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Category: neuroscience – Page 81

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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How key brain cells help replay and store memories during rest and sleep

How does the brain store knowledge so that you actually remember what you have learned the next day or even later? To find out, researchers at the University of Oslo disconnected one type of nerve cell in the brain of mice while the animals rested after having learned something new. This gave new answers to what actually happens when you remember earlier experiences for later use. The study is published in the journal Science Advances.

In the first phase of this experiment, were trained to recognize that an image with a particular pattern meant that they would be given a reward in the form of a sweet drink. Two different groups of mice were then put in front of a computer screen where they were able to see several images containing different patterns. In order to demonstrate that they remembered which image led to a reward, the mice had to lick a small “nozzle” that dispensed the drink.

While the mice performed this action, researchers at the University of Oslo monitored the activity in their using a special microscope. “It took some time before the mice understood which pattern triggered a reward. We could see what was happening with their neurons while they mastered the task,” says researcher Kristian K. Lensjø, who works at the Institute of Basic Medical Sciences and the Department of Biosciences at the University of Oslo.

Newborns have elevated levels of a biomarker for Alzheimer’s

Newborn babies and patients with Alzheimer’s disease share an unexpected biological trait: elevated levels of a well-known biomarker for Alzheimer’s, as shown in a study led by researchers at the University of Gothenburg and published in Brain Communications.

First author Fernando Gonzalez-Ortiz and senior author Professor Kaj Blennow recently reported that both newborns and Alzheimer’s patients have elevated blood levels of a protein called phosphorylated tau, specifically a form called p-tau217.

This protein has largely been used as a diagnostic test for Alzheimer’s disease, where an increase in p-tau217 blood levels is proposed to be driven by another process, namely the aggregation of b-amyloid protein into amyloid plaques. Newborns (for natural reasons) do not have this type of pathological change, so interestingly, in newborns increased plasma p-tau217 seems to reflect a completely different—and entirely healthy—mechanism.

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