Social cognition may exert a central role in the daily lives of MS patients

An international team of multiple sclerosis (MS) researchers showed that longitudinal changes in social cognition are associated with psychological outcomes of daily living, suggesting that x. The article, "Social Cognition in Multiple Sclerosis: A 3-Year Follow-Up MRI and Behavioral Study" (doi: 10.3390/diagnostics11030484) was published on March 9, 2021, in Diagnostics. It is available open access at

The authors are Helen M. Genova, PhD, of Kessler Foundation's Center for Neuropsychology and Neuroscience Research, and Stefano Ziccardi, PhD, Marco Pitteri, PhD, and Massimiliano Calabrese, MD, of the University of Verona. Dr. Genova also has an academic appointment at Rutgers University.

Some recent MS research, including work led by Dr. Genova, has shown that social cognition deficits may affect people with MS who otherwise have no other cognitive impairments. Social cognition, which is required to understand and process the emotions of others, is an extremely important skill set for forming successful relationships with others, and deficits in this area can significantly affect a person's quality of life.

Previous studies investigating the prevalence of social cognition impairment among people with MS suggested that impairment tracked with symptoms such as cognitive fatigue. More research was needed to clarify these results and determine whether changes to the area of the brain called the amygdala–known to be associated with emotions–correlated with social cognition. Moreover, no study had investigated the social cognition performance in people with MS with a longitudinal perspective, meaning that no data existed on the evolution of social cognition deficits over time.

In this three-year follow-up study, MS researchers conducted a longitudinal investigation of the evolution of social cognition deficits and amygdala damage in a group of 26 cognitively-normal people with relapsing-remitting MS. They analyzed the association between social cognition and several domains related to psychological well-being. Concurrently, they investigated the evolution of amygdala lesion burden and atrophy and their association with social cognition performance.

To gather data, the team used a battery of neuropsychological tests; social cognition tasks to assess theory of mind, facial emotion recognition, and empathy; and 3T-MRI to analyze structural amygdala damage. They then compared these findings to baseline data collected from participants three years prior.

The results confirmed that, despite being classified as cognitively normal, people with relapsing-remitting MS showed a significantly lower performance in several social cognition domains as compared to a matched group of healthy controls. These domains include facial emotion recognition, in particular fear and anger, as well as empathy. Longitudinal changes in the social cognition domain were also found to be associated with psychological outcomes of daily living, such as depression, anxiety, fatigue, and social functioning quality of life.

We confirmed the longitudinal stability of social cognition deficits in cognitively-normal people with relapsing-remitting MS, mirroring the amygdala structural damage and psychological well-being. These results confirm that social cognition exerts a key role in MS, affecting individuals' everyday lives. Our research highlights the need to identify treatments to improve social cognition in this population."

Dr. Helen M. Genova, PhD, of Kessler Foundation's Center for Neuropsychology and Neuroscience Research


Kessler Foundation

Journal reference:

Ziccardi, S., et al. (2021) Social Cognition in Multiple Sclerosis: A 3-Year Follow-Up MRI and Behavioral Study. Diagnostics.

Posted in: Medical Research News | Medical Condition News

Tags: Amygdala, Anxiety, Biogen, Brain, Depression, Diagnostics, Disability, Evolution, Eye, Fatigue, Imaging, Laboratory, Medical School, Medicine, Multiple Sclerosis, Neuroimaging, Neuroscience, Research, Sclerosis, Traumatic Brain Injury, Virtual Reality

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How is RRMS Different from PPMS and SPMS?

Multiple sclerosis is a neurodegenerative disorder that damages the nerves in the brain and spinal cord, leading to problems with muscle movement, balance and vision. The illness is an example of a demyelinating disease, where the protective coating called myelin that surrounds nerve fibres becomes damaged.

Multiple sclerosis follows a different course in every individual but there are three main ways in which the disease can progress depending on which form of the illness a patient has.

Relapsing remitting multiple sclerosis

Around 80% of all individuals with multiple sclerosis have the relapsing remitting form of the disease. These individuals have periods where their symptoms are mild or absent (remission), followed by periods of symptom relapse. Symptoms may occur suddenly and in acute bouts or exacerbations.

During these periods of relapse, symptoms may become worse each time and the relapsing remitting form of this condition may eventually progress to secondary progressive multiple sclerosis, where there are few or no periods of remission. Relapsing remitting multiple sclerosis may be diagnosed when two episodes of relapse are separated by more than 30 days or there has only been one relapse but there is MRI evidence of newly scarred or damaged myelin three months later.

