ArticleProceedings of the National Academy of Sciences of the United States of America2013
Dnr1 mutations cause neurodegeneration in Drosophila by activating the innate immune response in the brain.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 137 papers.
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137 citing papers in PubMed, 208 citations in OpenAlex.
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- The caterpillar Manduca sexta brain shows changes in gene expression and protein abundance correlating with parasitic manipulation of behaviour.Scientific reports · 2024Article
- Glucocerebrosidase deficiency leads to neuropathology via cellular immune activation.PLoS genetics · 2024Article
- Emerging roles of antimicrobial peptides in innate immunity, neuronal function, and neurodegeneration.Trends in neurosciences · 2024Review
- The NF-κB Factor Relish maintains blood progenitor homeostasis in the developing Drosophila lymph gland.PLoS genetics · 2024Article
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- Dysregulation of innate immune signaling in animal models of spinal muscular atrophy.BMC biology · 2024Article
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77 more citing papers are in PubMed but not listed here.
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4 authors at 1 institution in 1 country.
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Abstract
A growing body of evidence in humans implicates chronic activation of the innate immune response in the brain as a major cause of neuropathology in various neurodegenerative conditions, although the mechanisms remain unclear. In an unbiased genetic screen for mutants exhibiting neurodegeneration in Drosophila, we have recovered a mutation of dnr1 (defense repressor 1), a negative regulator of the Imd (immune deficiency) innate immune-response pathway. dnr1 mutants exhibit shortened lifespan and progressive, age-dependent neuropathology associated with activation of the Imd pathway and elevated expression of AMP (antimicrobial peptide) genes. To test the hypothesis that overactivation of innate immune-response pathways in the brain is responsible for neurodegeneration, we demonstrated that direct bacterial infection in the brain of wild-type flies also triggers neurodegeneration. In both cases, neurodegeneration is dependent on the NF-κB transcription factor, Relish. Moreover, we found that neural overexpression of individual AMP genes is sufficient to cause neurodegeneration. These results provide a mechanistic link between innate immune responses and neurodegeneration and may have important implications for the role of neuroinflammation in human neurodegenerative diseases as well.
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