Polyneuropathy, the most common form of peripheral neuropathy, is a condition in which neurons of the peripheral nervous system dysfunction progressively, over time, in a length dependent manner–the longest neurons being initially affected followed by sequentially shorter neurons. Many factors contribute to polyneuropathy but as with degenerative diseases of the nervous system such as Alzheimer’s disease and Parkinson’s disease, mitochondrial dysfunction–causing decreased ATP production and intraneuronal energy deficiency–may represent a common mechanism.
The ability of peripheral neurons to conduct action potentials is dependent upon, among other factors, the maintenance of a precise gradient of sodium and potassium ions across the neuronal cell membrane. The sodium-potassium pump, an array of membrane-resident macromolecules, maintains this gradient and, in so doing, consumes the majority of ATP produced by neuronal mitochondria. Inefficiencies in the functioning of the pump have been shown to cause polyneuropathy–as demonstrated in studies showing decreased pump activity, structural variations which decrease pump efficiency and fewer pumps molecules.
Because the pump consumes the majority of energy produced by neuronal mitochondria, it would be reasonable to hypothesize that damage to mitochondria or other conditions that impair ATP production would cause decreased pump activity and result in polyneuropathy.
The work of Bennett, et al. appears to support this hypothesis. They argue that cancer chemotherapy, HIV infection, and diabetes damage the mitochondria of peripheral sensory neurons–a condition they call mitotoxicity–reducing energy availability and causing distal symmetrical sensory peripheral neuropathy.
This hypothesis is also consistent with polyneuropathies associated with thiamine deficiency– diabetic polyneuropathy, alcoholic polyneuropathy, and others–in which thiamine deficiency impairs carbohydrate metabolism and reduces intraneuronal ATP production. These polyneuropathies often improve with thiamine replacement therapy and the increased ATP levels associated with it.
Although the causes of polyneuropathy are certainly multifactorial, decreased intraneuronal energy availability and its effect on sodium-potassium pump efficiency appear to be a factor in multiple etiologies. This hypothesis is supported by observations that mitochondrial damage and thiamine deficiency–both of which decrease intraneuronal energy availability–are often associated with polyneuropathy.
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