Secondary-progressive multiple sclerosis

Patients with this form of multiple sclerosis often experience phases of relapse followed by remission at first, but this later gives way to progressive disease, characterized by worsening symptoms and few or no periods of remission.

Primary-progressive multiple sclerosis

The least common form of multiple sclerosis is the primary progressive form which occurs in about 10% to 15% of all cases and usually in people aged over 40 years. In this form of the condition, symptoms get worse over time rather than occurring in bouts or as sudden attacks.

Primary progressive multiple sclerosis may be diagnosed if there have been no previous symptoms of relapse but the patient has become increasingly disabled over a period of at least one year.



Further Reading

  • All Multiple Sclerosis Content
  • Multiple sclerosis (MS)
  • Multiple Sclerosis Symptoms
  • Multiple Sclerosis Diagnosis
  • Multiple Sclerosis Causes

Last Updated: Aug 23, 2018

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Dr. Ananya Mandal

Dr. Ananya Mandal is a doctor by profession, lecturer by vocation and a medical writer by passion. She specialized in Clinical Pharmacology after her bachelor's (MBBS). For her, health communication is not just writing complicated reviews for professionals but making medical knowledge understandable and available to the general public as well.

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Functions of MHC in the Immune System

The major histocompatibility complex (MHC) is a group of genes that encode proteins on the cell surface that have an important role in immune response.

Credit: Juan Gaertner/

Their main role is in antigen presentation where MHC molecules display peptide fragments for recognition by appropriate T-cells. This is an important process in the immune system response for destroying invading pathogens.

The MHC complex on the cell surface is necessary for cell self-recognition and the prevention of the immune system targeting its own cells. Certain MHC alleles are associated with an increased risk of autoimmune disease such as Hodgkin’s lymphoma and multiple sclerosis.

Another function of the major histocompatibility complex is tissue allorecognition, an important factor in the prevention of successful organ transplantation.

MHC and antigen presentation

The MHC controls how the immune system detects and responds to specific antigens. Antigen specificity of T-cell recognition is controlled by MHC molecules with different antigen presentation between MHC class I and class II molecules.  

The two classes of MHC molecule have a similar function involving the delivery of short peptides to the cell surface for recognition by CD8+ and CD4+ T-cells respectively. MHC class I molecules present antigens that are intracellular or endogenous, whilst MHC class II molecules present antigens that are extracellular or exogenous. The MHC class I complex at the surface of the cell disconnects over time, leading to internalization into the endosome and entrance into the MHC class II pathway.

Cross presentation also occurs where MHC class I molecules present extracellular antigens to CD8+ T-cells. Degradation through autophagy can cause endogenous antigens to be presented by MHC class II molecules. Many viruses have evolved proteins that prevent antigen presentation by MHC molecules through the degradation or mislocalization of MHC molecules. Cross presentation is particularly important for responding to viruses that do not readily infect antigen-presenting cells.

MHC and autoimmunity

Certain MHC molecules are associated with an increased risk of autoimmune and inflammatory diseases. The MHC HLA-B antigens were first found to have increased frequency in patients with Hodgkin’s lymphoma in 1967. Other conditions associated with specific MHC molecules include multiple sclerosis, Crohn’s disease and rheumatoid arthritis.

A pooled analysis of MHC disease associations found that there is shared disease susceptibility to alleles that arise from HLA-DR4 haplotypes, indicating that there is both common and disease-specific associations between MHC and autoimmunity.

The mechanism behind the association between MHC and autoimmune disease has not been fully defined but is potentially reflecting a breakdown in tolerance to self-antigens in abnormal MHC class II molecule antigen presentation. Specific MHC class II alleles are therefore likely determinates of autoantigen targeting, resulting in disease association.

MHC and tissue allorecognition

Allorecognition is the ability of an organism to distinguish its tissues from those of another organism within the same species and has important implications for transplantation. A risk of organ transplantation is the alloresponse, where the histoincompatible antigen is recognized, producing an adaptive immune response via the employment of allospecific T-cells.

This can lead to rejection of the transplanted tissue. The MHC is involved in the direct mechanism of allorecognition where T-cells recognize determinants on the donor MHC molecule-peptide complex displayed at the cell surface. This is because the MHC molecules display an antigenic determinant called an epitope that is either self or non-self, with antigens from the transplanted cells recognized as non-self.  

