Multiple sclerosis is a chronic inflammatory disease that affects the brain and spinal cord, or central nervous system (CNS), leading to sensory and motor impairments. MS is more common in women than in men and is typically diagnosed between the ages of 20 and 40. Approximately 400,000 individuals in the United States currently have MS and more than 2.1 million people worldwide live with the disease. MS is diagnosed as one of two forms, either relapsing-remitting (RRMS) or primary progressive (PPMS). The vast majority of patients are initially diagnosed with RRMS, which is characterized by periods of exacerbation, or flare-ups, followed by periods of remission. Patients with PPMS do not experience remissive phases. Most of the medications approved for MS treatment are aimed toward ameliorating the relapsing-remitting disease course. Currently, MS is commonly treated with an interferon beta (IFN beta) drug, which reduces disease activity, in combination with other medications that target the various symptoms experienced by patients (2).
The clinical presentation of MS varies from person to person; however, pathologically, the disease results from an autoimmune attack on myelin sheath (a protective covering around nerve fibers). Immune cells (lymphocytes) become self-reactive against certain proteins that make up myelin and subsequently destroy it. This process is called demyelination. When the myelin sheath is damaged, signaling between nerve cells becomes slowed or prevented altogether. As a result, simple tasks like walking become quite difficult, and patients may experience vision impairments, episodes of numbness and tingling, loss of balance and coordination, as well as other symptoms. Unfortunately, the mechanism through which an individual develops MS is not entirely understood, and therefore, the repertoire of treatment targets is limited. In order to gain a better understanding of the cause and progression of MS, researchers use various animal models of the disease. The most commonly used MS model is experimental autoimmune encephalomyelitis (EAE), which can be induced in a variety of animal species including certain rodents and non-human primates. In the upcoming November issue of the Journal of Neuropathology and Experimental Neurology, a study by Kap and colleagues investigates whether or not B cell depletion (an experimental treatment for MS) is a valid therapeutic target (1). The authors employed an EAE study in the common marmoset (monkey species). Marmosets were first utilized to examine the clinical and pathological features of MS in 1996, and have been found to exhibit a disease course more closely related to human MS than that observed in rodent models. The marmoset EAE model demonstrates widespread demyelination in both white matter and grey matter of the CNS, strongly resembling the conditions of MS in humans. Furthermore, marmosets have similar immune and nervous system genes to humans, establishing another advantage of using this model (3).