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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 changes the structure of brain cells in a way that disrupts crucial communication between neurons that make the 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.

Subtle molecular changes in brain cells may be linked to autism and schizophrenia

A team of researchers at NYU Abu Dhabi has uncovered a key mechanism that helps shape how our brains are wired, and what can happen when that process is disrupted.

In a new study published in Cell Reports, the RNA-MIND Lab at NYU Abu Dhabi, led by Professor of Biology Dan Ohtan Wang, with Research Associate Belal Shohayeb, reveals how a small molecular mark on messenger RNA, called m6A methylation, regulates the production of essential proteins inside growing neurons. This process plays a critical role in the development of axons, the long extensions that neurons use to connect and communicate with each other.

The study shows that this molecular mark controls the production of a protein called (APC), which helps organize the internal structure of nerve cells and is needed to locally produce β-actin, a key building block of the cytoskeleton to support axon growth. Importantly, the team also found that linked to autism and schizophrenia can interfere with this process, potentially affecting how the brain develops.

Neuroscientists remain steadfastly uncertain about how the brain encodes memory

Researchers from Monash University, in collaboration with the European Biostasis Foundation and Apex Neuroscience, have revealed that although most neuroscientists agree that long-term memories depend primarily on neuronal connectivity patterns, significant uncertainties persist regarding precisely how these memories are structurally encoded.

Brains can retain memories for days, months and even across a lifetime of decades, through mechanisms that remain elusive to those at the cutting edge of neuroscience. Long-term memory enables animals to shape behaviors by linking past experiences with present contexts.

There are fragile memories, like recalling the name of someone you just met, or the location of where the keys were set down, that can seemingly escape the brain’s data capture. And there are durable memories that can survive periods of global neuronal inactivity and disruption, indicating that ongoing neural activity is not required to maintain stored information.

Low-intensity brain stimulation may restore neuron health in Alzheimer’s disease

Alzheimer’s disease (AD) is a debilitating neurodegenerative condition that affects a significant proportion of older people worldwide. Synapses are points of communication between neural cells that are malleable to change based on our experiences. By adding, removing, strengthening, or weakening synaptic contacts, our brain encodes new events or forgets previous ones.

In AD, , the brain’s ability to regulate the strength of synaptic connections between neurons, is significantly disrupted. This worsens over time, reducing cognitive and memory functions and leading to reduced quality of life. To date, there is no effective cure for AD, and only limited treatments for managing the symptoms.

Studies have shown that (rTMS), a noninvasive brain stimulation technique that uses electromagnetic pulses to target specific brain regions, has therapeutic potential to manage dementia and related diseases. From previous studies, we know that rTMS can promote synaptic plasticity in healthy nervous systems. Moreover, it is already used to treat certain neurodegenerative and neuropsychiatric conditions. However, individual responses to rTMS for AD management are variable, and the underlying mechanisms are not clearly understood.

Fast targeted gene transfection and optogenetic modification of single neurons using femtosecond laser irradiation

Year 2013 face_with_colon_three Basically this is the light based nanotransfection version that can eventually be put on a simple smartphone or smartwatch that can be an entire hospital in one touch healing the entire body in one touch or just areas that need healing.


Antkowiak, M., Torres-Mapa, M., Witts, E. et al. Sci Rep 3, 3,281 (2013). https://doi.org/10.1038/srep03281

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