To prevent an alloresponse in non-tolerant recipients, immunosuppressive drugs are provided but are known to cause long-term adverse effects. Increased understanding of the MHC role in tissue allorecognition may produce future targets for immunomodulation, reducing the requirement for long-term immunosuppression in transplant patients.



  • The major histocompatibility complex and its functions.
  • British Society for Immunology: Antigen Processing and Presentation.
  • Towards a systems understanding of MHC class I and MHC class II antigen presentation.
  • Defining the Role of the MHC in Autoimmunity: A Review and Pooled Analysis.
  • Pathways of major histocompatibility complex allorecognition.

Further Reading

  • All Immunology Content
  • What is Immunology?
  • Classical Immunology
  • Clinical Immunology
  • Developmental Immunology

Last Updated: Aug 23, 2018

Written by

Shelley Farrar Stoakes

Shelley has a Master's degree in Human Evolution from the University of Liverpool and is currently working on her Ph.D, researching comparative primate and human skeletal anatomy. She is passionate about science communication with a particular focus on reporting the latest science news and discoveries to a broad audience. Outside of her research and science writing, Shelley enjoys reading, discovering new bands in her home city and going on long dog walks.

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Medication may improve thinking skills in advanced multiple sclerosis: study

People with the advanced form of multiple sclerosis (MS) called secondary progressive MS who took the drug siponimod for one to two years had improved cognitive processing speed compared to those who did not take the drug, according to a new study published in the December 16, 2020, online issue of Neurology, the medical journal of the American Academy of Neurology.

Cognitive processing speed is the amount of time it takes someone to take in information, process it and then react to solve a problem or complete a task. It can affect many aspects of a person’s daily life including employment, driving skills and social activities.

While most people with MS are initially diagnosed with relapsing-remitting MS, marked by symptom flare-ups followed by periods of remission, most eventually transition to secondary progressive MS, which does not have wide swings in symptoms but instead a slow, steady, worsening of the disease.

“Multiple sclerosis is a neurodegenerative disease, meaning neurons in the brain can break down or die, and this can greatly affect a person’s thinking skills,” said study author Ralph H. B. Benedict, Ph.D., of the University of Buffalo in New York, and a member of the American Academy of Neurology. “While there are currently no drugs on the market in the United States approved for the treatment of cognitive impairment in MS, our study found that siponimod, which is prescribed to slow the progression of physical disability in MS, may also help improve cognitive processing speed in people with advanced MS.”

For the study, 1,651 people with secondary progressive MS with an average age of 48 were followed for up to two years. Two-thirds of the group was prescribed two milligrams a day of siponimod. One-third of the group was prescribed a placebo. All people in the study were given cognitive tests at the start of the study and again every six months.

One of those tests, the Symbol Digit Modalities Test, measures cognitive processing speed. It is widely recognized as a particularly sensitive and reliable test in MS studies. The person taking the test is given a key of symbols matched to numbers. They are then shown a series of symbols and must say the corresponding number for each symbol as quickly as possible. The test result is the number of items correctly answered in 90 seconds.

Researchers found that on average the group of people taking siponimod improved their scores on this test after one year, 18 months and again at two years, compared to the group of people taking placebo, in whom the score stayed the same.

People taking siponimod had a 28% higher chance of having a sustained improvement of four or more points compared to those taking a placebo. An increase or decrease of four or more points is considered clinically meaningful and is associated with quality of life outcomes and disability progression. People taking siponimod also had a 21% lower chance of having a four-point or lower decrease in score.

Among all participants, 35% of people taking siponimod improved their scores by four or more points compared to 27% of people taking a placebo, 41% taking siponimod had no change compared to 42% taking a placebo, and 25% taking siponimod had lower scores by four or more points compared to 32% of people taking a placebo.

Scores on two other thinking and memory tests did not differ between the two groups.

“We are impressed to see that siponimod may improve cognitive processing speed in people with MS, however more research is needed to confirm our results,” said Benedict.

He cautioned, “Because we did not see changes on two other cognitive tests, more research should further examine how siponimod affects scores on a broader array of thinking and memory tests. This research is needed before prescribing siponimod for cognition can be considered.”

Side effects that occured more frequently in people taking siponimod versus placebo included high blood pressure, higher levels of liver enzymes, eye swelling, shingles and convulsions.

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