Author: Rachael Hansford

Tecfidera lowers risk of first MS symptoms in RIS

Treatment with Tecfidera (dimethyl fumarate) significantly reduces the risk of experiencing the first multiple sclerosis (MS) symptoms in adults with radiologically isolated syndrome (RIS), according to data from a Phase 4 clinical trial which may lead to changes in practice.

RIS is a condition in which patients have MS-like lesions on MRI scans, but lack typical symptoms of the disease.

This is the first clinical trial demonstrating the benefit of disease-modifying therapies (DMTs) in people with RIS — the “earliest detectable pre-clinical phase of multiple sclerosis,” Darin Okuda, MD, the trial’s principal investigator, said in an oral presentation at the 38th Congress of the European Committee for Treatment and Research in Multiple Sclerosis (ECTRIMS).

Okuda is a Professor of Neurology and the Director of the MS and Neuroimmunology Imaging Programme, as well as Director of the Neuroinnovation Programme, at University of Texas Southwestern Medical Center, in Dallas, US.

The trial’s results, “Multi-center, randomized, double-blinded assessment of dimethyl fumarate in extending the time to a first clinical demyelinating event in radiologically isolated syndrome (ARISE),” were shared by Okuda at the ECTRIMS 2022 Congress, held October 26–28, both virtually and in Amsterdam, Netherlands. Biogen, which developed and markets Tecfidera as a DMT, funded the trial.

EMD Serono highlights new data for Evobrutinib

First BTKi to demonstrate sustained clinical benefit for people with RMS through three and a half years of treatment

  • Phase II clinical trial data of evobrutinib demonstrated low disease activity and stable EDSS, with NfL levels, a marker of neuronal injury, remaining low in people with RMS after three and a half years of therapy
  • Late-breaking data showed evobrutinib-treated patients mounted an antibody response to mRNA COVID vaccinations similar to that of healthy subjects
  • Evobrutinib is an investigational highly-selective, oral, CNS-penetrant BTK inhibitor with the potential to become a best-in-class treatment option for people living with RMS

EMD Serono, the Healthcare business sector of Merck KGaA, Darmstadt, Germany, in the US and Canada, announced on 26th October 2022 findings which demonstrated that annualised relapse rates (ARR) remained low and Expanded Disability Status Scale (EDSS) scores were stable in people with relapsing multiple sclerosis (RMS) treated with investigational evobrutinib through more than three and half years. Additionally, the number of T1 gadolinium-enhancing (Gd+) lesions and T2 lesion volume remained low for the duration of the open-label extension (OLE) of the Phase II clinical trial. These data, presented at the 38th Congress of the European Committee for Treatment and Research in Multiple Sclerosis (ECTRIMS), suggest the long-term positive benefits of evobrutinib for people with RMS as a potential best-in-class therapy.

Evobrutinib is an oral, highly selective, central nervous system (CNS) penetrant immunomodulator that has the potential to become a safe and highly efficacious treatment option for RMS by addressing both peripheral and central drivers of inflammation through inhibition of Bruton’s tyrosine kinase (BTK) signaling in B cells as well as microglia. The dual-faceted approach of evobrutinib may offer better control of silent progression of the disease in between attacks on top of strong relapse control in people living with RMS.

Disease progression is a top concern in the MS community. Learning more about silent disease progression without relapses will help us further our understanding of MS, along with potential treatments, as it has not just physical but also cognitive and mental deleterious impact. In this longest-running and most extensive analysis of any BTK inhibitor in development for RMS, evobrutinib maintained disease stability for up to three and half years. It also has the potential to directly address smoldering inflammation in RMS which contributes to the silent causes of disease progression. It has previously shown promising results in targeting central inflammation, including through its modulatory effects on microglia.

Patrick Vermersch, MD, PhD, Vice President, Research in Biology and Health, University of Lille

The OLE of the Phase II clinical trial evaluated the long-term treatment effect of evobrutinib on ARR, EDSS scores and several magnetic resonance imaging (MRI) outcomes, in people with RMS:

  • Patients assigned to the initial 75mg twice-daily arm, maintained a low ARR of 0.13 throughout the course of the OLE. In addition, switching from 75mg once-daily to 75mg twice-daily in the OLE reduced ARR from 0.19 to 0.09
  • Overall, mean EDSS scores, as well as MRI lesion activity remained low and stable throughout the entire study

These data points further strengthen the observations made previously that maximal BTK occupancy throughout the dosing interval achieved with twice-daily dosing is correlated to higher ARR reductions with evobrutinib.

