[Research progress on the correlation mechanism between innate immune imbalance and Alzheimer's disease based on Drosophila model].

Authors

Shasha Chen, Minghan He, Yumeng Huo, Fan Xing, Yufei Gao, Yichen Dai, Ning Gao, Songna Yin

Published in

Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology. Volume 42. Issue 10. Pages 931-937.

Abstract

Innate immune dysregulation is a common pathological basis for the development and progression of both infectious diseases and various chronic diseases. Drosophila melanogaster, owing to its highly conserved immune system, well-established genetic manipulation tools, and intact in vivo physiological environment, has become an important model for studying human immune-related diseases. This article systematically reviews the latest research progress on the Drosophila model regarding the "infection-innate immune dysregulation-Alzheimer's disease (AD)" axis. Studies using Drosophila models have shown that Gram-positive bacteria and fungi activate the Toll pathway, while Gram-negative bacteria activate the immune deficiency (Imd) pathway, leading to innate immune dysregulation; all of the above pathogen infections are associated with the pathological progression of AD. Peripheral immune dysregulation can mediate cross-organ inflammatory transmission through the gut-brain axis and the oral-gut-brain axis, thereby contributing to the exacerbation of AD pathological damage. The Drosophila tumor necrosis factor α (TNF-α) homolog Eiger, via activation of the tumor necrosis factor-c-Jun N-terminal kinase (TNF-JNK) pathway, mediates peripheral-immune-driven remote central neuroinflammation. These findings suggest that precise regulation of the innate immune system is critical for maintaining organismal homeostasis, and its dysregulation serves as a link between infectious diseases and AD. The Drosophila model provides a unique perspective for dissecting the pathological progression of "infection-innate immune dysregulation-AD," laying a theoretical foundation for AD intervention strategies targeting immune pathways, the gut-brain axis, and the oral-gut-brain axis, and also offering a reference for translational research on innate immunity-related diseases. It should be noted that the above conclusions are mainly based on mechanistic studies in the Drosophila model, and their extrapolation to human AD still requires further validation.

PMID:
42851057
Bibliographic data and abstract were imported from PubMed on 09 Oct 2026.

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