̽��ֱ�� of Cambridge - John van Geest Centre for Brain Repair

Lab-grown ‘mini brains’ hint at treatments for neurodegenerative diseases

cjb250 — Thu, 21 Oct 2021 15:00:41 +0000

A common form of motor neurone disease, amyotrophic lateral sclerosis, often overlaps with frontotemporal dementia (ALS/FTD) and can affect younger people, occurring mostly after the age of 40-45. These conditions cause devastating symptoms of muscle weakness with changes in memory, behaviour and personality. Being able to grow small organ-like models (organoids) of the brain allows the researchers to understand what happens at the earliest stages of ALS/FTD, long before symptoms begin to emerge, and to screen for potential drugs.

In general, organoids, often referred to as ‘mini organs’, are being used increasingly to model human biology and disease. At the ̽��ֱ�� of Cambridge alone, researchers use them to repair damaged livers, study SARS-CoV-2 infection of the lungs and model the early stages of pregnancy, among many other areas of research.

Typically, researchers take cells from a patient’s skin and reprogramme the cells back to their stem cell stage – a very early stage of development at which they have the potential to develop into most types of cell. These can then be grown in culture as 3D clusters that mimic particular elements of an organ. As many diseases are caused in part by defects in our DNA, this technique allows researchers to see how cellular changes – often associated with these genetic mutations – lead to disease.

Scientists at the John van Geest Centre for Brain Repair, ̽��ֱ�� of Cambridge, used stem cells derived from patients suffering from ALS/FTD to grow brain organoids that are roughly the size of a pea. These resemble parts of the human cerebral cortex in terms of their embryonic and fetal developmental milestones, 3D architecture, cell-type diversity and cell-cell interactions.

Although this is not the first time scientists have grown mini brains from patients with neurodegenerative diseases, most efforts have only been able to grow them for a relatively short time frame, representing a limited spectrum of dementia-related disorders. In findings published today in Nature Neuroscience, the Cambridge team reports growing these models for 240 days from stem cells harbouring the commonest genetic mutation in ALS/FTD, which was not previously possible – and in unpublished work the team has grown them for 340 days.

Dr András Lakatos, the senior author who led the research in Cambridge’s Department of Clinical Neurosciences, said: “Neurodegenerative diseases are very complex disorders that can affect many different cell types and how these cells interact at different times as the diseases progress.

“To come close to capturing this complexity, we need models that are more long-lived and replicate the composition of those human brain cell populations in which disturbances typically occur, and this is what our approach offers. Not only can we see what may happen early on in the disease – long before a patient might experience any symptoms – but we can also begin to see how the disturbances change over time in each cell.”

While organoids are usually grown as balls of cells, first author Dr Kornélia Szebényi generated patient cell-derived organoid slice cultures in Dr Lakatos’ laboratory. This technique ensured that most cells within the model could receive the nutrients required to keep them alive.

Dr Szebényi said: “When the cells are clustered in larger spheres, those cells at the core may not receive sufficient nutrition, which may explain why previous attempts to grow organoids long term from patients’ cells have been difficult.”

Using this approach, Dr Szebényi and colleagues observed changes occurring in the cells of the organoids at a very early stage, including cell stress, damage to DNA and changes in how the DNA is transcribed into proteins. These changes affected those nerve cells and other brain cells known as astroglia, which orchestrate muscle movements and mental abilities.

“Although these initial disturbances were subtle, we were surprised at just how early changes occurred in our human model of ALS/FTD,” added Dr Lakatos. “This and other recent studies suggest that the damage may begin to accrue as soon as we are born. We will need more research to understand if this is in fact the case, or whether this process is brought forward in organoids by the artificial conditions in the dish.”

As well as being useful for understanding disease development, organoids can be a powerful tool for screening potential drugs to see which can prevent or slow disease progression. This is a crucial advantage of organoids, as animal models often do not show the typical disease-relevant changes, and sampling the human brain for this research would be unfeasible.

̽��ֱ��team showed that a drug, GSK2606414, was effective at relieving common cellular problems in ALS/FTD, including the accumulation of toxic proteins, cell stress and the loss of nerve cells, hence blocking one of the pathways that contributes to disease. Similar drugs that are more suitable as medications and approved for human use are now being tested in clinical trials for neurodegenerative diseases.

