How to Restore Walking After Spinal Cord Injury

A new study by scientists at the .NeuroRestore research center has identified the type of neuron that is activated and remodeled by spinal cord stimulation, allowing patients to stand up, walk and rebuild their muscles – thus improving their quality of life. This discovery, made in  nine patients, marks a fundamental, clinical breakthrough.

In a multi-year research program coordinated by the two directors of  .NeuroRestore – Grégoire Courtine, a neuroscience professor at EPFL, and  Jocelyne Bloch, a neurosurgeon at Lausanne University Hospital (CHUV) – patients who had been paralyzed by a spinal cord injury and who underwent  targeted epidural electrical stimulation of the area that controls leg movement  were able to regain some motor function.

You must be logged in to view this content.

Synthetic Neurons

Synthetic neurons made of hydrogel could one day be used in sophisticated artificial tissues to repair organs such as the heart or the eyes. Hagan Bayley at the University of Oxford and his colleagues devised a synthetic material that can act in a similar way to a human neuron. Made from hydrogel, the artificial neurons are about 0.7 millimetres across ­– about 700 times wider than a human neuron, but similar to giant axons found in squid. They can also be made up to 25 millimetres long, which is similar in length to a human optic nerve running from the eye to the brain.
When a light is shone on the synthetic neuron, it activates proteins that pump hydrogen ions into the cell. These positively charged ions then move through the neuron, carrying an electrical signal. The speed of transmission was too fast to measure with the team’s equipment and is probably faster than the rate in natural neurons, says Bayley. When the positive charge reaches the tip of the neuron, it makes adenosine triphosphate (ATP) – a neurotransmitter chemicalmove from one water droplet to another. In future work, the researchers hope to make the synthetic neuron interact with another via an ATP signal, just as neurons connect with each other at synapses.
The team bundled seven of the neurons together to work in parallel as a synthetic nerve. “This allows us to send multiple signals simultaneously,” says Bayley. “They can all have very different frequencies and so it’s a very versatile signal.” The main purpose is to send different pieces of information down the same pathway, he says.

Artificial nerve cells made from biocompatible materials have been made in a lab for the first time. The innovation may one day be used in synthetic tissues to repair organs such as the heart or the eyes. 

However, the artificial neurons still have a long way to go. Unlike real neurons, there is no mechanism to recycle and create new neurotransmitters in the synthetic system. The neurons therefore only work for a few hours, says Bayley. “The more you do science, the more you find out how clever science is by virtue of evolution.” Alain Nogaret at the University of Bath in the UK says the innovation could play a major role in improving neuro-implants such as artificial retinas by the end of the decade. “The emulation of nervous activity in soft materials is a major step towards non-invasive brain-machine interfaces and solutions addressing neurodegenerative disease.”

Bayley hopes to eventually use these synthetic neurons to deliver different types of drugs simultaneously to treat wounds more quickly and precisely. “Using light, we could maybe release drug molecules in a patterned way,” he says.
Source: https://www.nature.com/ 
AND
https://www.scientiststudy.com/

Brain Surgery Without a Scalpel

The School of Medicine from the University of Virginia (UVA) researchers have developed a noninvasive way to remove faulty brain circuits that could allow doctors to treat debilitating neurological diseases without the need for conventional brain surgery. The UVA team, together with colleagues at Stanford University, indicate that the approach, if successfully translated to the operating room, could revolutionize the treatment of some of the most challenging and complex neurological diseases, including epilepsy, movement disorders and more. The approach uses low-intensity focused ultrasound waves combined with microbubbles to briefly penetrate the brain’s natural defenses and allow the targeted delivery of a neurotoxin. This neurotoxin kills the culprit brain cells while sparing other healthy cells and preserving the surrounding brain architecture.

A new alternative to brain surgery developed at UVA can wipe out out problematic neurons, a type of brain cell, without causing collateral damage.

This novel surgical strategy has the potential to supplant existing neurosurgical procedures used for the treatment of neurological disorders that don’t respond to medication,” said researcher Kevin S. Lee, PhD, of UVA’s Departments of Neuroscience and Neurosurgery and the Center for Brain Immunology and Glia (BIG). “This unique approach eliminates the diseased brain cells, spares adjacent healthy cells and achieves these outcomes without even having to cut into the scalp.”

The new approach is called PING, and it has already demonstrated exciting potential in laboratory studies. For instance, one of the promising applications for PING could be for the surgical treatment of epilepsies that do not respond to medication. Approximately a third of patients with epilepsy do not respond to anti-seizure drugs, and surgery can reduce or eliminate seizures for some of them. Lee and his team, along with their collaborators at Stanford, have shown that PING can reduce or eliminate seizures in two research models of epilepsy. The findings raise the possibility of treating epilepsy in a carefully-targeted and noninvasive manner without the need for traditional brain surgery.

