StemCell Therapy

Charcot-Marie-Tooth disease (CMT), known also as Hereditary Motor and Sensory Neuropathy (HMSN), Hereditary Sensorimotor Neuropathy (HSMN), or Peroneal Muscular Atrophy, is a heterogeneous inherited disorder of nerves (neuropathy) that is characterized by loss of muscle tissue and touch sensation, predominantly in the feet and legs but also in the hands and arms in the advanced stages of disease. Presently incurable, this disease is one of the most common inherited neurological disorders, with 37 in 100,000 affected.[1]

Charcot-Marie-Tooth disease is caused by mutations that cause defects in neuronal proteins. Nerve signals are conducted by an axon with a myelin sheath wrapped around it. Most mutations in CMT affect the myelin sheath. Some affect the axon.

The most common cause of CMT (70-80% of the cases) is the duplication of a large region in chromosome 17p12 that includes the gene PMP22 . Some mutations affect the gene MFN2, which codes for a mitochondrial protein. Cells contain separate sets of genes in their nucleus and in their mitochondria. In nerve cells, the mitochondria travel down the long axons. In some forms of CMT, mutated MFN2 causes the mitochondria to form large clusters, or clots, which are unable to travel down the axon towards the synapses . This prevents the synapses from functioning.[2] CMT is divided into the primary demyelinating neuropathies (CMT1, CMT3, and CMT4) and the primary axonal neuropathies (CMT2), with frequent overlap.

Another cell involved in CMT is the Schwann cell, which creates the myelin sheath, by wrapping its plasma membrane around the axon in a structure that is sometimes compared to a.[3]

Neurons, Schwann cells, and fibroblasts work together to create a working nerve. Schwann cells and neurons exchange molecular signals that regulate survival and differentiation. These signals are disrupted in CMT. [3]

Demyelinating Schwann cells causes abnormal axon structure and function. They may cause axon degeneration. Or they may simply cause axons to malfunction.[1] The myelin sheath allows nerve cells to conduct signals faster. When the myelin sheath is damaged, nerve signals are slower, and this can be measured by a common neurological test, electromyography. When the axon is damaged, on the other hand, this results in a reduced compound muscle action potential (CMAP).[4]

Stem Cells

A growing body of evidence suggests strongly that the use of stem cells to address the primary componants of both inflammation and demylination has a direct effect on this disease. Much of the research, that also applies, has focused on Multiple Sclerosis another demylinationg disease with a larger incidence world wide. There is a growing body of literature supporting the contention that with stem cell therapy Schwann cells and other componants of the immune system, that adversely affect CMT patients, can be influenced to reverse their typical progressive dysfunction.

Our patients have now documented significant changes in multiple areas of function. Most notable has been in their ability to walk, maintain balance and have more consistent and higher levels of energy. These changes allow for a substantial quality of life changing affair.Interestingly we have seen progressive improvements over the period of a year post treatment. Only time will determine the nature of how much change can take place. It should be understood that currently all the CMT patients are seniors. We expect that with earlier treatment even better results can be achieved.

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Stem Cell Therapy for CMT Stem Cells CMT

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