Dr Gabriel Balmus from the UK Dementia Research Institute at the ̽��ֱ�� of Cambridge, collaborating senior author, said: “By modelling some of the mechanisms that lead to DNA damage in nerve cells and showing how these can lead to various cell dysfunctions, we may also be able to identify further potential drug targets.”

Dr Lakatos added: “We currently have no very effective options for treating ALS/FTD, and while there is much more work to be done following our discovery, it at least offers hope that it may in time be possible to prevent or to slow down the disease process.

“It may also be possible in future to be able to take skin cells from a patient, reprogramme them to grow their ‘mini brain’ and test which unique combination of drugs best suits their disease.”

̽��ֱ��study was primarily funded by the Medical Research Council UK, Wellcome Trust and the Evelyn Trust.

Reference

Szebényi, K et al. Human ALS/FTD Brain Organoid Slice Cultures Display Distinct Early Astrocyte and Targetable Neuronal Pathology. Nature Neuroscience; 21 Oct 2021; DOI: 10.1038/s41593-021-00923-4

Cambridge researchers have developed ‘mini brains’ that allow them to study a fatal and untreatable neurological disorder causing paralysis and dementia – and for the first time have been able to grow these for almost a year.

Not only can we see what may happen early on in the disease – long before a patient might experience any symptoms – but we can also begin to see how the disturbances change over time in each cell

András Lakatos

Andras Lakatos

Mini brain organoids showing cortical-like structures

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Scientists reverse age-related memory loss in mice

sc604 — Thu, 22 Jul 2021 14:18:03 +0000

In a study published in Molecular Psychiatry, the team show that changes in the extracellular matrix of the brain – ‘scaffolding’ around nerve cells – lead to loss of memory with ageing, but that it is possible to reverse these using genetic treatments.

Recent evidence has emerged of the role of perineuronal nets (PNNs) in neuroplasticity – the ability of the brain to learn and adapt – and to make memories. PNNs are cartilage-like structures that mostly surround inhibitory neurons in the brain. Their main function is to control the level of plasticity in the brain. They appear at around five years old in humans, and turn off the period of enhanced plasticity during which the connections in the brain are optimised. Then, plasticity is partially turned off, making the brain more efficient but less plastic.

PNNs contain compounds known as chondroitin sulphates. Some of these, such as chondroitin 4-sulphate, inhibit the action of the networks, inhibiting neuroplasticity; others, such as chondroitin 6-sulphate, promote neuroplasticity. As we age, the balance of these compounds changes, and as levels of chondroitin 6-sulphate decrease, so our ability to learn and form new memories changes, leading to age-related memory decline.

Researchers at the ̽��ֱ�� of Cambridge and ̽��ֱ�� of Leeds investigated whether manipulating the chondroitin sulphate composition of the PNNs might restore neuroplasticity and alleviate age-related memory deficits.

To do this, the team looked at 20-month old mice – considered very old – and using a suite of tests showed that the mice exhibited deficits in their memory compared to six-month old mice.

For example, one test involved seeing whether mice recognised an object. ̽��ֱ��mouse was placed at the start of a Y-shaped maze and left to explore two identical objects at the end of the two arms. After a short while, the mouse was once again placed in the maze, but this time one arm contained a new object, while the other contained a copy of the repeated object. ̽��ֱ��researchers measured the amount of time the mouse spent exploring each object to see whether it had remembered the object from the previous task. ̽��ֱ��older mice were much less likely to remember the object.

̽��ֱ��team treated the ageing mice using a ‘viral vector’, a virus capable of reconstituting the amount of 6-sulphate chondroitin sulphates to the PNNs and found that this completely restored memory in the older mice, to a level similar to that seen in the younger mice.

Dr Jessica Kwok from the School of Biomedical Sciences at the ̽��ֱ�� of Leeds said: “We saw remarkable results when we treated the ageing mice with this treatment. ̽��ֱ��memory and ability to learn were restored to levels they would not have seen since they were much younger.”

To explore the role of chondroitin 6-sulphate in memory loss, the researchers bred mice that had been genetically-manipulated such that they were only able to produce low levels of the compound to mimic the changes of ageing. Even at 11 weeks, these mice showed signs of premature memory loss. However, increasing levels of chondroitin 6-sulphate using the viral vector restored their memory and plasticity to levels similar to healthy mice.

