fight Parkinson’s disease?

An international team has succeeded in using a magnetic field to target structures deep within the brain. The researchers injected magnetic nanoplatelets into the relevant region. By doing so, they succeeded in treating movement deficits in mice suffering from Parkinson’s-like symptoms. The new method is less invasive than standard stimulation procedures using implanted electrodes that are currently used to treat certain Parkinson’s disease patients.

The study from Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), RWTH Aachen and the Universities of Maastricht (the Netherlands) and Leuven (Belgium) has been published in the journal Advanced Science.

In Parkinson’s disease, nerve cells in the brain that produce the neurotransmitter dopamine gradually deteriorate. This affects the motor circuits and leads to tremors and other movement disorders. A brain pacemaker may help some patients. This is a small device that is implanted under the collarbone. From there, it stimulates a region deep within the brain called the subthalamic nucleus (STN for short). This changes pathological activity in these neural circuits and can alleviate movement disorders.

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