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.

Multiple Sclerosis: New trial to test vaccine against common virus to treat MS

A new clinical trial will test whether vaccination against a common virus found in almost all people with multiple sclerosis (MS) could help treat the condition.

Researchers at the University of Edinburgh will initially evaluate the safety of the vaccine, which aims to support the body’s immune response to the Epstein-Barr virus (EBV), while also examining its potential effect on new MS disease activity.

Targeting the virus could offer a possible new treatment strategy for MS, but further evidence is needed to determine the approach’s safety and effectiveness, experts say. 

EBV infects more than 90% of people in the UK. It usually causes no symptoms but can lead to glandular fever. Once infected, the virus remains hidden in the body for life but can become active again. 

The investigational vaccine aims to help train the immune system to keep the hidden virus, which is thought to be a potential underlying cause of MS, suppressed.

Professor David Hunt, National Chief Investigator for the trial and Director of the MS and Neuroimmunology Hub at the Anne Rowling Clinic said: “This is an important and innovative trial to treat multiple sclerosis by targeting EBV infection using a vaccine. Currently, almost all of our disease-modifying treatments for multiple sclerosis work by suppressing the body’s immune system. The discovery that EBV plays an important role in the development of multiple sclerosis is opening new avenues for treating the condition.”

The University of Edinburgh is leading the Horizon trial in the UK, with pharmaceutical firm Moderna sponsoring the research.

Up to 10 UK sites will participate, recruiting patients as part of a global cohort of 180 people.

Alzheimer’s disease: Research could help Alzheimer’s patients remember loved ones

A US study may have uncovered why people with Alzheimer’s disease no longer recognise their loved ones, offering fresh hope for new treatments.

Scientists from the University of Virginia School of Medicine say the breakdown of protective barriers in the brain, known as perineuronal nets, causes patients to forget their family and friends.

They found that lab mice with damaged nets lost their “social memory” or the ability to recognise familiar mice, even though they could still form new memories and distinguish between familiar objects in their surroundings.

This pattern closely mirrors what happens in people with Alzheimer’s, where social memory often fades before object memory.

“Finding a structural change that explains a specific memory loss in Alzheimer’s is very exciting,” said Sontheimer, chair of UVA’s Department of Neuroscience and member of the UVA Brain Institute. “It is a completely new target, and we already have suitable drug candidates in hand.”

Building on this discovery, UVA’s Harald Sontheimer and his colleagues tested whether MMP inhibitors – a class of drugs already being studied for their potential to treat cancer and arthritis – could prevent the loss of perineuronal nets.

The treatment worked, preventing further damage and helping the mice keep their memories of one another.

“In our research with mice, when we kept these brain structures safe early in life, the mice suffering from this disease were better at remembering their social interactions,” said Lata Chaunsali, another study author.

Turning these discoveries into a treatment will take time and further study, but Sontheimer is optimistic.

“Although we have drugs that can delay the loss of perineuronal nets, and thereby delay memory loss in disease, more research needs to be done regarding safety and effectiveness of our approach before this can be considered in humans,” he said.

MND: New drug could significantly slow MND progression, scientists say

UK scientists have discovered a new drug that they say could substantially slow the progression of motor neuron disease (MND).

The drug, known as M102, works by protecting nerve cells damaged by MND.

In pre-clinical trials, researchers at the University of Sheffield’s Institute for Translational Neuroscience (SITraN), preserved muscle function in mice with MND, improving movement, gait, and nerve function.

The drug also protected motor neurons grown in the laboratory from damage caused by MND patient cells known as astrocytes.

The findings, published in the journal Molecular Neurodegeneration, suggest M102 could significantly extend length and quality of life for people living with MND.

Professor Dame Pamela Shaw, Director of SITraN and lead investigator of the study, said: “MND is one of the cruellest diseases, robbing people of their mobility and independence often at an alarming speed. We are now at a point where scientific understanding is finally catching up. Our discovery of M102 gives real hope that we can substantially slow the progression of this disease.”

M102 works by activating two major protective systems inside cells — called NRF2 and HSF1.

Together, these systems help nerve cells combat stress, reduce inflammation, improve energy generation and clear away damaged proteins — all of which are known to contribute to motor neuron injury in MND.

The University of Sheffield has partnered with Aclipse Therapeutics, a biotech company based in the United States, to conduct the research.

The team will enter clinical trials in humans once funding has been secured.

Parkinson’s and Alzheimer’s: Scientists discover common brain signalling pathway in both diseases

A study has identified a shared molecular pathway in Parkinson’s and Alzheimer’s, improving understanding of how symptoms of both diseases are produced.

Researchers at the Okinawa Institute of Science and Technology (OIST) investigated how brain cell communication across synapses in the brain is disrupted by disease-related protein buildup.

They found a pathway that interferes with synaptic vesicle recycling, the process by which small sacs called vesicles store and release neurotransmitters, the brain’s chemical messengers.

First author Dr. Dimitar Dimitrov of OIST's Synapse Biology Unit said: “Synapses are communication hubs in the brain involved in different neuronal circuits controlling different functions.

“Therefore, protein accumulation in synapses of one neuronal circuit may impact memory, while in another it may impair motor control. This helps to explain how a shared mechanism of synaptic dysfunction can lead to the distinct symptoms of both Alzheimer’s and Parkinson’s diseases.” 

For sustained signalling, vesicles must be retrieved from the cell membrane, refilled with neurotransmitters, and then reused.  

In this study, the researchers identified a molecular cascade which interrupts this process, disrupting normal brain function.  

“When disease-related proteins accumulate in brain cells, they cause over-production of protein filaments called microtubules, which are normally essential in cell structure and function,” explained Dr. Dimitrov.

“When over-produced, these microtubules trap a protein called dynamin, which is responsible for the retrieval of emptied vesicles from cell membranes, playing a crucial role in vesicle recycling. With less dynamin, vesicle retrieval and recycling slow, thereby interrupting signalling and communication between brain cells.”