Professor James Fawcett from the John van Geest Centre for Brain Repair at the ̽��ֱ�� of Cambridge said: “What is exciting about this is that although our study was only in mice, the same mechanism should operate in humans – the molecules and structures in the human brain are the same as those in rodents. This suggests that it may be possible to prevent humans from developing memory loss in old age.”

̽��ֱ��team have already identified a potential drug, licensed for human use, that can be taken by mouth and inhibits the formation of PNNs. When this compound is given to mice and rats it can restore memory in ageing and also improves recovery in spinal cord injury. ̽��ֱ��researchers are investigating whether it might help alleviate memory loss in animal models of Alzheimer's disease.

̽��ֱ��approach taken by Professor Fawcett’s team – using viral vectors to deliver the treatment – is increasingly being used to treat human neurological conditions. A second team at the Centre recently published research showing their use for repairing damage caused by glaucoma and dementia.

̽��ֱ��study was funded by Alzheimer’s Research UK, the Medical Research Council, European Research Council and the Czech Science Foundation.

Reference
Yang, S et al. Chondroitin 6-sulphate is required for neuroplasticity and memory in ageing. Molecular Psychiatry; 16 July 2021; DOI: doi.org/10.1038/s41380-021-01208-9

Scientists at Cambridge and Leeds have successfully reversed age-related memory loss in mice and say their discovery could lead to the development of treatments to prevent memory loss in people as they age.

Although our study was only in mice, the same mechanism should operate in humans – the molecules and structures in the human brain are the same as those in rodents. This suggests that it may be possible to prevent humans from developing memory loss in old age

James Fawcett

Michael Shribak, Marine Biological Laboratory, Woods Hole, MA

Spatially oriented neurons (mouse brain)

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Gene therapy technique shows potential for repairing damage caused by glaucoma and dementia

cjb250 — Wed, 31 Mar 2021 18:00:54 +0000

Gene therapy – where a missing or defective gene is replaced by a healthy version – is becoming increasingly common for a number of neurological conditions including Leber’s Congenital Amaurosis, Spinal Muscular Atrophy and Leber’s Hereditary Optic Neuropathy. However, each of these conditions is rare, and monogenic – that is, caused by a single defective gene. ̽��ֱ��application of gene therapy to complex polygenic conditions, which make up the majority of neurodegenerative diseases, has been limited to date.

A common feature of neurodegenerative diseases is disruption of axonal transport, a cellular process responsible for movement of key molecules and cellular ‘building blocks’ including mitochondria, lipids and proteins to and from the body of a nerve cell. Axons are long fibres that transmit electrical signals, allowing nerve cells to communicate with other nerve cells and muscles. Scientists have suggested that stimulating axonal transport by enhancing intrinsic neuronal processes in the diseased central nervous system might be a way to repair damaged nerve cells.

Two candidate molecules for improving axonal function in injured nerve cells are brain-derived neurotrophic factor (BDNF) and its receptor tropomyosin receptor kinase B (TrkB).

In research published today in Science Advances, scientists at the ̽��ֱ�� of Cambridge show that delivering both of these molecules simultaneously to nerve cells using a single virus has a strong effect in stimulating axonal growth compared to delivering either molecule on its own. They tested their idea in two models of neurodegenerative disease known to be associated with reduced axonal transport, namely glaucoma and tauopathy (a degenerative disease associated with dementia).

Dr Tasneem Khatib from the John van Geest Centre for Brain Repair at the ̽��ֱ�� of Cambridge, the study’s first author, said: “ ̽��ֱ��axons of nerve cells function a bit like a railway system, where the cargo is essential components required for the cells to survive and function. In neurodegenerative diseases, this railway system can get damaged or blocked. We reckoned that replacing two molecules that we know work effectively together would help to repair this transport network more effectively than delivering either one alone, and that is exactly what we found.

“This combined approach also leads to a much more sustained therapeutic effect, which is very important for a treatment aimed at a chronic degenerative disease.

“Rather than using the standard gene therapy approach of replacing or repairing damaged genes, we used the technique to supplement these molecules in the brain.”

Glaucoma is damage to the optic nerve often, but not always, associated with abnormally high pressure in the eye. In an experimental glaucoma model, the researchers used a tracer dye to show that axonal transport between the eye and brain was impaired in glaucoma. Similarly, a reduction in electrical activity in the retina in response to light suggested that vision was also impaired.

