The first wave of data Penn State’s HEALthy Brain and Child Development study is now available to researchers interested in addressing a wide-range of questions, including how environments and substances impact infant and child development.
Category: neuroscience
Proteins important in brain communication have different roles than previously thought
Cellular communication between neurons within our brain is complex and busy, much like a USPS mailroom.
To keep things running smoothly, the brain uses specialized molecules, termed alpha-2-delta (α2δ) proteins, to coordinate the sending and receival of signals between nerve cells in the brain.
Genetic variations in these types of proteins can impact important brain messaging and function, resulting in chronic pain, autism spectrum disorders, epilepsy, migraines, and other conditions.
Triglycerides may play an important role in brain metabolism
While glucose, or sugar, is a well-known fuel for the brain, Weill Cornell Medicine researchers have demonstrated that electrical activity in synapses—the junctions between neurons where communication occurs—can lead to the use of lipid or fat droplets as an energy source.
The study, published in Nature Metabolism, challenges “the long-standing dogma that the brain doesn’t burn fat,” said principal investigator Dr. Timothy A. Ryan, professor of biochemistry and of biochemistry in anesthesiology, and the Tri-Institutional Professor in the Department of Biochemistry at Weill Cornell Medicine.
The paper’s lead author, Dr. Mukesh Kumar, a postdoctoral associate in biochemistry at Weill Cornell Medicine who has been studying the cell biology of fat droplets, suggested that it makes sense that fat may play a role as an energy source in the brain like it does with other metabolically demanding tissues, such as muscle.
Inhibiting enzyme could halt cell death in Parkinson’s disease, study finds
Putting the brakes on an enzyme might rescue neurons that are dying due to a type of Parkinson’s disease that’s caused by a single genetic mutation, according to a new Stanford Medicine-led study conducted in mice.
The study has been published in Science Signaling.
The genetic mutation causes an enzyme called leucine-rich repeat kinase 2, or LRRK2, to be overactive. Too much LRRK2 enzyme activity changes the structure of brain cells in a way that disrupts crucial communication between neurons that make the neurotransmitter dopamine and cells in the striatum, a region deep in the brain that is part of the dopamine system and is involved in movement, motivation and decision-making.
Scientists reprogram ant behavior using brain molecules
Leafcutter ants live in highly organized colonies where every ant has a job, and now researchers can flip those jobs like a switch. By manipulating just two neuropeptides, scientists can turn defenders into nurses or gardeners into leaf harvesters. These same molecular signals echo in naked mole-rats, revealing a deep evolutionary link in how complex societies function, even across species. The study also teases out a possible connection to insulin and longevity, hinting at new frontiers in understanding human behavior and lifespan.
Researchers identify neural mechanism behind memory prioritization
To study what happened in the brain during this task, the researchers used functional magnetic resonance imaging, which measures blood flow as a proxy for neural activity. They scanned the brains of 11 participants while they performed the memory task over multiple sessions. By applying a complex decoding model to the imaging data, the researchers were able to estimate not only what participants were remembering but also how uncertain they were about each memory. The model treated neural activity as a probabilistic code, where stronger or more focused patterns of activity reflected more confident memory representations.
The results showed that neural signals in the visual cortex—the area of the brain involved in processing visual information—were more intense for the high-priority memory items. These stronger signals translated to smaller memory errors and greater confidence. On average, participants remembered the high-priority items more accurately and responded more quickly when asked to recall them. Their eye movements were closer to the correct location, and they took less time to respond. These behavioral improvements matched the patterns observed in the brain data.
The study also found that the magnitude of neural activity in the frontal cortex predicted how well participants could distinguish between high-and low-priority memories. This suggests that the frontal cortex plays a regulatory role, sending signals that adjust the strength of memory representations in visual areas depending on how important each item is. In other words, the frontal brain regions help direct the mental spotlight, increasing the “volume” of the memories that matter most.
Dual electrical stimulation at spinal-muscular interface reconstructs spinal sensorimotor circuits after spinal cord injury
Electrical signals with characteristic parameters for reconstructing neural circuits remain incompletely understood, limiting the therapeutic potential of electrical neuromodulation techniques. Here, the authors demonstrate that dual electrical stimulation at 10–20 Hz rebuilds the spinal sensorimotor neural circuit after spinal cord injury, indicating the characteristic signals of circuit remodeling.
Engineered protein can turn off tissue-damaging immune cells in autoimmune diseases
An engineered protein turns off the kind of immune cells most likely to damage tissue as part of type-1 diabetes, hepatitis, multiple sclerosis, shows a new study in mice.
In these autoimmune diseases, T cells mistakenly target the body’s own tissues instead of invading viruses or bacteria as they would during normal immune responses. Treatments focused on T cells have been elusive because blocking their action broadly weakens the immune system and creates risk for infections and cancer.
Published online June 30 in the journal Cell, the study revealed that holding closely together two protein groups (signaling complexes) on T cells, including one found more often on T cells involved in autoimmune disease, shuts down those T cells in a limited way.