Drugs in Multiple Sclerosis

Treatments that modify the immune response without completely suppressing it.

A cytokine that modulates the immune response and reduces inflammation, particularly in MS.

A synthetic polymer that acts as a decoy to prevent immune attack against myelin.

A drug that targets the proliferation of rapidly dividing immune cells (T & B lymphocytes).

Targets of treatment in diseases affecting the immune system.

Reducing inflammatory cell movement and modifying surface antigens.

Flu-like symptoms, injection site reactions, potential liver damage, and potentially depression or leukopenia.

Strategies focused on the immune system to alleviate inflammation and slow down the progression of MS.

Macrophages consume myelin-autoantibody complexes, leading to myelin damage and neuronal harm.

Myelin loss exposes axons to harmful substances, initiating axonal damage.

Demyelination makes axons susceptible to inflammatory triggers like cytokines and reactive molecules.

Certain immune cells directly harm neurons and axons in MS.

Long-term inflammation and myelin loss cause progressive axonal destruction.

Damaged myelin hinders the rapid transmission of signals in nerve fibers.

Problems with nerve signal transmission cause symptoms like muscle weakness, sensory loss, vision issues, and cognitive problems in MS.

The central nervous system has limited capacity to repair myelin.

T cells, especially CD4+ and CD8+, are involved in MS by triggering and contributing to inflammation and directly attacking myelin and neurons.

B cells generate antibodies, contributing to auto-immune responses that target myelin in MS, making auto-antibodies and triggering inflammation.

Microglia, the resident macrophages of the central nervous system, become highly active and contribute to inflammation and neuronal damage in MS.

Astrocytes support neurons and maintain the blood-brain barrier. They also contribute to the inflammatory response in MS.

Cytokines (e.g., TNF-α, IL-6) and chemokines (e.g., CCL2, CXCL10) promote inflammation, and immune cell recruitment to the CNS, in MS.

Myelin-specific autoantibodies target myelin in MS, accelerating destruction.

Relapsing-remitting multiple sclerosis; characterized by clear relapses (flare-ups) followed by periods of remission.

Disease-modifying therapies; treatments meant to reduce MS disease activity and severity.

Highly effective RRMS treatment that slows disease progression, but carries a PML risk.

Primary progressive multiple sclerosis; a relentless, steady progression of disability without clear relapses/remissions.

The only approved DMT for PPMS; targets CD20+ B cells.

Reduces inflammation & oxidative stress in RRMS treatment.

Focuses on controlling symptoms, maintaining function (mobility), and supportive care alongside limited disease-modifying therapies.

A sphingosine-1-phosphate receptor modulator that sequesters lymphocytes in lymph nodes, preventing their migration to the CNS.

A drug that interacts with DNA to disrupt replication and repair, inhibits macrophage activity, and reduces immune-mediated CNS damage.

A monoclonal antibody that binds to a protein on immune cells (alpha-4 integrin), preventing these cells from entering the central nervous system (CNS) and causing inflammation.

A drug that traps lymphocytes (immune cells) in lymph nodes, reducing their ability to reach the CNS and cause inflammation.

A drug that reduces inflammation by modulating the immune response and protecting myelin sheath.

A drug that targets specific receptors on immune cells to reduce their activation and prevent them from causing inflammation.

A monoclonal antibody that targets B cells (a specific type of immune cell) to reduce inflammation and prevent damage to myelin.

A drug that depletes lymphocytes (immune cells) by interfering with their DNA synthesis, slowing down disease progression.

The way in which a drug works at the cellular level to achieve its therapeutic effect.

Treatment options often used initially for relapsing-remitting MS due to their generally good safety profile and moderate efficacy. Examples include interferon-beta, glatiramer acetate, and dimethyl fumarate.

Treatments for relapsing-remitting MS that demonstrate strong effectiveness in reducing relapse rates and slowing disease progression, but may have more severe side effects. Examples include natalizumab, fingolimod, and alemtuzumab.

A serious complication associated with some MS therapies, particularly natalizumab, where a virus that typically lies dormant can reactivate and cause brain damage. This risk requires close monitoring.

Some MS therapies, like fingolimod, can negatively impact heart function, requiring careful monitoring and risk assessment. This is especially critical at the initial dose.