Dr Khatib and colleagues used ‘viral vectors’ – gene therapy delivery systems – to deliver TrkB and BDNF to the retina of rats. They found that this restored axonal transport between the retina and the brain, as observed by movement of the dye. ̽��ֱ��retinas also showed an improved electrical response to light, a key prerequisite for visual restoration.

Next, the team used transgenic mice bred to model tauopathy, the build-up of ‘tangles’ of tau protein in the brain. Tauopathy is seen in a number of neurodegenerative diseases including Alzheimer’s disease and frontotemporal dementia. Once again, injection of the dye showed that axonal transport was impaired between the eye and the brain – and that this was restored using the viral vectors.

Intriguingly, the team also found preliminary evidence of possible improvement in the mice’s short-term memory. Prior to treatment, the researchers tested the mice on an object recognition task. ̽��ֱ��mouse was placed at the start of a Y-shaped maze and left to explore two identical objects at the end of the two arms. After a short while, the mouse was once again placed in the maze, but this time one arm contained a new object, while the other contained a copy of the repeated object. ̽��ֱ��researchers measured the amount of the time the mouse spent exploring each object to see whether it had remembered the object from the previous task.

This task was repeated after the viral vector had been injected into the mouse’s brain and the results were suggestive of a small improvement in short-term memory. While the results of this particular study did not quite achieve statistical significance – a measure of how robust the findings are – the researchers say they are promising and a larger study is now planned to confirm the effect.

Professor Keith Martin from the Centre for Eye Research Australia and the ̽��ֱ�� of Melbourne, who led the study while at Cambridge, added: “While this is currently early stage research, we believe it shows promise for helping to treat neurodegenerative diseases that have so far proved intractable. Gene therapy has already proved effective for some rare monogenic conditions, and we hope it will be similarly useful for these more complex diseases which are much more common.”

̽��ֱ��research was supported by Fight for Sight, Addenbrooke’s Charitable Trust, the Cambridge Eye Trust, the Jukes Glaucoma Research Fund, Quethera Ltd, Alzheimer's Research UK, Gates Cambridge Trust, Wellcome and the Medical Research Council.

Reference
Khatib, TZ et al. Receptor-ligand supplementation via a self-cleaving 2A peptide-based gene therapy promotes CNS axon transport with functional recovery. Science Advances; 31 Mar 2021; DOI: 10.1126/sciadv.abd2590

Scientists at the ̽��ֱ�� of Cambridge have shown in animal studies that gene therapy may help repair some of the damage caused in chronic neurodegenerative conditions such as glaucoma and dementia. Their approach demonstrates the potential effectiveness of gene therapy in polygenic conditions – that is, complex conditions with no single genetic cause.

[Our] approach also leads to a much more sustained therapeutic effect, which is very important for a treatment aimed at a chronic degenerative disease

Tasneem Khatib

IAPB/VISION 2020

Screening for glaucoma

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Technique to regenerate the optic nerve offers hope for future glaucoma treatment

cjb250 — Thu, 05 Nov 2020 10:00:30 +0000

Axons – nerve fibres – in the adult central nervous system (CNS) do not normally regenerate after injury and disease, meaning that damage is often irreversible. However, over the past decade there have been a number of discoveries that suggest it may be possible to stimulate regeneration.

In a study published today in Nature Communications, scientists tested whether the gene responsible for the production of a protein known as Protrudin could stimulate the regeneration of nerve cells and protect them from cell death after an injury.

̽��ֱ��team, led by Dr Richard Eva, Professor Keith Martin and Professor James Fawcett from the John van Geest Centre for Brain Repair at the ̽��ֱ�� of Cambridge, used a cell culture system to grow brain cells in a dish. They then injured their axons using a laser and analysed the response to this injury using live-cell microscopy. ̽��ֱ��researchers found that increasing the amount or activity of Protrudin in these nerve cells vastly increased their ability to regenerate.

Nerve cells in the retina, known as retinal ganglion cells, extend their axons from the eye to the brain through the optic nerve in order to relay and process visual information. To investigate whether Protrudin might stimulate repair in the injured CNS in an intact organism, the researchers used a gene therapy technique to increase the amount and activity of Protrudin in the eye and optic nerve. When they measured the amount of regeneration a few weeks after a crush injury to the optic nerve, the team found that Protrudin had enabled the axons to regenerate over large distances. They also found that the retinal ganglion cells were protected from cell death.