The Company also presented new long-term data from the Phase II clinical trial OLE which found reductions of blood neurofilament light chain (NfL) levels, a key biomarker which may predict future brain volume loss and disease progression. Patients experienced sustained and ongoing reductions in blood NfL levels compared to the double-blind period (DBP) and OLE baseline values. A dose of 75mg twice-daily significantly reduced NfL levels from week 12 (DBP), compared to placebo/evobrutinib 25mg once-daily showing an early dose-response. This reduction in NfL provides evidence evobrutinib may reduce neuronal damage in people with RMS.

“This is the first time that evidence of sustained efficacy out to three and a half years could be shown with a BTK inhibitor in RMS,” said Jan Klatt, Senior Vice President, Head of Development Unit Neurology and Immunology, Merck KGaA, Darmstadt, Germany. “Combined with our previous data demonstrating reduced volume of slowly expanding lesions, indicative of an effect on microglia, and reduced neurofilament levels, a marker of neuronal injury, we are confident evobrutinib has the potential to offer best-in-class efficacy for people living with RMS.”

Late-breaking data from a post hoc analysis of vaccinated patients (n=24) in the Phase II OLE were also presented, showing 96% of people with RMS treated with evobrutinib (75mg twice daily) were able to mount an antibody response following two doses of an mRNA COVID-19 vaccine, similar to untreated RMS patients and healthy subjects. The increase in antibody response in seronegative and seropositive patients demonstrated a preserved response to novel and recall antigens. This is the first time this could be shown with a BTK inhibitor in RMS and these findings are consistent with the modulation of B cell function, providing a potentially alternative treatment to B cell depletion approaches.

About Evobrutinib
Evobrutinib is an oral, highly selective CNS-penetrant inhibitor of Bruton’s tyrosine kinase (BTK) in clinical development as a potential treatment for relapsing multiple sclerosis (RMS). It is the first BTK inhibitor to demonstrate clinical efficacy in the largest Phase II study with follow-up beyond three years as well as demonstrate an impact on early biomarkers of ongoing central inflammation that correlate with disease progression. Evobrutinib is designed to modulate B cell responses such as proliferation and antibody and cytokine release, as well as modulate macrophage/microglia activation. It significantly reduced SEL volume and levels of blood NfL, markers of ongoing central inflammation and neurodegeneration that predict long-term disability. Evobrutinib was optimized for efficacy through the most comprehensive BTK inhibitor dose-finding study in RMS which demonstrated 75mg twice-daily dosing achieves maximal efficacy across endpoints by sustaining BTK inhibition throughout the dosing interval (>95% BTK occupancy maintained in 98% of patients before next dose). It is currently under clinical investigation and is not approved for any use anywhere in the world.

About the Open-Label Extension (OLE) Phase II Clinical Trial
In the 48 week double-blind period (DBP), patients with RMS were assigned to one of five treatment groups: placebo (switching to 25mg once-daily evobrutinib after 24 weeks), 25mg or 75mg once-daily evobrutinib, 75mg twice-daily evobrutinib, or open-label dimethyl fumarate (120mg twice daily for the first week and 240mg twice daily thereafter). At week 48, patients could enter the OLE and received evobrutinib 75mg once daily for a mean time of 49.8 weeks before switching to 75mg twice daily for the remainder of the OLE.

Laser Therapy for Epilepsy now available on the NHS

NHS England has accepted the recommendation of the Clinical Priorities Advisory Group to roll out LITT (laser interstitial thermal therapy) on the NHS. LITT is a laser treatment for epilepsy offering a less invasive alternative to conventional neurosurgery. It is a stereotactic procedure with the potential for seizure reduction results similar to those of open resection, with fewer side-effects or complications.

LITT allows for individualised neurological treatment with a small wound, a much faster recovery time, less pain, and minimal risk of infection, adverse neurocognitive deficits, or other side effects.

This pioneering laser beam treatment for epilepsy patients is life-changing and will offer hope to hundreds of people every year who have not had success in preventing seizures with traditional drugs. By replacing invasive neurosurgery with a cutting-edge laser therapy, allowing clinicians to better target the parts of the brain causing the epilepsy, we not only dramatically reduce risks to these patients, but drastically reduce their recovery time both in and out of hospital.

