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.
Stroke: Post-stroke injection could prevent brain damage during life-saving treatment
Scientists in the US have developed an injection that could protect the brain during post-stroke treatment.
When a person has a stroke, physicians must restore blood flow to the brain as quickly as possible to save their life. But, that same rush of blood can also trigger a second wave of damage, killing brain cells, fuelling inflammation and increasing the odds of long-term disability.
Now, Northwestern University scientists have developed an injectable regenerative nanomaterial that helps protect the brain during this vulnerable window.
In a new preclinical study, the team delivered a single intravenous dose, immediately after restoring blood flow, in a mouse model of ischemic stroke, the most common type of stroke.
The therapy successfully crossed the blood-brain barrier to reach and repair brain tissue. The material significantly reduced brain damage and showed no signs of side effects or organ toxicity.
The findings suggest the new therapy could eventually complement existing stroke treatments by limiting secondary brain injury and supporting recovery.
Dr. Ayush Batra, Associate Professor for neurology and pathology at Northwestern University Feinberg School of Medicine, said: “Any treatment that facilitates neuronal recovery and minimizes injury would be very powerful, but that holy grail doesn’t yet exist. This study is promising because it’s leading us down a pathway to develop these technologies and therapeutics for this unmet need.”
The injectable therapy is based on supramolecular therapeutic peptides (STPs), a platform developed by Northwestern’s Samuel Stupp.
A study published in 2021 in the journal Science demonstrated the use of an STP technology — nicknamed “dancing molecules” — because of the dynamic nature of its therapeutic agents that could reverse paralysis and repair tissue in mice after a single injection at the site of severe spinal cord injury.
The new study found scientists can administer similar dynamic assemblies of molecules intravenously, without requiring surgery or an invasive injection directly into the brain.
“One of the most promising aspects of this study is that we were able to show this therapeutic technology, which has shown incredible promise in spinal cord injury, can now begin to be applied in a stroke model and that it can be delivered systemically,” said Stupp, co-corresponding author of the study.
Multiple Sclerosis: UCL identifies two types of MS using AI
Artificial intelligence has identified two biologically distinct types of multiple sclerosis (MS), in research led by University College London.
During the study involving 634 patients, scientists looked at blood levels of a protein called serum neurofilament light chain (sNfL). The protein indicates the level of nerve cell damage and acts as a useful measure of how active the disease is.
These sNfL levels were combined with magnetic resonance imaging (MRI) brain scans, which showed the level of disease spread, and interpreted by a UCL-developed machine learning model, called SuStaIn (Subtype and Stage Inference).
The results revealed two distinct types of MS: early sNfL and late sNfL.
In the first type appears to be more aggressive and active, with patients having high levels of sNfL early on in the disease, along with visible damage to a part of the brain called the corpus callosum. Patients in this group also developed brain lesions quickly.
In the second type, patients showed brain shrinkage in areas like the limbic cortex and deep grey matter before sNfL levels went up. This type seems to be slower, with overt damage happening later.
Researchers say the breakthrough will enable doctors to predict much more precisely which patients are at higher risk of developing new brain lesions, paving the way for more personalised care.
Lead author of the study, Dr Arman Eshaghi (UCL Queen Square Institute of Neurology and UCL Hawkes Institute in UCL Computer Science) said: “MS is not one disease and current subtypes fail to describe the underlying tissue changes, which we need to know to treat it.
“By using an AI model combined with a highly available blood marker with MRI, we have been able to show two clear biological patterns of MS for the first time. This will help clinicians understand where a person sits on the disease pathway and who may need closer monitoring or earlier, targeted treatment.”
Parkinson’s disease: Protein discovery by Yale scientists could lead to new treatments
Two proteins found on the surface of motor neurons in the brain may be essential in the progression of Parkinson’s disease, according to a new study.
Parkinson’s disease is a neurodegenerative condition where neurons in the brain slowly die. This process is caused by the accumulation of a misfolded protein called α-synuclein, which spreads from neuron to neuron.
The mechanism by which α-synuclein spreads among cells, however, remains unknown. Now, research by the Yale School of Medicine suggests that two membrane proteins—mGluR4 and NPDC1—are major players in transporting misfolded α-synuclein into healthy neurons after it escapes from dying neurons.
