Is Expression of Mutational/ Deletional Genetic Lesions Determined Chiefly by Specifically Altered Myelin-axonal Interactions in Peripheral Neuropathy?

Simple pathways of interactive influence constituted by the Schwann cell and by a myelin sheath/axon complex might involve effective modes of induced expression of genetic lesions of a mutational or deletional type. Indeed, the Schwann cell itself would perhaps help characterize how such genetic lesions in hereditary peripheral neuropathy would be expressed in specific clinical forms of involvement that pathobiologically are demyelinative or axonal independent of actual distinction between dynamics of myelin deposition or axonal viability. In simple terms, one might perhaps realize paradoxical systems of expression and of progression of hereditary peripheral neuropathies inherent to disturbed control of genetic lesion expression. Indeed, disturbed gene expression as induced by mutation or deletion of genes would appear further modulated by essential attributes of myelin sheath and axonal interactions, as further reflected particularly in terms of Schwann cell participation. In terms of a range of types of peripheral neuropathies of hereditary and acquired type, mechanistic pathways of axonal and Schwann cell response would participate in actually creating various modulated forms of expression of gene interaction. Gene expression itself might itself constitute integrative interaction between neuronal axon and Schwann cell participation in peripheral neuropathies of both inherited and acquired type.