The treatment is yet another example of how the NHS continues to deliver on its NHS Long Term Plan commitment to secure the latest medical innovations for patients while also using our commercial means to ensure value for money.

Professor Sir Stephen Powis, NHS national medical director

Find the clinical commissioning policy here.

AssistiveTech in the UK

Ecosystem Overview and ATLAS Advocacy Launched in House of Lords

AssistiveTech poised for rapid growth in the UK, tackling key socio-economic challenges.

The official launch event and key findings of the new ‘AssistiveTech in the UK’ interactive report, developed by ATLAS (Assistive Technology, Longevity and Ageing Society) with the support of Aging Analytics Agency and Deep Knowledge Philanthropy was launched in the House of Lords on Tuesday October 4th, 2022.

The event brought together key industry and ecosystem participants, thought leaders, founders of AssistiveTech and AgeTech organisations across governance, policy, charity, academia and industry in a bid to harness the power of technology for social good.

Co-launched with the report was UK-based advocacy initiative, ATLAS, which seeks to help inform and guide the public and private sectors to embrace the UK’s growing Assistive tech, Longevity and Agetech industries.

TLAS’ analysis depicts five segments of companies within AssistiveTech in the UK: Assistive Care Services, Devices and Apps, Education and Consulting, Tech-Enabled Home Care, and Smart Homes technologies.

The report provides insights on numerous AssistiveTech ecosystem participants and stakeholders, major trends and obstacles, and highlights the government’s developmental role in this emerging ecosystem.

Study reveals high neurodegenerative risk among former international rugby players

A study led by the University of Glasgow has revealed the first major insights into lifelong health outcomes in former international rugby union players.

In findings published in the Journal of Neurology, Neurosurgery and Psychiatry, the researchers found that former international rugby players had an approximately two and a half times higher risk of neurodegenerative disease than expected, with risk of disease varying by subtype, but not by player position.  

Led by Consultant Neuropathologist Prof Willie Stewart, Honorary Professor at the University of Glasgow, the research team compared health outcomes among 412 male, Scottish, former international rugby players and over 1,200 matched individuals from the general population.

The results showed that while age at death was slightly higher among former rugby players, they were also at higher risk of a neurodegenerative disease diagnosis compared to their matched controls. This risk varied by disease subtype ranging from around a doubling of risk of a dementia diagnosis, to an over 10-fold risk of motor neuron disease diagnosis.

In their previous findings from the landmark FIELD study, which was funded by The Football Association and The Professional Footballers Association, the research team reported the first data on neurodegenerative risk among former professional footballers.  

The current study is a continuation of this ground-breaking research into brain health outcomes among former contact sports athletes, and represents the largest study to date looking in this detail at neurodegenerative disease risk among former rugby players.

Prof Willie Stewart said: “This latest work under our FIELD program of research demonstrates that risk of neurodegenerative disease is not isolated to former footballers, but also a concern for former rugby players.

This latest work under our FIELD program of research demonstrates that risk of neurodegenerative disease is not isolated to former footballers, but also a concern for former rugby players. As such, this study provides further insight into the association between contact sports and neurodegenerative disease risk. Of particular concern are the data on motor neuron disease risk among our rugby players, which is even higher than that for former professional footballers. This finding requires immediate research attention to explore the specific association between rugby and the devastating condition of motor neuron disease.

Prof Willie Stewart

The study also found that, although rugby union players had a higher risk of death overall from neurodegenerative disease, they were less likely to die of respiratory disease. And while deaths in former rugby players were lower than expected up to age 70, they was no difference to matched population controls over that age.

Dr Emma Russell, researcher at the University of Glasgow and first author on the study, said: “An important aspect of this work has been the ability to look across a range of health outcomes in former professional rugby players, allowing us to build a clear picture of health in this population.

Our data show that, in contrast to our previous findings in former professional football players, rugby players do not appear to benefit from a reduced risk of death due to cardiovascular disease or cancer, suggesting the possibility of sport-specific influences on lifelong health.

Dr Emma Russell

The study used national electronic health records on death certificates, data on hospitalisation and dispensed prescribing for dementia and causes of death in Scottish former international rugby union players. Players included were all aged 30 years or over at the end of 2020. The final cohort for analysis comprised 412 former international rugby players and a comparison group of 1,236 matched members of the general population.

In parallel work, also led by Professor Stewart, a specific pathology linked to brain injury exposure, known as chronic traumatic encephalopathy (CTE), has been described in a high proportion of the brains of former contact sport athletes, including former rugby players.

