Controlled scar formation in the brain — ScienceDaily

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from research organizations

Date:

March 26, 2021

Source:

Charité – Universitätsmedizin Berlin

Summary:

When the brain suffers injury or infection, glial cells surrounding the affected site act to preserve the brain’s sensitive nerve cells and prevent excessive damage. A team of researchers has been able to demonstrate the important role played by the reorganization of the structural and membrane elements of glial cells.

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When the brain suffers injury or infection, glial cells surrounding the affected site act to preserve the brain’s sensitive nerve cells and prevent excessive damage. A team of researchers from Charité — Universitätsmedizin Berlin have been able to demonstrate the important role played by the reorganization of the structural and membrane elements of glial cells. The researchers’ findings, which have been published in Nature Communications, shed light on a new neuroprotective mechanism which the brain could use to actively control damage following neurological injury or disease.

The nervous system lacks the ability to regenerate nerve cells and is therefore particularly vulnerable to injury. Following brain injury or infection, various cells have to work together in a coordinated manner in order to limit damage and enable recovery. ‘Astrocytes’, the most common type of glial cell found in the central nervous system, play a key role in the protection of surrounding tissues. They form part of a defense mechanism known as ‘reactive astrogliosis’, which facilitates scar formation, thereby helping to contain inflammation and control tissue damage. Astrocytes can also ensure the survival of nerve cells located immediately adjacent to a site of tissue injury, thereby preserving the function of neuronal networks. The researchers were able to elucidate a new mechanism which explains what processes happen inside the astrocytes and how these are coordinated.

“We were able to show for the first time that the protein ‘drebrin’ controls astrogliosis,” says study lead Prof. Dr. Britta Eickholt, Director of Charité’s Institute of Biochemistry and Molecular Biology. “Astrocytes need drebrin in order to form scars and protect the surrounding tissue.” By switching off the production of drebrin inside astrocytes, the researchers were able to study its role in brain injury in an animal model. They used electron microscopy and high-resolution light microscopy to investigate cellular changes in the brain, in addition to undertaking real-time investigations using isolated astrocytes in cell culture. “Loss of drebrin results in the suppression of normal astrocyte activation,” explains Prof. Eickholt. She adds: “Instead of engaging in defensive reactions, these astrocytes suffer complete loss of function and abandon their cellular identity.” Without protective scar formation, normally harmless injuries will spread, and more and more nerve cells will die.

To enable scar formation, drebrin controls the reorganization of the actin cytoskeleton, an internal scaffold responsible for maintaining astrocyte mechanical stability. By doing so, drebrin also induces the formation of long cylindrical membrane structures known as tubular endosomes, which are used in the uptake, sorting and redistribution of surface receptors and are needed for the defensive measures of astrocytes. Summing up the researchers’ findings, Prof. Eickholt says: “Our findings also show how drebrin uses the dynamic and versatile cytoskeleton as well as membrane structures to control astrocyte functions which are fundamental to the defense mechanism against injury.” She continues: “In particular, the membrane tubules which are formed during this process have not previously been described in this manner, neither in cultured astrocytes nor in the brain.”

“Drebrin’s role as a cytoskeletal regulator suggests that it may be a risk factor for severe outcomes in both neurological and other disorders, because loss of the protein can produce similar changes in astrocytes,” says Prof. Eickholt. She adds: “It is also possible that individuals with defects in the drebrin gene — comparable to those in the animal model — might remain without symptoms until triggers like cellular stresses, environmental toxins or diseases occur.” It is hoped that investigations involving patient samples will elucidate the extent to which drebrin also plays a role in degenerative brain disorders, such as Alzheimer’s disease.

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Story Source:

Materials provided by Charité – Universitätsmedizin Berlin. Note: Content may be edited for style and length.

