ArticleCellular and molecular neurobiology2026
Indoleamine 2,3-Dioxygenase: A Potential Biomarker for Neural Damage Severity of Leprosy Neuropathy.
Article in Cellular and molecular neurobiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Neural damage, which could be characterized by demyelination and neuropathic pain, is a hallmark of leprosy, driven primarily by the interaction of Mycobacterium leprae with peripheral nerves, particularly Schwann cells. The role of indoleamine 2,3-dioxygenase (IDO) in neuroinflammation and neurodegeneration has been suggested; however, its precise contribution to leprosy-associated neuropathy remains poorly understood. This study aimed to determine whether variations in serum IDO activity, inferred from the kynurenine/tryptophan (Kyn/trp) ratio, could assist in distinguishing leprosy-associated neuropathy from other peripheral neuropathies. Additionally, we investigated the potential correlation between the increase in the Kyn/trp ratio and the extent of neural impairment. Based on clinical and electrophysiological evaluations, neural damage was classified into four severity types. Kyn/trp ratio was significantly higher in patients with leprosy neuropathy than in those with non-leprosy neuropathies. Moreover, we observed that patients exhibiting no sensory or motor responses have the highest IDO levels. Thus, the data presented here suggest that given the challenges in diagnosing leprosy neuropathy, IDO-1 activity may serve as a complementary diagnostic tool to help distinguish leprosy from other peripheral neuropathies.
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