Professor Stewart said: “Taking these new results in rugby, together with our pathology work and previous FIELD studies in football, the risk exposure of concern must remain repetitive head impacts and head injuries. As such, precautionary approaches should be adopted to reduce unnecessary head impacts and better manage head injuries across all contact sports.”

The paper ‘Neurodegenerative disease risk among former international rugby union players.’ is published in Journal of Neurology, Neurosurgery and Psychiatry, and also includes funding from The US National Institutes of Neurological Disorders and Stroke and NHS Research Scotland.

NICE publishes draft guidance on access to Duchenne treatment Translarna

NICE has published draft guidance stating that although Translarna (also known as ataluren) is clinically effective and an innovative treatment, there is doubt as to its cost effectiveness. NICE’s draft recommendation is that people currently receiving Translarna should continue to have access to it until they and their NHS clinician consider it appropriate to stop, but that it shouldn’t be provided for new patients after January 2023.

On 30 September 2022, NICE published its draft guidance on Translarna (also known as ataluren). Translarna is used to treat Duchenne muscular dystrophy with a nonsense mutation in the dystrophin gene and is currently available through a Managed Access Agreement (MAA), which ends in January 2023. Duchenne muscular dystrophy affects around 2,500 people in the UK, and it is estimated that approximately 10% of these people carry a nonsense mutation in the dystrophin gene. 

The draft guidance recognises the clinical effectiveness of Translarna and that the treatment is likely to slow the progression of Duchenne muscular dystrophy. It also recognises that Translarna has a positive impact on the lives of people receiving it and on caregivers. However, at this stage NICE is concerned about the cost effectiveness of the treatment.

This has led to the draft guidance recommending that while anyone currently receiving Translarna should continue to do so after the MAA ends in January 2023, the NHS should not provide the treatment to newly diagnosed patients after that date. This draft recommendation is now subject to consultation until 21 October 2022, with a final decision likely by January 2023. 

NICE guidance is usually mirrored in Wales and Northern Ireland. In Scotland, Translarna is available through the ultra-orphan pathway until early 2024.

The uncertainties around the cost-effectiveness of Translarna highlighted in the draft guidance include how quality-of-life differences between people receiving Translarna and other people with Duchenne muscular dystrophy are measured, how caregivers’ quality of life is measured, and the age at which people are likely to start receiving Translarna.

Action Duchenne, MDUK and Duchenne UK will be submitting a joint response to the NICE consultation and will shortly highlight key areas of input needed.

Take part in the NICE consultation by visiting the ataluren section of the NICE website

Related articles

First Publication of Real-World Data Showing Translarna (ataluren) Significantly Preserves Ability to Walk for Longer in Children with Duchenne Muscular Dystrophy | ACNR

What is the role for preconception carrier screening in neurology? | ACNR Journal

Investigation of hereditary muscle disorders in the genomic era | ACNR

Sir William Gowers (1845-1915): a centenary celebration, with an examination of his comments on cognitive dysfunction | ACNR

Breakthrough in identifying common neural processes in Parkinson’s disease

New research could lead to treatments that halt the advance of Parkinson’s disease. Study from University of Haifa could have significant implications for how Parkinson’s disease is treated following a breakthrough in identifying common neural processes for the first time.

A new study conducted by University of Haifa has identified processes that may help prevent the spread of Parkinson’s disease. The study, published in NJP Parkinson’s Disease, has for the first time identified neural processes that are common to various different types of the disease. 

The processes relate to the ability of cells to connect to the extracellular matrix and their capacity to create new synopses. Thanks to the use of the innovative Sendai Reprogramming technique, the researchers were able to show for the first time that even in sporadic Parkinson patients for which no animal model has yet been developed, these processes are also impaired. 

Parkinson’s patients suffer from massive loss of nerve cells in the area of the brain known as the Substantia nigra, which is packed with dopaminergic neurons. Dopamine is required in the process of transfer of messages between brain cells and plays a key role in the ability to perform motor actions properly. One of the problems in the research – and development of drugs – is the fact that only 15 percent of Parkinson’s cases are caused by known genetic factors, while 85 percent are defined as “sporadic.” Accordingly, it is only possible to create a model for the disease in animals relating to those 15 percent of the cases.