̽��ֱ��researchers showed that this technique may help protect against glaucoma, a common eye condition. In glaucoma, the optic nerve that connects the eye to the brain is progressively damaged, often in association with elevated pressure inside the eye. If not diagnosed early enough, glaucoma can lead to loss of vision. In the UK, round one in 50 people over the age of 40, and one in ten people over the age of 75 is affected by glaucoma.

To demonstrate this protective effect of Protrudin against glaucoma, the researchers used a whole retina from a mouse eye and grew it in a cell-culture dish. Usually around a half of retinal neurons die within three days of retinal removal, but the researchers found that increasing or activating Protrudin led to almost complete protection of retinal neurons.

Dr Veselina Petrova from the Department of Clinical Neurosciences at the ̽��ֱ�� of Cambridge, the study’s first author, said: “Glaucoma is one of leading causes of blindness worldwide. ̽��ֱ��causes of glaucoma are not completely understood, but there is currently a large focus on identifying new treatments by preventing nerve cells in the retina from dying, as well as trying to repair vision loss through the regeneration of diseased axons through the optic nerve.

“Our strategy relies on using gene therapy – an approach already in clinical use – to deliver Protrudin into the eye. It’s possible our treatment could be further developed as a way of protecting retinal neurons from death, as well as stimulating their axons to regrow. It’s important to point out that these findings would need further research to see if they could be developed into effective treatments for humans.”

Protrudin normally resides within the endoplasmic reticulum, tiny structures within our cells. In this study, the team showed that the endoplasmic reticulum found in axons appears to provide materials and other cellular structures important for growth and survival in order to support the process of regeneration after injury. Protrudin stimulates transport of these materials to the site of injury.

Dr Petrova added: “Nerve cells in the central nervous system lose the ability to regenerate their axons as they mature, so have very limited capacity for regrowth. This means that injuries to the brain, spinal cord and optic nerve have life-altering consequences.

“ ̽��ֱ��optic nerve injury model is often used to investigate new treatments for stimulating CNS axon regeneration, and treatments identified this way often show promise in the injured spinal cord. It’s possible that increased or activated Protrudin might be used to boost regeneration in the injured spinal cord.”

̽��ֱ��research was supported by the Medical Research Council, Fight for Sight, the Bill and Melinda Gates Foundation, Cambridge Eye Trust and the National Eye Research Council.

Reference
Petrova, V et al. Protrudin functions from the endoplasmic reticulum to support axon regeneration in the adult CNS. Nat Comms; 5 Nov 2020; DOI: 10.1038/s41467-020-19436-y

Scientists have used gene therapy to regenerate damaged nerve fibres in the eye, in a discovery that could aid the development of new treatments for glaucoma, one of the leading causes of blindness worldwide.

It’s possible our treatment could be further developed as a way of protecting retinal neurons from death, as well as stimulating their axons to regrow

Veselina Petrova

TobiasD

Eye

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Spinal injury and ‘biorobotic control’ of the bladder

cjb250 — Tue, 16 Feb 2016 13:27:49 +0000

Spinal cord injury is, in many respects, a testosterone disease, says Professor James Fawcett.

What he means by this is that four out of five spinal cord injuries happen to men, and the most common age group is early adulthood. “Men are not good at assessing risk at that age,” he says. “Females are much more sensible.”

It is perhaps not surprising, then, that when asked about their priorities, most quadriplegic people will select a return of sexual function as second after the use of arms and hands. Third on the list, above being able to walk, is a return of bladder and bowel control. “Way down the list is walking, because wheelchairs work reasonably well and patients can get used to using them,” says Fawcett, who heads the John van Geest Centre for Brain Repair at Cambridge.

Restoring bladder and bowel control is a particular challenge, however. Currently, patients have to fill their bladder with botulinum toxin (botox) to paralyse it and catheterise themselves several times a day. This may be the simplest method, but catheterisation can cause infection and scarring in the urethra.

Instead, Fawcett is developing a device based on the ‘Brindley device’, named after physiologist Giles Brindley, who trained at Cambridge after the Second World War. ̽��ֱ��Brindley device is an implant to which an external stimulator is applied manually, causing the bladder to contract and empty itself. It has been used in thousands of patients, but it, too, is not without problems: it necessitates severing sensory nerves from the pelvis into the spinal cord, causing weakening of the pelvic muscles – and loss of sexual function. (For most male patients, Viagra can at least help them maintain an erection, but this is only half the problem. ‘Well OK, doc,’ they say, ‘you’ve given me an erection, but what’s the use if I can’t feel it?’”)