Journal Reference:

1. Juliane Schiweck, Kai Murk, Julia Ledderose, Agnieszka Münster-Wandowski, Marta Ornaghi, Imre Vida, Britta J. Eickholt. Drebrin controls scar formation and astrocyte reactivity upon traumatic brain injury by regulating membrane trafficking. Nature Communications, 2021; 12 (1) DOI: 10. 1038/s41467-021-21662-x

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Charité – Universitätsmedizin Berlin. “Controlled scar formation in the brain.” ScienceDaily. ScienceDaily, 26 March 2021. <www.sciencedaily.com/releases/2021/03/210326104659.htm>.

Charité – Universitätsmedizin Berlin. (2021, March 26). Controlled scar formation in the brain. ScienceDaily. Retrieved July 2, 2023 from www.sciencedaily.com/releases/2021/03/210326104659.htm

Charité – Universitätsmedizin Berlin. “Controlled scar formation in the brain.” ScienceDaily. www.sciencedaily.com/releases/2021/03/210326104659.htm (accessed July 2, 2023).

Blood protein triggers scars in the brain after injury; New target might help aid recovery for patients with traumatic injuries — ScienceDaily

Science News

from research organizations

Date:

April 28, 2010

Source:

Society for Neuroscience

Summary:

A protein called fibrinogen that is known to help form blood clots also triggers scar formation in the brain and spinal cord, according to new research. Researchers found that fibrinogen carries a dormant factor that activates when it enters the brain after an injury, prompting brain cells to form a scar. Scars in the brain or spinal cord can block connections between nerve cells and often keep injury patients from reaching full recovery.

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A protein called fibrinogen that is known to help form blood clots also triggers scar formation in the brain and spinal cord, according to new research in the April 28 issue of the Journal of Neuroscience. Researchers found that fibrinogen carries a dormant factor that activates when it enters the brain after an injury, prompting brain cells to form a scar. Scars in the brain or spinal cord can block connections between nerve cells and often keep injury patients from reaching full recovery.

A fundamental question in studies of damage to the central nervous system has been the origin of the first signal for scar growth. In this study, a group of neuroscientists led by Katerina Akassoglou, PhD, of the Gladstone Institutes at the University of California, San Francisco, looked at molecules in the bloodstream.

“Our study shows that a blood clotting factor is an important player in glial scar formation,” Akassoglou said. Current treatments to improve nerve cell regeneration after injury focus on minimizing existing scar tissue; this new result suggests that suppressing these blood proteins might be a way to stop scars from even forming, Akassoglou said.

After a traumatic injury in the nervous system, such as a stab wound or stroke, fibrinogen leaks from damaged blood vessels into the brain and scar tissue begins to form. This process cordons off the wounded area, but also prevents nerve cells from reconnecting and communicating with one another. Rewired nerve cells are essential if a patient is to regain normal function.

To determine what role fibrinogen plays in scar formation, the researchers used a mouse model of brain trauma. When fibrinogen was effectively removed from the blood stream, the mice had dramatically smaller scars after injury. The authors found that fibrinogen carries an inactive type of scar-inducing substance called TGF-ß that switches “on” when it encounters local cells in the brain. When the brain pathways associated with TGF-ß were blocked, scars didn’t form.

“These new findings offer an entirely new avenue to explore potentially important therapeutic agents that interfere with this interesting function of fibrinogen,” said Jerry Silver, PhD, of Case Western Reserve University, who was unaffiliated with the study. “This is the first time that a major blood-associated trigger of reactive scar-forming cells has been reported in the literature.”

The research was supported by the National Institute of Neurological Disorders and Stroke of the National Institutes of Health, the American Heart Association, and the German Research Foundation.

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Society for Neuroscience. (2010, April 28). Blood protein triggers scars in the brain after injury; New target might help aid recovery for patients with traumatic injuries. ScienceDaily. Retrieved July 1, 2023 from www.sciencedaily.com/releases/2010/04/100427171804.htm

Society for Neuroscience. “Blood protein triggers scars in the brain after injury; New target might help aid recovery for patients with traumatic injuries.” ScienceDaily. www.sciencedaily. com/releases/2010/04/100427171804.htm (accessed July 1, 2023).

causes, signs and diagnosis |Treatment of hippocampal sclerosis in Moscow

Contents↓[show]

Hippocampal sclerosis is one of the forms of epilepsy, the cause of which is the pathology of the parts of the limbic system of the brain. The main generator of epileptic activity is gliosis in combination with atrophy of the cortical plate of the underlying white matter. To diagnose the disease, neurologists at the Yusupov Hospital use modern methods of instrumental research, perform laboratory tests and minimally invasive diagnostic procedures.