The finding could help develop more effective treatments for Parkinson’s disease, according to senior author Stephen Strittmatter.
Misfolded α-synuclein is “the pathologic hallmark of Parkinson’s disease,” he said.
“If we understood how it gets into neurons, we could perhaps block or slow down the progression of the disease,” he added.
People with Parkinson’s disease often experience motor issues, which are caused by the accumulation of misfolded α-synuclein in motor cells in the brain. As this protein spreads between neurons, symptoms worsen.
One way α-synuclein could enter new cells is by binding to surface proteins. To determine whether this was the case, the team at Yale created 4,400 batches of cells, each expressing different cell surface proteins, and observed whether they bound to misfolded α-synuclein.
Most cell surface proteins did not, but 16 did, including two found in the human dopamine neurons of the substantia nigra, a region of the brain that degenerates in Parkinson’s disease. The researchers found that these two, called mGluR4 and NPDC1, transported misfolded α-synuclein into the cell.
These results suggested to researchers that the two proteins could be involved in moving α-synuclein from neuron to neuron. To test this, the researchers genetically modified mice to have non-functional copies of either mGluR4 or NPDC1 and then introduced misfolded α-synuclein.
In regular mice, misfolded α-synuclein accumulated in their brains once introduced, and the mice developed Parkinson’s-like symptoms. But mice without working mGluR4 or NPDC1 did not. The researchers also found that knocking out the genes for these two cell surface proteins in a mouse model of Parkinson's disease helped reduce the risk of death and progression of symptoms.
The findings offer a potential avenue for treating Parkinson’s disease, Strittmatter said.
Alzheimer’s disease: New way to prevent TBIs triggering Alzheimer’s identified
University of Virginia School of Medicine researchers have uncovered a potential approach to preventing Alzheimer’s occurring in patients following a traumatic brain injury (TBI).
John Lukens, director of UVA’s Harrison Family Translational Research Center in Alzheimer’s and Neurodegenerative Diseases, and his collaborators found that a single mild TBI brings about harmful changes in the brain that facilitate the onset of Alzheimer’s.
They were able to prevent those changes in lab mice by using a hollowed-out virus to deliver repair supplies into the brain’s protective membranes.
“Our findings indicate that fixing brain drainage following head trauma can provide a much-needed strategy to limit the development of Alzheimer’s disease later in life,” said Lukens.
“Our hope is that these discoveries will inspire the design of novel brain drainage-boosting therapeutics that can be deployed to accelerate recovery of the injured brain and limit the risk of developing Alzheimer’s disease.”
Traumatic brain injuries are known to increase the risk for Alzheimer’s and other neurodegenerative diseases significantly, but scientists have had little understanding of why.
Lukens’ research suggests that such injuries impair the function of lymphatic vessels that connect the brain and the immune system.
These vessels, located in the brain’s protective membranes (or “meninges”), were thought not to exist until they were discovered by UVA neuroscience researchers in 2015. Now the vessels are known to play a vital role in cleaning and protecting the brain.
The research suggests TBI accelerates the accumulation of harmful tau protein associated with Alzheimer’s disease, and that these tau tangles are not necessarily confined to the site of the injury. In lab mice, a single mild TBI worsened overall brain health and spurred neurodegeneration.
The scientists were able to identify specific effects caused by mild TBI, including harmful changes to the activity of immune cells called macrophages that act as brain defenders and debris removers.
“This research builds on our understanding of some of the devastating long-term outcomes after brain injury and how they pertain to neurodegenerative disease,” said Ashley Bolte, a medical doctor at UVA and member of the research team. “Traumatic brain injury is a condition where we have very few medical interventions currently, so a prospective therapeutic target is very exciting.”
The scientists found they could act within 24 hours of an injury to protect the brain and restore the function of the vital lymphatic vessels. They used a hollowed-out virus shell to deliver a substance called VEGFC directly into the meninges.
This “lymphatic growth factor” is naturally produced in the body to promote vessel growth and repair, and administering it to the meninges prevented harmful tau production.
More research will be needed before the approach could be used as a treatment in people, but the scientists say it holds exciting promise for preventing TBI-related neurodegeneration.