Please write one page on the cellular biology behindCharcot-Marie-Tooth disease in continuation to the excerpt below.NO INTRODUCTION OR CONCLUSION!!! Simply add one page of information without repeating the things listed below. I need one page to be attached following this piece so I am asking that someone writes one page that I can directly place toadd to the end of the piece below.

Charcot-Marie-Tooth (CMT) Disease is classified as a genetic, neuromuscular condition. Its inheritance pattern is autosomal dominant, so it is more likely to be inherited by an individual’s progeny. The development of this condition can stem from one of three mutations. The most significant mutation is a 1.5 Mb duplication on chromosome 17, which includes the PMP22 gene. This gene encodes for peripheral myeline protein 22, which is responsible for expression of myelin sheaths around the neurons of the peripheral nervous system (PNS). The mutation inhibits the expression this protein, which leaves peripheral neurons more vulnerable to damage, as well as less functional. The second mutation that can occur is a dominant mutation in the MFN2 gene on chromosome 1. This gene is associated with inter-mitochondrial fusing within the cell. Although there is not yet evidence for the specific translational difference between the wild-type and CMT mutated forms of this gene, it is understood that in CMT-afflicted individuals, the mitochondria will aggregate excessively within the cell. These aggregates can be disruptive and even prevent entire cells from functioning. More specifically, in neurons, mitochondrial masses block axonal pathways, inhibiting the transmission of their electrical signals to their target destination. The third mutation includes several missense mutations in the GJB1 gene, which is responsible for gap junction beta 1 protein. This protein helps develop connexin 32 bridges to enhance cell communication between neurons and their complementary Schwann cells in the PNS, and neurons and their complementary oligodendrocytes in the CNS. This specific mutation, unlike the previous two, is X-linked. 

The presence and combination of any of these mutations causes severe damage to the nervous system of afflicted individuals. The result from them is that over time, if an individual afflicted with CMT does not maintain daily activity, they will be more prone to the loss of function of their damaged neurons. They may develop symptoms such as loss of feeling in their extremities, as well as muscle tension and cramps, which can be painful.