Zihan Huang
Xueji Dai
Baichun Jiang
Yan Kong- 1Department of Biochemistry and Molecular Biology, School of Medicine, Southeast University, Nanjing, China
- 2Department of Genetics, School of Basic Medical Sciences, Cheeloo College of Medicine, Shandong University, Jinan, China
Editorial on the Research Topic
Model organisms in neuroinflammation and neuropathy: Drosophila melanogaster
Neuroinflammation is the activated inflammatory response in the central nervous systems, including dysregulated cytokine release, reactive cytokine release, and activation of immune cells (Han et al., 2021). A plethora of evidence showed that neuroinflammation contributes to the pathogenesis of neurological disorders including Alzheimer's disease, Parkinson's disease, anxiety, and major depressive disorder (Leng and Edison, 2021; Sampson et al., 2016; Guo et al., 2023; Wu and Zhang, 2023). With evolutionally conserved mechanisms of immune response and convenience for genetic manipulation, Drosophila melanogaster is a widely used model organism to study the molecular mechanisms of neuropathy (Suzuki et al., 2023; Bussmann and Storkebaum, 2017; Muqit and Feany, 2002). To provide the overview of this Research Topic, we have selected four original research and review articles focusing on the neuroinflammation and neuropathy using Drosophila melanogaster.
In one research article, Zhao et al. investigated the role of total ginsenosides (TGGR) from ginseng on senescence. Feeding with TGGR during early adulthood extended the lifespan of Drosophila melanogaster dramatically. The food intake and reproductive capacity were not influenced by TGGR. Additionally, it improved the motility, intestine barrier, biorhythm homeostasis, and resilience to various stresses. Transcriptome profiling and molecular study showed that TGGR exert beneficial effects on longevity by targeting on genes involved in insulin, TOR and MAPK signaling. This study highlighted the translational value of active components in the traditional Chinese medicine on aging.
Dravecz et al. studied the contribution of Insulin/IGF-like signaling (IIS) to lifespan and health span. They previously found that targeted inhibition of neuronal IIS extended the lifespan. However, the negative geotaxis was unaffected and the exploratory walking behavior was worsened. This disconnection made them clarify the role of IIS in different types of neurons. They overexpressed the dominant negative form of insulin receptor to impair IIS in neuron type specific manner. Lifespan and locomotion abilities were used as redouts. Interestingly, IIS reduction selectively in serotonergic neurons extended the lifespan without influencing locomotion. In contrast, IIS inhibiton in cholinergic, GABAergic, dopaminergic, glutamatergic, and octopaminergic neurons had no effects or detrimental effects on lifespan and locomotor senescence. This study gave new ideas for neuron type-specific roles in lifespan and health span.
In a review article contributed by Asthana and Shravage, the role of mitophagy in Parkinson's disease Drosophila model was systemically discussed. As the second prevalent neurodegenerative disorder, Parkinson's disease is characterized as the degeneration of dopaminergic neurons, aggregation of α-synuclein (α-syn), and locomotor defects. Mitophagy is one of the major types of autophagy and regulates mitochondrial homeostasis. Impaired mitophagy was tightly correlated with PD. This review focused on the role of mitophagy modulators and potential PD drugs targeting mitophagy in Drosophila model. This review will accelerate the research of PD related mitophagy and targeting strategy in the future.
The mini-review by Bhattacharya shed light on peripheral neuropathy and axon degeneration. Traumatic, toxic, or genetically-induced insults impair the peripheral axons. They discussed the model establishment of peripheral nerve injury and neuropathy in Drosophila. The effects of injury on neurons and glias were systemically summarized. The peripheral axon injury models also gave platforms to clarify genes that participate in the pathogenesis and potential intervention strategies.
We expect the selected reviews and research articles could further our understanding of neuroinflammation and neuropathy. They also highlight the great value of Drosophila melanogaster as model organisms for the research of molecular pathogenesis and treatments in the field.
Author contributions
ZH: Writing – original draft. XD: Writing – original draft. BJ: Writing – original draft. YK: Conceptualization, Funding acquisition, Writing – original draft, Writing – review & editing.
Funding
The author(s) declare financial support was received for the research, authorship, and/or publication of this article. This study was supported by the National Natural Science Foundation of China (82371532).
Conflict of interest
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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References
Bussmann, J., and Storkebaum, E. (2017). Molecular pathogenesis of peripheral neuropathies: insights from Drosophila models. Curr. Opin. Genet. Dev. 44, 61–73. doi: 10.1016/j.gde.2017.01.011
Guo, B., Zhang, M., Hao, W., Wang, Y., Zhang, T., and Liu, C. (2023). Neuroinflammation mechanisms of neuromodulation therapies for anxiety and depression. Transl. Psychiat. 13:5. doi: 10.1038/s41398-022-02297-y
Han, V. X., Patel, S., Jones, H. F., and Dale, R. C. (2021). Maternal immune activation and neuroinflammation in human neurodevelopmental disorders. Nat. Rev. Neurol. 17, 564–579. doi: 10.1038/s41582-021-00530-8
Leng, F., and Edison, P. (2021). Neuroinflammation and microglial activation in Alzheimer disease: where do we go from here? Nat. Rev. Neurol. 17, 157–172. doi: 10.1038/s41582-020-00435-y
Muqit, M. M., and Feany, M. B. (2002). Modelling neurodegenerative diseases in Drosophila: a fruitful approach? Nat. Rev. Neurosci. 3, 237–243. doi: 10.1038/nrn751
Sampson, T. R., Debelius, J. W., Thron, T., Janssen, S., Shastri, G. G., Ilhan, Z. E., et al. (2016). Gut microbiota regulate motor deficits and neuroinflammation in a model of Parkinson's disease. Cell 167, 1469–1480.e12. doi: 10.1016/j.cell.2016.11.018
Suzuki, M., Kuromi, H., Shindo, M., Sakata, N., Niimi, N., Fukui, K., et al. (2023). A Drosophila model of diabetic neuropathy reveals a role of proteasome activity in the glia. iScience 26:106997. doi: 10.1016/j.isci.2023.106997
Keywords: neuroinflammation, neuropathy, Drosophila model, neurological disorder, aging
Citation: Huang Z, Dai X, Jiang B and Kong Y (2024) Editorial: Model organisms in neuroinflammation and neuropathy: Drosophila melanogaster. Front. Aging Neurosci. 16:1502502. doi: 10.3389/fnagi.2024.1502502
Received: 27 September 2024; Accepted: 02 October 2024;
Published: 14 October 2024.
Edited and reviewed by: Yu-Min Kuo, National Cheng Kung University, Taiwan
Copyright © 2024 Huang, Dai, Jiang and Kong. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: Yan Kong, kongyancn@163.com