Most of the current studies were undertaken on a small number of familiar Parkinson’s mutations caused by genetic factors, since it is not possible to create models for sporadic forms of the disease. Thanks to the ability to create induced pluripotent stem cells for patients with “sporadic” disease, we managed to show for the first time the presence of impaired neural and cellular mechanisms in a similar manner across all the types of disease we examined.

Study author Dr. Shani Stern, a senior lecturer at the University’s Sagol Department of Neurobiology.

In recent years, however, a method has been developed based on the “reprogramming of mature cells into induced pluripotent stem cells.” According to this method, which was used in the current study, the researchers take cells from specific individuals, reprogramme them into stem cells, and then differentiate them as cells of a different type carrying the same genetic load of the individual from whom they were taken.

In the current instance, Dr. Stern along with Prof. Fred Gage from the Salk Institute; Prof. Alexis Brice from ICM, Paris; Prof. Juergen Winkler from FAU, Germany; and Prof. Irit Sagi from the Weizmann Institute worked on skin cell samples taken from nine patients suffering from Parkinson’s disease. 

Some of the patients were diagnosed with genetic mutations while others had the “sporadic” disease. The skin cells were “restored” to stem cells, which the researchers then differentiated into dopaminergic neurons, so that the cells carried the genetic load of each specific patient and were effectively “sick” with the same type of Parkinson’s disease as that participant. The process was also used for four healthy participants constituting a control group. In the second stage, the researchers sequenced the RNA expressed in the dopaminergic cells and prepared an electrophysiological profile of the cells, measuring electric currents and potentials in the nerve cells.

The study found additional evidence of a possible damage to the structures of the extracellular matrix – a decline in the quantity of the proteins that build the matrix – in both the genetic and sporadic form of the disease. It likely leads to the emergence of an unstable structure that in turn causes instability, disconnection, and death in the cells. The researchers also found a decline in the synaptic activity responsible for the transmission of neural messages to the target cells among all the Parkinson’s patients in the study. “It seems that one of the results of the decline in matrix proteins is a decline in synaptic activity and in the ability of the cells to create functional synapses,” Dr. Stern noted.

The dopaminergic neurons we examined were derived from patients through the reprogramming which rejuvenates them into young cells. In other words, we can see changes in the electric activity, genes, and proteins of the extracellular matrix even when the cells are young. This implies that these changes exist in Parkinson’s patients long before they are aware of a disease process that is occurring in their brain. If we perform this sequencing in a young person and find a similar picture to that found among people who have developed Parkinson’s disease, we can assume that this individual will develop the disease at a later stage. 

Dr Stern

“Currently, most of the treatments are intended to prevent the exacerbation of the disease rather than to prevent it. If we can identify the potential to develop Parkinson’s disease at an early stage and develop treatments that can halt the advancement of the disease, we will be able to start preventative treatment at a stage when the nerve cell mortality is limited. This will allow us to significantly slow down the progression of the disease,” Dr. Stern concluded.

AJOVY®▼ (fremanezumab) for treatment of migraine in patients with co-morbid depression

  • Two separate analyses1,2 presented at the Migraine Trust International Symposium (MTIS) demonstrate the effectiveness of AJOVY▼(fremanezumab) for the treatment of migraine in patients with migraine and co-morbid depression
  • Depression and anxiety are common co-morbidities experienced by around half of all patients with migraine3,4  and are associated with more pain, disability and a reduced quality of life1,2
  • AJOVY▼(fremanezumab) has been shown to be an effective migraine preventive treatment in a range of patients including those with depression and anxiety5,6,7

Teva Pharmaceutical  Industries Ltd. announced on 8th September 2022 the results of two studies1,2 presented at the Migraine Trust International Symposium (MTIS) in London, UK, which demonstrate the efficacy of AJOVY▼ (fremanezumab) in migraine patients who also experience depression or anxiety.  AJOVY▼ (fremanezumab) is indicated for the prevention of migraine in adults with at least 4 migraine days per month.8

In both studies, quarterly and monthly dosing of fremanezumab demonstrated efficacy in reducing monthly migraine attacks by more than 50% compared to placebo.1,2 This is an important outcome because psychiatric disorders are a common co-morbidity in patients suffering from migraine. Population-based samples of people with migraine show up to 47% have co-morbid depression, and up to 58% have co-morbid anxiety4 with many patients experiencing both psychiatric conditions.

