Neuro Rehab, the UK's leading event for rehabilitation professionals, brings you the latest research findings from studies conducted around the world. These studies explore various pioneering treatments for patients affected by neurological conditions or injuries, and potential new ways of improving diagnosis and long-term outcomes.
Spinal injury
World’s first spinal cord implant could allow paralysed patients to walk again
Israeli researchers are preparing for what is believed to be the first spinal cord implant using human tissues.
The surgery, expected to take place within a year, aims to help paralysed patients stand and walk again by replacing damaged tissue with lab-grown cells.
Currently, the human body is unable to regenerate nerve cells when damage occurs. But researchers at Tel Aviv University (TAU) say they have developed a process to overcome this challenge.
Blood cells are taken from the patient and reprogrammed through genetic engineering to behave like embryonic stem cells, capable of becoming any type of cell in the body.
Meanwhile, fat tissue from the same patient is used to extract substances such as collagen and sugars. These are used to produce a unique hydrogel.
Prof. Tal Dvir, of TAU’s Sagol Center for Regenerative Biotechnology, explains: “The beauty of this gel is that it’s also personalised, just like the cells. We take the cells that we’ve reprogrammed into embryonic-like stem cells, place them inside the gel, and mimic the embryonic development of the spinal cord.
The result is a complete three-dimensional implant. “At the end of the process, we don’t just turn the cells into motor neurons — because cells alone won’t help us but into three-dimensional tissue: neuronal networks of the spinal cord. After about a month, we obtain a 3D implant with many neurons that transmit electrical signals. These 3D tissues are then implanted into the damaged area.”
Stroke
NHS stroke centres given AI tool that triples recovery rates
People who experience a stroke in England are now three times as likely to make a full recovery thanks to a new AI scanning system.
The NHS confirmed that it has potentially helped thousands of patients avoid serious disability after deploying the technology in 107 NHS stroke centres across the country.
The innovative system analyses brain CT scans of stroke patients arriving at hospital, taking just a minute to identify the type and severity of stroke and the most appropriate treatment.
Early analysis shows the AI technology reduces hospital admission to treatment time by 60 minutes – from 140 minutes to 79 minutes.
Quicker treatment means that the proportion of patients recovering with no or only slight disability has tripled, from 16% to 48%.
The system could transform care for the 80,000 people in England who have a stroke each year.
David Hargroves, NHS national clinical director for stroke, said: “NHS stroke teams have been leading the way in rolling out AI, and with every stroke centre now using the technology, it is already playing a key role in improving the care of thousands of people in England every year.”
Parkinson’s
Overworked brain cells linked to Parkinson’s disease
Researchers have long known that a particular subset of neurons die as Parkinson’s disease progresses. Now fresh evidence could explain why this is the case.
A new study published by scientists at Gladstone Institutes in San Francisco shows that in mice, chronic activation of dopamine-producing neurons can directly cause their demise.
The scientists hypothesize that in Parkinson’s, neuron overactivation could be triggered by a combination of genetic factors, environmental toxins, and the need to compensate for other neurons that are lost.
In the new study, Ken Nakamura, who led the research, and his colleagues introduced a receptor specifically into dopamine neurons in mice that allowed them to increase the cells’ activity by treating the animals with a drug, clozapin-N-oxide (CNO).
Within a few days of over-activating dopamine neurons, the animals’ typical cycle of daytime and nighttime activities became disrupted. After one week, the researchers could detect degeneration of the long projections (called axons) extending from some dopamine neurons. By one month, the neurons were beginning to die.
Importantly, the changes mostly affected one subset of dopamine neurons—those found in the region of the brain known as the substantia nigra, which is responsible for movement control—while sparing dopamine neurons in brain regions responsible for motivation and emotions. This is the same pattern of cellular degeneration seen in people with Parkinson’s disease.
Motor Neuron Disease
New study uncovers how DNA damage can lead to MND
Researchers at the University of Bath have discovered how DNA damage caused by a faulty DNA protection and repair system can lead to neurodegenerative disorders such as Motor Neurone Disease (MND).
MND, also known as Amyotrophic Lateral Sclerosis (ALS), is a terminal neurodegenerative disease which causes progressive loss of the neurones that control the muscles.
Several faulty genes have been linked to MND, including mutations of the gene that codes for a protein called CFAP410.
This protein is found on the surface of some cells called cilia, which are involved in many cell functions including signalling pathways crucial for brain development.
The researchers used gene editing techniques in mouse embryonic stem cells to investigate the effects of two mutations of CFAP410 commonly found in patients with MND.
After introducing the mutated gene, the researchers induced the cells to make neurones and observed the effects on cilia formation and the response of the cells to chemical stress leading to DNA damage.
Previous work by others has shown that knocking out the CFAP410 gene harms cilia formation, however the Bath researchers found that cilia were unaffected in neurones edited to contain the mutated gene.
Instead, the mutations in CFAP410 changed the protein’s interaction with another protein called Nek1, which activates the cell’s DNA repair system. This resulted in the motor neurone cells being more susceptible to DNA damage.
These cells were less able to repair the damage and were more sensitive to various chemical stressors, leading to higher rates of cell death.
Publishing in the journal iScience, the authors say their findings suggest it is this DNA damage that is likely to cause MND.
Dr Vasanta Subramanian, who led the research, said: “Whilst CFAP410 has been linked with MND previously, we’ve used gene editing for the first time to show that mutations in this gene contribute to the disease by making cells more vulnerable to DNA damage and stress, ultimately leading to death of the motor neurones.
“Our findings identify new insights into the mechanisms underlying MND and highlights potential targets for new therapies.”