Multiple On the other hand, PPMS is a

Multiple Sclerosis (MS) is a degenerative
disease that primarily affects the Central Nervous System (CNS)1.
There are a variety of theories pertaining to the cause of MS and there is
currently no cure available. Although there is no cure, treatments may help
reduce the effects of symptoms and slow progression of the disease. With this
autoimmune disease, multiple lesions are usually found on the brain/spinal cord
which in turn affect neural transmission. These lesions can slow down or block
neural transmission, leading to weakness, sensory loss, and other neurological
symptoms. Currently, there are 4 recognizable subtypes of MS, these include
Relapsing Remitting MS (RRMS), Secondary Progressive MS (SPMS), Primary
Progressive MS (PPMS) and Progressive Relapsing MS (PRMS). RRMS is
characterized by relapsing periods of neurological dysfunction that can last
from days to months followed by a partial/full recovery. The recovery period is
often a very stable time in between the relapses. Similarly, SPMS initially
begins as a relapse/remission pattern that eventually changes into a steady
progression of the disease. On the other hand, PPMS is a continuous decline of
neurologic function with minimal recovery. Lastly PRMS consists of periods of
relapses with minimal recovery, resulting in the disease progressively getting
worse from the onset.

Multiple Sclerosis is a common
inflammatory disease and can result in demyelination, axon loss and
inflammation2.
The CNS is responsible for integrating and responding to the sensory
information received from the body and it consists of the brain & spinal
cord. Nerves cells are the specialized cells involved in the CNS and
demyelination involves the breakdown of the myelin sheath that
surrounds/insulates these nerve cells. It can be due to the direct damage to
myelin by inflammatory cells which results in neurons being more susceptible to
apoptosis. By losing its myelin sheath, neurons become more susceptible to the
binding of agents that induce apoptosis.

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In contrast to demyelination, the
mechanisms that underlie the progression of axon loss are currently unknown.3
Theories for causes of axonal damage include direct cytotoxic attack, antibody
mediated lesion, or exposure to glutamate. Moreover, it has been discovered
that acute damage to the axon occurs mostly in the early stages with a tendency
to slow as the disease progresses and has been linked to chronic disabilities
in those with MS4. Similarly, the inflammatory aspect of MS has also
been linked to functional disability and is primarily the result of the
overproduction inflammatory cytokines. Autoreactive T-Cells stimulate
microglial, astrocytes and antibody production while also secreting the
cytokines that recruit inflammatory cells4.
Microglial cells are similar to macrophages in which they destroy cells
perceived to be pathogenic and remove damaged cells. Alternatively, the role of
astrocytes in MS is a poorly understood mechanism, however there are several
suggested mechanisms that could contribute to MS. These mechanisms include
astrocytes being a part of the innate immune system, a source of cytotoxic
factors, an inhibitor to remyelination or a contributor to axonal mitochondrial
dysfunction5.
Anti-myelin antibodies in addition to microglial cells and astrocytes, each contribute
to produce demyelination of the nerve cells.

To sum up,
Multiple Sclerosis is a degenerative disease that affects the nerve cells of
the Central Nervous System. Despite not having a cure, treatments for MS have
been able to combat symptoms and slow progression of the disease. MS can be
diagnosed via MRIs and can affect regions of the brain & spinal cord,
resulting in demyelination, axon loss and inflammation. With proper medical
treatment and physical therapy, symptoms such as fatigue, pain, balance and
depression can be controlled and managed.

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