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Updated: May 27, 2026

Lipidomics and Transcriptomics in Neurological Diseases
Published on: March 18, 2022
Alzheimer's and seizures: interleukin-18, indoleamine 2,3-dioxygenase and quinolinic Acid
1CRC, Rm 1/2, 1229 Dumbarton Road, Glasgow, Scotland, U.K.
Abstract:
Emergent seizures are common in Alzheimer's disease (AD), although the mechanisms mediating this are unknown. It is proposed that stress induced interleukin-18 (IL-18), via interferon-gamma (IFNy) and independently, increases indoleamine 2,3-dioxygenase (IDO) and subsequent quinolinic acid (QA) in microglia. QA increases seizures and concurrently contributes to neuronal loss via excitotoxicity. The ApoE4 allele interacts with IL-18 polymorphisms to increase the risk of AD, and seems likely to potentiate the emergence of seizures. Concurrent changes in IDO and the kynurenine pathways at the blood-brain-barrier (BBB) have implications for treatment, including in the efficacy of different anti-hypertensives. Melatonin is proposed to inhibit these overlapping excitotoxic and neurodegenerative processes, and would be a useful adjunctive treatment.
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