Fawcett and colleagues are developing a ‘biorobotic’ version of the Brindley device that can read signals from the sensory nerves in the pelvis, rather than requiring them to be cut. These signals would stop the bladder emptying itself at embarrassing times, tell the patient how full the bladder is, and allow them to use the electronics to empty it.

̽��ֱ��ability to record signals from individual nerves has applications beyond just bladder control: Fawcett envisioned the technology as enabling patients who had lost a limb – such as soldiers losing arms or legs – to control robotic limbs. “ ̽��ֱ��limbs themselves are quite sophisticated,” he says, “but what doesn’t work at all well is their interface with the nervous system.” ̽��ֱ��technology required for recording signals for a whole limb has proven to be extremely complicated, so the team is looking at the bladder-control device as a simpler demonstration of a proof of concept.

Biorobotics will be one focus of a proposed new Spinal Injury Research Centre to be based at Addenbrooke’s Hospital. Although still at the very early planning stages, the Centre will capitalise on Cambridge’s position as the regional trauma centre for the East of England (even though a lack of facilities means spinal injury patients have to be sent to Stoke Mandeville near Oxford for rehabilitation).

A simplified version of the adapted Brindley device has so far been trialled in around 50 dogs, in whom spinal cord injury is surprisingly common, particularly in dogs with longer spines, such as dachshunds. Many owners of injured dogs want to keep their pets but, as Fawcett explains, “the dogs are perfectly happy to paddle around with wheels under their back legs, but they do so dribbling urine around your house.”

In fact, a randomised controlled trial in 2013 showed that injured dogs may even be able to do away with their wheels. Professor Robin Franklin from the Wellcome Trust-Medical Research Council Cambridge Stem Cell Institute showed that transplanting cells found in the nasal cavity, known as olfactory ensheathing cells, into the injured spine could help restore movement to the previously paralysed limbs. Although the cell transplant did not restore bowel or bladder control, it was, says Franklin, “a landmark study” that offers the promise of translation into humans. Franklin’s colleague Dr Mark Kotter is currently seeking funding to carry out a trial in humans.

But as Fawcett says, the priority among injured patients is to recover use of their upper limbs. Spinal cord injury causes damage to motor nerve fibres travelling from the brain and to sensory nerve fibres travelling to the brain. Both are structurally different and need to be coaxed to regenerate across the site of the injury – but even getting the nerve fibres to span these couple of centimetres is a challenge.

“ ̽��ֱ��problem is scar tissue,” says Fawcett. “It’s very difficult for nerve fibres to grow through this tissue.” He has identified an enzyme, chondroitinase, which can dissolve scar tissue. ̽��ֱ��enzyme works in rats and is in preclinical development for use in humans by the US biotech company Acorda Therapeutics.

Once the scar tissue has been dissolved, the nerve fibres need to regenerate and make new connections. Although restoring motor nerve fibres is proving a challenge, Fawcett has managed to restore sensory nerve fibres in rats, which is an important start. “Patients need to be able to feel what they’re doing and to sense pain. If they turn on a hot tap, they can easily scald themselves if they can’t feel the heat. And of course, they want sensation back in their genitalia.”

In most spinal cord injuries, some nerve fibres will always survive, and Fawcett believes we may be able to harness these to bypass nerve damage if we can harness a remarkable property of the young brain known as plasticity, which enables new connections to be made as we learn new skills. If a young child receives a spinal injury, their chances of recovery are much better than for an adult as their brain can adapt, but as we age, a cartilage-like coating wraps around nerve fibres, cementing the connections in place. These molecules make it difficult for the brain of an injured adult to find a way to bypass the injury.

“Interestingly,” explains Fawcett, “one of the main constituents of this cartilage is the same as that which blocks nerve growth in scar tissue – and we know we can dissolve this using chondroitinase. This should make rehabilitation – teaching the brain to do useful things again – dramatically more successful.”

Inset image: Credit ̽��ֱ��District.

There are many challenges facing people with spinal cord injury – and walking again is often the least of their problems. Cambridge research could help patients take control of their lives once more.

This should make rehabilitation – teaching the brain to do useful things again – dramatically more successfull.

James Fawcett

Zeevveez

Wheelchair

̽��ֱ��text in this work is licensed under a Creative Commons Attribution 4.0 International License. For image use please see separate credits above.

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