Sclerosis of the hippocampus is accompanied by loss of neurons and scarring of the deepest part of the temporal lobe. Often caused by severe brain injury. It is left handed and right handed. Brain damage due to trauma, neoplasm, infection, lack of oxygen, or uncontrolled spontaneous seizures leads to the formation of scar tissue in the hippocampus. It begins to atrophy, neurons die and form scar tissue.

Based on structural changes, two main types of temporal lobe epilepsy are distinguished:

• with the presence of a volumetric process (tumor, congenital pathology, aneurysm of a blood vessel, hemorrhage) affecting the limbic system;
• without clearly verified volumetric changes in the area of ​​the medial temporal lobe.

Causes

The following causes of hippocampal sclerosis are known:

• hereditary predisposition;
• cerebral hypoxia;
• brain injury;
• infections.

Today the following theories of development of hippocampal sclerosis are considered to be the main ones:

• the influence of febrile convulsions leading to regional metabolic disorders and edema of the temporal lobe cortex. Neuronal death occurs, local gliosis and atrophy develop, as a result of which the volume of the hippocampus decreases, reactive expansion of the sulcus and the lower horn of the lateral ventricle.
• acute circulatory disorders in the basin of the terminal and lateral branches of the posterior cerebral artery cause basal ischemia of the temporal lobe, secondary diapedetic sweating, neuronal death, gliosis and atrophy occur.
• violation of the development of the temporal lobe during embryogenesis.

Symptoms

Sclerosis of the hippocampus usually leads to focal epilepsy. Epileptic seizures appear in groups or individually. They are complex, starting with strange indescribable sensations, hallucinations or illusions, followed by a numb gaze, food and rotational automatisms. They last about two minutes. With progression, generalized tonic-clonic seizures may occur.

Attacks in hippocampal sclerosis may be accompanied by various symptoms:

• change in behavior;
• loss of memory;
• headaches;
• increased anxiety;
• sleep problems;
• panic attacks.

Patients develop impaired cognitive abilities (memory, thinking, ability to concentrate). Seizures that disrupt brain activity can lead to sudden loss of consciousness, as well as autonomic cardiac dysfunction. Patients with left-sided hippocampal sclerosis have more severe parasympathetic dysfunction compared to patients with right-sided mesial sclerosis.

Seizures of epilepsy are accompanied by auditory or vestibular hallucinations, eructations or vegetative manifestations, paresthesias and unilateral facial twitches. Patients note the difficulty of learning, memory impairment. They are conflicted, emotionally labile, have an increased sense of duty.

Doctors of the Yusupov hospital use the following examination methods to diagnose the disease:

• neuroradiological diagnostics;
• computed tomography;
• nuclear magnetic resonance spectroscopy;
• angiography;
• electroencephalography.

The study is performed on modern equipment from the world’s leading manufacturers.

Treatment

Neurologists at the Yusupov hospital prescribe antiepileptic drugs to reduce the symptoms of the disease. The first choice is carbamazepine. Second choice drugs include Valproate, Difenin, and Hexamidin. After treatment, some patients stop having seizures, and a long-term remission occurs.

In case of resistance to ongoing therapy and progression of hippocampal sclerosis, surgical treatment is carried out in partner clinics. It consists in removing the temporal lobe of the brain (lobectomy). After surgery, in 70-95% of cases, the number of seizures decreases. If you are faced with the problem of hippocampal sclerosis and wish to receive qualified specialized medical care, call us. You will be booked in for a consultation with a neurologist at the Yusupov Hospital.

