What is Multiple Sclerosis (MS)?

Multiple sclerosis (MS) is a chronic autoimmune disease that affects the central nervous system (CNS), which includes the brain and spinal cord. In MS, the body’s immune system mistakenly attacks the protective covering of nerve fibers called myelin. This attack leads to inflammation, damage to the myelin sheath, and sometimes to the underlying nerve fibers. As a result of this damage, communication between the brain, spinal cord, and the rest of the body is disrupted.


What is the relationship between MS and oxidative stress?

The relationship between multiple sclerosis (MS) and oxidative stress is a topic of ongoing research, and while the precise mechanisms are not fully understood, oxidative stress is believed to play a significant role in the pathogenesis and progression of MS. Here’s how MS and oxidative stress are interconnected:


  • Inflammatory Response: MS is characterized by inflammation in the central nervous system (CNS), which leads to damage of the myelin sheath surrounding nerve fibers and subsequent neurodegeneration. Inflammatory processes in MS involve the activation of immune cells, such as T cells and microglia, which produce pro-inflammatory cytokines and reactive oxygen species (ROS). These ROS can cause oxidative damage to lipids, proteins, and DNA within the CNS, exacerbating tissue injury and inflammation.


  • Mitochondrial Dysfunction: Mitochondria are the primary source of cellular energy production and play a crucial role in maintaining cellular function and integrity. Dysfunction of mitochondria has been implicated in MS, leading to impaired energy metabolism, increased production of ROS, and oxidative stress. Mitochondrial dysfunction may result from direct damage by inflammatory mediators or from genetic and environmental factors associated with MS.


  • Myelin Degradation: Myelin, the fatty substance that insulates nerve fibers in the CNS, is a primary target of the immune attack in MS. Degradation of myelin by immune cells and inflammatory mediators releases lipid breakdown products and exposes axons to oxidative damage. Oxidative stress can further exacerbate myelin degradation and disrupt the repair processes that are essential for remyelination in MS lesions.


  • Blood-Brain Barrier Dysfunction: The blood-brain barrier (BBB) is a selective barrier that regulates the passage of molecules and immune cells between the bloodstream and the CNS. Dysfunction of the BBB in MS allows infiltration of inflammatory cells and molecules into the CNS, contributing to neuroinflammation and oxidative stress. Disruption of the BBB integrity may also facilitate the entry of blood-derived ROS and inflammatory mediators into the CNS, exacerbating oxidative damage.


  • Axonal Injury and Neurodegeneration: In addition to demyelination, MS is associated with axonal injury and neurodegeneration, which contribute to disability progression in the disease. Oxidative stress has been implicated in axonal injury and neuronal death in MS, as ROS can directly damage axonal structures and impair axonal transport and function. Oxidative stress-mediated neurodegeneration may occur independently of demyelination and contribute to irreversible neurological deficits in MS.


Overall, oxidative stress is a common feature of MS pathology and contributes to various aspects of the disease, including inflammation, demyelination, neurodegeneration, and disability progression.