Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:4.1.2.13 (aldolase)
 3,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

On the whole, the treatment of peripheral neuropathies is disappointing, even when a cause has been identified, because nerve lesions, and particularly axonal diseases, are frequently severe, and the mechanisms or peripheral nerve fibre repair is very slow. However, during the last few years important advances have been made in the treatment of acute and chronic acute inflammatory demyelinating polyneuropathies, most probably of dysimmune origin, with plasma exchanges and, more recently, intravenous human plasma immunoglobulins. Therapeutic trials are in progress in neuropathies associated with monoclonal gammopathies, notably IgM. In diabetic neuropathy numerous studies are going on, in particular with aldolase reductase inhibitors and with gangliosides.
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PMID:[Therapeutic approach in peripheral neuropathies]. 131 14

The duration of diabetes, age and genetic predispositions are admitted agents of risk in diabetic neuropathy. The reasons of diabetic neuropathy are suspected in cooperation with various factors among which metabolic disturbances and ischaemia are the most important. The abnormal activation of sorbitol tract is very significant agent of development of diabetic neuropathy. The excess of sorbitol which is accumulating also in nervous tissue causes its damage in osmotic way. At the same time decreasing concentration of myoinositol reduces ATP-ase Na+/K+ activity which is important in impulse conduction. The overproduction of free oxygenic radical (oxidative lesion) and nitrogen oxide (vasodilator) deficiency is inducted by hyperglycaemia and the activation of aldolase reductase. Metabolic disturbances cause the decrease of carnitine concentration what deteriorates nerve sensitivity on growth factor. The activation of sorbitol tract leads to nonenzymatic proteins glycation which causes thickening of basement membrane and proliferation of endothelium cells. In this way increased vascular resistance decreases tissue perfusion and induces nerve hypoxia. The impairment of nerve blood supply depends on altered in diabetes rheological properties. They are inconveniently changed through hyperglycaemia, hyperlypidaemia, dysproteinaemia and excessive aggregation and rigidity of morphotic elements of blood.
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PMID:[Contemporary views on the pathogenesis of diabetic neuropathy]. 968 30