ArticleCell death & disease2023
Blocking dPerk in the intestine suppresses neurodegeneration in a Drosophila model of Parkinson's disease.
Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- Revealing the Mechanisms of Alzheimer's, Parkinson's and Huntington's Diseases Through Invertebrate Models.Biology · 2026Review
- Insights into PINK1/Parkin function and dysfunction from Drosophila models.The Biochemical journal · 2025Review
- 4EHP and NELF-E regulate physiological ATF4 induction and proteostasis in disease models of Drosophila.Nature communications · 2025Article
- Imaginal discs produce neuropeptide-like precursor 1 to alleviate ER stress in response to warm temperatures.Communications biology · 2025Article
- Oral intake of aripiprazole compromises male fertility in Drosophila.Biology direct · 2025Article
- Emerging roles for integrated stress response signaling in homeostasis.The FEBS journal · 2025Review
- Oral administration of aripiprazole to Drosophila causes intestinal toxicity.Disease models & mechanisms · 2025Article
- Research progress on natural products in regulating the gut microbiota in Parkinson's disease.Frontiers in pharmacology · 2025Review
- Modeling neurodegenerative and neurodevelopmental disorders in theLearning & memory (Cold Spring Harbor, N.Y.) · 2024Review
- Measuring Constipation in a Drosophila Model of Parkinson's Disease.Journal of visualized experiments : JoVE · 2023Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Parkinson's disease (PD) is characterised by selective death of dopaminergic (DA) neurons in the midbrain and motor function impairment. Gastrointestinal issues often precede motor deficits in PD, indicating that the gut-brain axis is involved in the pathogenesis of this disease. The features of PD include both mitochondrial dysfunction and activation of the unfolded protein response (UPR) in the endoplasmic reticulum (ER). PINK1 is a mitochondrial kinase involved in the recycling of defective mitochondria, and PINK1 mutations cause early-onset PD. Like PD patients, pink1 mutant Drosophila show degeneration of DA neurons and intestinal dysfunction. These mutant flies also lack vital proteins due to sustained activation of the kinase R-like endoplasmic reticulum kinase (dPerk), a kinase that induces the UPR. Here, we investigated the role of dPerk in intestinal dysfunction. We showed that intestinal expression of dPerk impairs mitochondrial function, induces cell death, and decreases lifespan. We found that suppressing dPerk in the intestine of pink1-mutant flies rescues intestinal cell death and is neuroprotective. We conclude that in a fly model of PD, blocking gut-brain transmission of UPR-mediated toxicity, is neuroprotective.
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