Researchers investigate platelet dysfunction in multiple sclerosis
Why does increased thromboembolic activity of platelets occur in multiple sclerosis? Scientists are conducting research that can help clarify this issue.
According to the researchers, in the future understanding these processes may help in the treatment of one of the most common neurological diseases.
According the World Health Organization (WHO) estimates, approx. 2.3 million people worldwide suffer from multiple sclerosis (MS), and MS is one of the main causes of disability in young people.
According to Angela Dziedzic from the Department of General Biochemistry, Faculty of Biology and Environmental Protection of the University of Lodz, the exact causes of multiple sclerosis are still unknown. Autoimmune factor is considered to be one of them.
The patient`s body begins to produce proteins - autoantibodies that destroy myelin, its own nerve fibres. "This, in consequence, causes the patient`s body to attack itself, which leads to neurological problems and symptoms of the disease" - she adds.
Some studies show that patients with MS develop platelet dysfunction that may lead to an increased risk of so-called ischaemic diseases including stroke and myocardial infarction.
Research on platelets that can help explain the mechanism of their increased prothrombotic activity in multiple sclerosis is being conducted by researchers from the Department of General Biology, University of Lodz, under the supervision of Prof. Joanna Saluk-Bijak.
Researchers emphasize that platelets perform many tasks in the circulatory system. They also take part in various disorders, including neurological diseases.
The team from Lodz focuses on β-tubulin, one of the key proteins that make up the cytoskeleton in platelets. Preliminary studies have shown elevated β-tubulin levels in patients with secondary progressive multiple sclerosis (SPMS) compared to healthy volunteers.
According to the scientists, this may be an important cause of prothrombotic platelet activity in progressive multiple sclerosis and, for example, promote the formation of a blood clot in the area of a damaged blood vessel. This leads to the closure of the vessel and the occurrence of ischaemic disease, i.e. stroke or myocardial infarction.
In the project financed from the PRELUDIUM grant of the National Science Centre, several research phases and comparative analyses have been planned to explain the causes and consequences of differences in platelet β-tubulin concentration. Researchers will also investigate whether the abnormal amount of β-tubulin has a genetic background.
Angela Dziedzic emphasizes that understanding the mechanisms responsible for the formation of inflammatory factors in MS at the molecular level can help in the search for more effective therapies. Until now - due to unknown causes of the disease - only drugs that slow down its progress and temporarily relieve symptoms have been used.
"The role of platelets in multiple sclerosis indicates their important role as potential therapy targets" - believes the project leader.
The research project "Determination of structural and functional changes in the platelet cytoskeleton as potential factors of increased prothrombotic activity occurring in multiple sclerosis" will continue until mid-2021. (PAP)
szu/ zan/ kap/