The first study1 relating to this patient cohort was led by Richard Lipton MD, Department of Neurology, Psychiatry and Behavioural Sciences at Albert Einstein College of Medicine, New York.  This study is an analysis of pooled data from two previous six-month studies: HALO and FOCUS. The new study to be presented at MTIS sets out to analyse the efficacy of quarterly or monthly dosing of fremanezumab versus placebo in people with migraine and one or more psychiatric co-morbidities.1

Results at three months showed that 32% of patients on quarterly fremanezumab (n=61) and 36% of patients on monthly fremanezumab (n=75) achieved a ≥ 50% reduction in monthly-migraine-days (MMD) compared to 19% of those taking placebo (n=42), and that proportion increased after continuing or switching to fremanezumab at month six.1

The second study2 is a sub-analysis of patients from the double-blind, placebo-controlled phase 3b FOCUS study led by Patricia Pozo-Rosich, Vall d’Hebron University Hospital and Vall d’Hebron Institute of Research, Barcelona. The FOCUS study set out to evaluate the efficacy of quarterly or monthly fremanezumab in chronic or episodic migraine patients who had experienced an inadequate response to two to four classes of prior preventive migraine medication. The sub-analysis evaluated treatment efficacy on a sub-group of the migraine patients who had co-morbid depression.2

Reductions were observed in both monthly-migraine-days and monthly-headache-days with both quarterly and monthly fremanezumab compared with placebo. Differences were also seen in patient-reported depressive symptoms using a PHQ-9 questionnaire – a brief self-reporting instrument incorporating recognised depression criteria and other depressive symptoms9 suggesting that effective treatment of migraine can also positively impact depressive symptoms in patients with this co-morbidity.

Clinicians are becoming increasingly aware of the impact that co-morbidities can have on the management of migraine patients. I believe that we need to move towards more personalised treatment decisions that are tailored to the patient’s profile and co-morbidities. As depression and anxiety are commonly associated with migraine, it will be very important for treatments to demonstrate efficacy and safety in migraine patients with these particular co-morbidities.

Dr. Richard Lipton

Details of enrolment progress into the UNITE study were also revealed at MTIS.10 The 28-week study, led by Dr. Richard Lipton and supported by Teva, will be assessing the efficacy and safety of fremanezumab in adult patients with chronic and episodic migraine and major depressive disorder.  

Commenting on the study, Dr. Lipton said: “We are pleased to report that a total of237 patients have so far enrolled in the UNITE study with 19% from the U.S., 61% from Europe, and 20% from the rest of the world. Assessing the efficacy of fremanezumab in patients with migraine and major depressive disorder will help inform treatment decisions to improve care in this important patient population. We look forward to sharing the results in due course.”

Dr. Dieter Schultewolter, Vice President of Global Medical Affairs Neuroscience at Teva, said: “Teva is strongly committed to supporting further research into the role of fremanezumab in managing the full spectrum of migraine patients, including those who suffer from co-morbid depression and anxiety. We see this as an important step towards a much needed personalised treatment approach for people suffering from migraine in the future.” 


  1. Lipton et al. Efficacy of Quarterly and Monthly Fremanezumab in Patients With Migraine and Psychiatric Comorbidities. Abstract accepted for MTIS 2022. MTIS2022-229 
  2. Pozo-Rosich et al. Fremanezumab Efficacy in Migraine Patients With Prior Inadequate Response to ≥3 Preventive Migraine Medication Classes and Depressive Symptoms. Abstract accepted for MTIS 2022. MTIS2022-230
  3. Lanteri-Minet et al. Anxiety and depression associated with migraine: Influence on migraine subjects’ disability and quality of life, and acute migraine management. Pain. 2005; 118: 319- 326.
  4. Minen et al. Migraine and its psychiatric comorbidities. J Neurol Neurosurg Psychiatry. 2016; 87: 741- 749.
  5. Lipton et al. Long-Term Efficacy of Fremanezumab in Patients with Chronic Migraine and Comorbid Moderate to Severe Depression. Presented at the American Academy of Neurology 61st Annual Meeting Philadelphia, Pennsylvania, USA May 4–10, 2019.  P144
  6. Winner et al. Long-Term Efficacy of Fremanezumab in Chronic and Episodic Migraine Patients Who Failed at Least One Prior Migraine Preventive Medication: Results of a 1-Year Study. Presented at the American Headache Society 61st Annual Scientific Meeting, Philadelphia, Pennsylvania, USA July 11–14, 2019. P151
  7. Silberstein et al. Long-Term Efficacy of Fremanezumab in Chronic and Episodic Migraine Patients with Acute Medication Overuse at Baseline: Results of a 1-Year Study. Presented at the American Headache Society 61st Annual Scientific Meeting, Philadelphia, Pennsylvania, USA July 11–14, 2019. P107
  8. Ajovy EU SmPC [accessed 26 August 2022]
  9. PHQ-9 assessment tool. [accessed 26 August 2022]
  10. Lipton et al. A Phase 4 Study of Fremanezumab for Preventive Migraine Treatment in Patients With Major Depressive Disorder: Baseline Patient Characteristics in UNITE.  Abstract accepted for MTIS 2022. MTIS2022-231