Treatment options for MS that are taken by mouth, offering convenience and flexibility compared to injections or infusions. Examples include fingolimod, cladribine, siponimod, and dimethyl fumarate.

Types of MS that show a steady worsening of disability, with either minimal relapses (primary progressive MS) or a gradual progression after initial relapse periods (secondary progressive MS).

A form of MS where a relapsing-remitting phase transitions into steady, gradual worsening of disability. This phase is marked by ongoing neurodegeneration and limited remyelination.

For active relapsing-remitting MS without high-risk factors, starting with well-tolerated first-line agents like interferon-beta, glatiramer acetate, or dimethyl fumarate is often a good approach.

This therapy, though effective in reducing disease activity, has a limited lifetime dose due to the potential for serious cardiac toxicity and leukemia risk, requiring careful monitoring.

A newer oral treatment for secondary progressive MS, specifically targeting neuroinflammation and protecting the myelin sheath. It offers moderate efficacy and a side effect profile similar to fingolimod.

A chronic disease where the immune system attacks the central nervous system (CNS), leading to inflammation and damage to the myelin sheath that protects nerve fibers.

A fatty covering that insulates nerve fibers and allows for fast and efficient signal transmission.

The destruction or loss of the myelin sheath surrounding nerve fibers.

MS causes various neurological symptoms due to disrupted nerve signal transmission, including: fatigue, muscle weakness, vision problems, sensory disturbances, and cognitive difficulties.

In MS, the immune system mistakenly attacks the myelin sheath of nerve fibers, leading to inflammation and demyelination.

T cells are immune cells that directly attack infected or abnormal cells, while B cells produce antibodies that bind to foreign substances.

Treatments for MS aim to modify the immune system, reduce inflammation, and protect myelin from further damage.

A protective barrier that regulates what substances can enter the brain from the bloodstream.

A type of Multiple Sclerosis (MS) characterized by distinct periods of new or worsening neurological symptoms (relapses) followed by periods of partial or complete recovery (remissions).

A type of MS characterized by a continuous worsening of neurological function from the onset of symptoms, without distinct relapses or remissions. It is characterized by progressive neurodegeneration.

RRMS is marked by relapses and remissions, while SPMS shows a gradual worsening of symptoms even without relapses.

PPMS is defined by a consistent worsening of neurological function from the onset of the disease, without the clear relapses and remissions seen in RRMS.

SPMS usually develops after a period of RRMS, while PPMS is progressive from the onset.

SPMS is driven by neurodegenerative processes, leading to a loss of nerve cells and brain atrophy.

PPMS is characterized by progressive neurodegeneration, leading to continuous neurological decline.

A cytokine that modulates the immune response in MS by reducing the migration of inflammatory cells across the blood-brain barrier and potentially altering the expression of surface antigens on immune cells.

A synthetic polymer that mimics myelin basic protein, acting as a decoy to divert the immune response away from healthy myelin in MS.

A drug that targets the proliferation of rapidly dividing immune cells, like activated T and B lymphocytes, in MS.

Interferon-beta reduces the movement of inflammatory cells into the brain, alters cell surface antigens, and modulates overall immune responses, but its precise mechanism is still being investigated.

Common side effects include flu-like symptoms, injection site reactions, and potential liver damage. Less common, but more serious effects include depression and leukopenia.

Glatiramer acetate acts as a decoy, diverting the immune response away from myelin by mimicking a component of the myelin sheath.

Immune modulators modify specific aspects of the immune response without broadly suppressing it, restoring the balance of the immune system and targeting pathways or cells involved in the disease.

Immune modulators are particularly effective in autoimmune diseases like Multiple Sclerosis (MS) as they target specific pathways or types of immune cells involved in the disease process.

These drugs trap lymphocytes in lymph nodes, preventing them from reaching the CNS and causing inflammation.

These antibodies target specific molecules on immune cells, blocking their entry into the CNS or reducing their activity.

Risks include allergic reactions, increased infection risk, and a rare but serious brain infection called PML.

Common side effects include infusion reactions, respiratory infections, and skin infections. Long-term use can reduce immunoglobulin levels.