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Welcome to 2 minute neuroscience, where I simplistically explain neuroscience topics
in 2 minutes or less.
In this installment I will discuss multiple sclerosis.
Multiple sclerosis, or MS, is a central nervous system disorder that involves the abrupt appearance
of neurological symptoms, which usually occur for the first time between the ages of 20
and 50.
The symptoms of MS vary from person to person, and almost any nervous system function can
be disrupted in the disease.
The most common initial symptoms involve visual disturbances, abnormal sensations, and weakness.
The causes of the disease are not fully understood and are thought to involve genetic and environmental
factors.
Multiple sclerosis is characterized by damage to the myelin sheaths surrounding the axons
of neurons in the central nervous system.
This myelin damage disrupts the conduction of action potentials along these axons, which
is thought to cause many of the symptoms of the disease.
The myelin damage can also lead to the deterioration of axons.
The brains of MS patients can contain evidence of this damage in the form of plaques or lesions
that are visible with some types of neuroimaging.
The reason these attacks on a patient’s myelin occur is not fully understood, but
the damage in MS is most commonly attributed to an autoimmune attack.
According to this hypothesis, the immune system in a patient with MS targets myelin, treating
it as foreign.
This autoimmune attack and the associated inflammatory response leads to damage to myelin,
axons, and glial cells.
What prompts the autoimmune attack is not known, however, and some have argued that
MS is caused by a persistent infection instead.
Either way, MS seems to involve excessive immune system activation in some respect,
and the drugs that have proven most successful in treating it act to reduce inflammatory
or other immune responses.