About AJOVYq (fremanezumab-vfrm) injection
AJOVY is indicated for prophylaxis of migraine in adults who have at least 4 migraine days per month. AJOVY is available as a 225 mg/1.5 mL single dose injection in a pre-filled syringe or, in some countries, in a pre-filled pen. Two dosing options are available: 225 mg once monthly administered as one subcutaneous injection (monthly dosing), or 675 mg every three months (quarterly dosing), which is administered as three subcutaneous injections. AJOVY can be administered either by a healthcare professional or at home by a patient or caregiver. No starting dose is required to begin treatment. AJOVYq European SmPC can be found here.

▼This medicinal product is subject to additional monitoring. Adverse events should be reported. Reporting forms and information can be found at Adverse events should also be reported to Teva UK Limited on +44 (0) 207 540 7117 or

Blood type may be linked to risk of early stroke

Gene variants associated with a person’s blood type may be linked to their risk of early stroke, according to a new meta-analysis published in the August 31, 2022, online issue of Neurology®, the medical journal of the American Academy of Neurology. The meta-analysis included all available data from genetic studies that included young adult ischaemic stroke, which is caused by a blockage of blood flow to the brain.

“Non-O blood types have previously been linked to a risk of early stroke, but the findings of our meta-analysis showed a stronger link between these blood types with early stroke compared to late stroke, and in linking risk mostly to blood type A,” said study author Braxton D. Mitchell, PhD, MPH, of University of Maryland School of Medicine in Baltimore.

Specifically, our meta-analysis suggests that gene variants tied to blood types A and O represent nearly all of those genetically linked with early stroke. People with these gene variants may be more likely to develop blood clots, which can lead to stroke.

Braxton D. Mitchell

The meta-analysis involved a review of 48 studies on genetics and ischaemic stroke from North America, Europe and Asia. The studies included 16,927 people with stroke and 576,353 people who did not have a stroke. Of those with stroke, 5,825 people had early onset stroke and 9,269 people had late onset stroke. Early onset stroke was defined as an ischaemic stroke occurring before age 60 and late onset stroke was older than 60.

Researchers looked across all the chromosomes to identify genetic variants associated with stroke. They found a link between early stroke and the area of the chromosome that includes the gene that determines A, AB, B or O blood type.

They then divided participants into A, AB, B and O blood types. They compared the prevalence of those blood types in people with early stroke, late stroke and people who did not have a stroke.

Researchers found that people with early stroke were more likely to have blood type A and less likely to have blood type O compared to people with late stroke and people without stroke. Both early and late stroke were also more likely to have blood type B compared to controls.

When looking at people of European ancestry and comparing 5,825 people with early stroke to 29,320 people who did not have a stroke, the meta-analysis found that 48% of people with early stroke had blood type A compared to 45% of people with late stroke and 44% of people without stroke. They also found 35% of people with early stroke had blood type O compared to 39% of those with late stroke and 41% of people without stroke.

After adjusting for sex and other factors, researchers found those who had blood type A had a 16% higher risk of having an early stroke than people with other blood types. Those who had blood type O had a 12% lower risk of having a stroke than people with other blood types.

“This work deepens our understanding of early onset stroke development and changes,” said Jennifer Juhl Majersik, MD, MS, of the University of Utah and Fellow of the American Academy of Neurology, who wrote an editorial accompanying the study. “Future research is needed to help develop a more precise understanding of how stroke develops. This could lead to targeted preventative treatments for early onset stroke, which could result in less disability during people’s most productive years.”

A limitation of the study was the limited amount of diversity among participants, although 35% of the participants were of non-European ancestry.

The study was supported by the National Institutes of Health and Department of Veterans Affairs.