ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012
β-secretase cleavage of the fly amyloid precursor protein is required for glial survival.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
22 citing papers in PubMed, 29 citations in OpenAlex.
- Amyloid-β disrupts APP-regulated protein aggregation and dissociation from recycling endosomal membranes.The EMBO journal · 2025Article
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- Nutraceutical and Probiotic Approaches to Examine Molecular Interactions of the Amyloid Precursor Protein APP inInternational journal of molecular sciences · 2021Review
- Developing a Rational, Optimized Product ofFrontiers in nutrition · 2021Article
- Better Sleep at Night: How Light Influences Sleep inFrontiers in physiology · 2020Review
- A Role forFrontiers in cellular neuroscience · 2019Article
- Restoring Tip60 HAT/HDAC2 Balance in the Neurodegenerative Brain Relieves Epigenetic Transcriptional Repression and Reinstates Cognition.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Alzheimer's Disease and Sleep-Wake Disturbances: Amyloid, Astrocytes, and Animal Models.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Review
- Drosophila Full-Length Amyloid Precursor Protein Is Required for Visual Working Memory and Prevents Age-Related Memory Impairment.Current biology : CB · 2018Article
- Neuronal migration during development and the amyloid precursor protein.Current opinion in insect science · 2016Review
- Amyloid Precursor Proteins Are Dynamically Trafficked and Processed during Neuronal Development.Frontiers in molecular neuroscience · 2016Article
- Analysis of Amyloid Precursor Protein Function in Drosophila melanogaster.Frontiers in molecular neuroscience · 2016Review
- Modeling the complex pathology of Alzheimer's disease in Drosophila.Experimental neurology · 2015Review
- Manipulations of amyloid precursor protein cleavage disrupt the circadian clock in aging Drosophila.Neurobiology of disease · 2015Article
- Mutations in PNPLA6 are linked to photoreceptor degeneration and various forms of childhood blindness.Nature communications · 2015Article
- Amyloid-β Peptide Exacerbates the Memory Deficit Caused by Amyloid Precursor Protein Loss-of-Function in Drosophila.PloS one · 2015Article
- Probing the enigma: unraveling glial cell biology in invertebrates.Current opinion in neurobiology · 2013Review
- Presenilin controls kinesin-1 and dynein function during APP-vesicle transport in vivo.Human molecular genetics · 2013Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
β-secretase (or BACE1) is the key enzyme in the production of β-amyloid (Aβ), which accumulates in the senile plaques characteristic for Alzheimer's disease. Consequently, the lack of BACE1 prevents β-processing of the amyloid precursor protein and Aβ production, which made it a promising target for drug development. However, the loss of BACE1 is also detrimental, leading to myelination defects and altered neuronal activity, functions that have been associated with the cleavage of Neuregulin and a voltage-gated sodium channel subunit. Here we show that the Drosophila ortholog of BACE, dBACE, is required for glial survival. Cell-specific knockdown experiments reveal that this is a non-cell autonomous function, as a knockdown of dBACE in photoreceptor neurons leads to progressive degeneration of glia in their target zone, the lamina. Interestingly, this phenotype is suppressed by the loss of the fly amyloid precursor protein (APPL), whereas a secretion-deficient form of APPL enhances the degeneration. This shows that full-length APPL in neurons promotes the death of neighboring glial cells and that β-processing of APPL is needed to prevent glial death. These results therefore not only demonstrate a novel function for an APP protein in glia, but they also show this function specifically requires regulation by β-cleavage.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.