Relapsing-remitting MS – signs, symptoms, who treats, who treats

Multiple sclerosis damages the central nervous system, which includes the brain and spinal cord. Multiple sclerosis causes the immune system to attack the myelin that protects the nerves. The nerves themselves can also be damaged, and when damaged, scar tissue forms – sclerosis. When myelin or nerves are damaged, the transmission of nerve impulses is also impaired. Different types of multiple sclerosis affect patients differently. One type is called relapsing-remitting multiple sclerosis, in which the patient experiences disease flares or relapses. Between exacerbations there are periods of recovery or remission. Most patients diagnosed with multiple sclerosis begin with a relapsing-remitting type. In most cases, the course of the disease changes over several decades and then steadily worsens.

What causes relapsing-remitting multiple sclerosis?

Multiple sclerosis occurs when the body’s immune system attacks the central nervous system, damaging the myelin that protects nerve fibers. Experts believe that environmental factors trigger the disease in those patients whose genetics make them susceptible to multiple sclerosis.

Who is at risk for relapsing-remitting multiple sclerosis

• Multiple sclerosis can be caused by an infection that lies dormant in the body, such as the Epstein-Barr virus (the virus that causes infectious mononucleosis)
• Some patients may have a genetic predisposition.

Symptoms of relapsing-remitting multiple sclerosis

Early symptoms of multiple sclerosis:

• Vision problems
• Hypersensitivity to heat
• Numbness, especially in the legs
• Weakness
• Fatigue
• Confusion of thoughts
• Depression
• Urgent urge to urinate
• Impaired balance and coordination.

Relapsing-remitting multiple sclerosis is characterized by relapses lasting at least 24 hours. During a relapse, symptoms worsen. A relapse will be followed by a remission. During the remission period, the symptoms partially or completely disappear.

How a doctor diagnoses relapsing-remitting multiple sclerosis

A neurologist diagnoses and treats relapsing-remitting multiple sclerosis. Differential diagnosis of multiple sclerosis involves many examinations, since it is extremely important for a doctor to rule out other diseases that can cause similar symptoms. A neurologist examines vision, a sense of balance and other functions of the patient’s body; for this, an MRI of the brain and an MRI of the entire spine may be prescribed. An MRI with contrast can detect areas of damage in the brain or spinal cord associated with multiple sclerosis. In addition, the patient is prescribed blood and cerebrospinal fluid tests.

How a doctor treats relapsing-remitting multiple sclerosis

Multiple sclerosis is not considered curable, but various therapies are available to reduce inflammation and slow progress. As a rule, the following drugs are prescribed to the patient:

• Beta-interferon
• Glatiramer acetate
• Monoclonal antibodies
• Dimethyl fumarate
• Fingolimod.

Other medications are used to treat symptoms such as:

• Muscle spasms
• Urge to urinate
• Depression
• Erectile dysfunction
• Fatigue.

Your doctor may also suggest steroids to reduce symptoms during flare-ups. If steroids are not effective, then the doctor may prescribe plasmapheresis, a blood purification procedure.

Complications of relapsing-remitting multiple sclerosis

Most cases of relapsing-remitting multiple sclerosis are mild, although the patient may need to use a cane or other aid to move around. In some cases, the disease is severe and makes it impossible to take care of yourself. Rarely causes death.

Certain steps are also recommended for the patient to manage their condition:

• Physiotherapy can help relieve muscle spasms
• Diet low in saturated fat and trans fat
• Overheating avoidance
• Moderate physical activity and adequate sleep.

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Scientific sources

1. Markov D.A., Leonovich A.L. Multiple sclerosis. Moscow: Medicine, 1976.
2. Alaev B.A. Features of the spread of multiple sclerosis. J. Neuropathology and psychiatry. 1988, no. 2, p. 119-124.
3. Wayne A.M. and others. The course of multiple sclerosis in men and women. // J. Neurology and psychiatry. 1995, no. 4, p. 43-44.
4. Gordeev Ya.Ya. Clinical and pathological bases of diagnosis and treatment of multiple sclerosis. //Author. dis. cand.ped. Sciences. L., 1988, 25 p.
5. Gushchin V.M. Clinic and treatment of multiple sclerosis. // Healthcare of Kazakhstan. 1990, no. 2, p. 49-51.

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