Another important potential advantage of PING is that it could encourage the surgical treatment of appropriate patients with epilepsy who are reluctant to undergo conventional invasive or ablative surgery. In a scientific paper newly published in the Journal of Neurosurgery, Lee and his collaborators detail the ability of PING to focally eliminate neurons in a brain region, while sparing non-target cells in the same area. In contrast, currently available surgical approaches damage all cells in a treated brain region.

A key advantage of the approach is its incredible precision. PING harnesses the power of magnetic-resonance imaging (MRI) to let scientists peer inside the skull so that they can precisely guide sound waves to open the body’s natural blood-brain barrier exactly where needed. This barrier is designed to keep harmful cells and molecules out of the brain, but it also prevents the delivery of potentially beneficial treatments.

The UVA group’s new paper concludes that PING allows the delivery of a highly targeted neurotoxin, cleanly wiping out problematic neurons, a type of brain cell, without causing collateral damage.

Source: https://newsroom.uvahealth.com/

AI Closer To The Efficiency Of The Brain

Computers and artificial intelligence continue to usher in major changes in the way people shop. It is relatively easy to train a robot’s brain to create a shopping list, but what about ensuring that the robotic shopper can easily tell the difference between the thousands of products in the store?

Purdue University researchers and experts in brain-inspired computing think part of the answer may be found in magnets. The researchers have developed a process to use magnetics with brain-like networks to program and teach devices such as personal robots, self-driving cars and drones to better generalize about different objects.

Our stochastic neural networks try to mimic certain activities of the human brain and compute through a connection of neurons and synapses,” said Kaushik Roy, Purdue’s Edward G. Tiedemann Jr. Distinguished Professor of Electrical and Computer Engineering. “This allows the computer brain to not only store information but also to generalize well about objects and then make inferences to perform better at distinguishing between objects.

The stochastic switching behavior is representative of a sigmoid switching behavior of a neuron. Such magnetic tunnel junctions can be also used to store synaptic weights. Roy presented the technology during the annual German Physical Sciences Conference earlier this month in Germany. The work also appeared in the Frontiers in Neuroscience.

The switching dynamics of a nano-magnet are similar to the electrical dynamics of neurons. Magnetic tunnel junction devices show switching behavior, which is stochastic in nature.  The Purdue group proposed a new stochastic training algorithm for synapses using spike timing dependent plasticity (STDP), termed Stochastic-STDP, which has been experimentally observed in the rat’s hippocampus. The inherent stochastic behavior of the magnet was used to switch the magnetization states stochastically based on the proposed algorithm for learning different object representations. “The big advantage with the magnet technology we have developed is that it is very energy-efficient,” said Roy, who leads Purdue’s Center for Brain-inspired Computing Enabling Autonomous Intelligence. “We have created a simpler network that represents the neurons and synapses while compressing the amount of memory and energy needed to perform functions similar to brain computations.

Source: https://www.purdue.edu/

New Hope To Fight Alzheimer’s

It is known that the onset of Alzheimer’s disease (AD) is associated with the accumulation of Amyloid beta () peptides in small molecular clusters known as oligomers. These trigger the formation of so-called ‘neurofibrillary tangles’ within neurons hamper their workings, ultimately causing cell death and so significant cognitive decline. Very large Aβ oligomers which form plaques outside neurons, alongside neuroinflammation have also been found to play a key part in the progression of the disease.


The EU-funded iRhom2 in AD project took as its starting point the protein iRhom2, which has been identified as a genetic risk factor for AD due to its pro-inflammatory properties. The team were able to explore further the influence of iRhom2 on neuroinflammation in mice. iRhom2 recently emerged as a protein of note in AD as it aids the maturation of an enzyme called TACE (tumor necrosis factor-α converting enzyme) guiding it towards a cell’s plasma membrane where the enzyme releases a cell-signalling cytokine (TNFα), implicated in the regulation of inflammatory processes. While mice studies have shown that TNFα-dependent inflammation can lead to sepsis and rheumatoid arthritis, it is also thought that the process contributes to neuroinflammatory signalling events, which can cause harm in the brain.

The EU-funded iRhom2 in AD project worked with mice that are prone to develop the hallmarks of AD, amyloid plaques and memory deficits. The team genetically altered iRhom2 in the mice then analysed the progression of the pathology using an array of biochemical and histological methods, together with a number of behavioural tests to assess cognitive decline. The results were somewhat surprising.

We initially hypothesised that iRhom2 would affect one specific aspect of neuroinflammation in AD. What we discovered was even more exciting as it actually affects several different aspects of neuroinflammation simultaneously. So modulating iRhom2 appears particularly well suited to interfere with AD,” explains project coordinator Prof. Dr. Stefan Lichtenthaler.

Source: https://cordis.europa.eu/