ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2015
The full-length form of the Drosophila amyloid precursor protein is involved in memory formation.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed.
- Amyloid precursor protein ortholog Appl acts with Vnd during mushroom body axon growth in Drosophila.Genetics · 2026Article
- Astrocyte-to-neuron HNature metabolism · 2025Article
- Exploring the multifaceted functions of APPL in metabolism and memory using Drosophila melanogaster.Molecules and cells · 2025Article
- The Drosophila amyloid precursor protein homologue mediates neuronal survival and neuroglial interactions.PLoS biology · 2020Article
- Glutamate Receptor Trafficking and Protein Synthesis Mediate the Facilitation of LTP by Secreted Amyloid Precursor Protein-Alpha.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Drosophila Full-Length Amyloid Precursor Protein Is Required for Visual Working Memory and Prevents Age-Related Memory Impairment.Current biology : CB · 2018Article
- Article
- Anti-Aβ single-chain variable fragment antibodies restore memory acquisition in a Drosophila model of Alzheimer's disease.Scientific reports · 2017Article
- Amyloid Precursor Protein inThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- APP Protein Family Signaling at the Synapse: Insights from Intracellular APP-Binding Proteins.Frontiers in molecular neuroscience · 2017Review
- Role of APP Interactions with Heterotrimeric G Proteins: Physiological Functions and Pathological Consequences.Frontiers in molecular neuroscience · 2017Review
- APP as a Protective Factor in Acute Neuronal Insults.Frontiers in molecular neuroscience · 2017Review
- Neuronal migration during development and the amyloid precursor protein.Current opinion in insect science · 2016Review
- Drosophila Neprilysins Are Involved in Middle-Term and Long-Term Memory.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Role ofFrontiers in molecular neuroscience · 2016Review
- Amyloid Precursor Proteins Are Dynamically Trafficked and Processed during Neuronal Development.Frontiers in molecular neuroscience · 2016Article
- The APP Intracellular Domain Is Required for Normal Synaptic Morphology, Synaptic Plasticity, and Hippocampus-Dependent Behavior.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Amyloid-β Peptide Exacerbates the Memory Deficit Caused by Amyloid Precursor Protein Loss-of-Function in Drosophila.PloS one · 2015Article
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3 authors.
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No grant is acknowledged in the PubMed record.
Abstract
The APP plays a central role in AD, a pathology that first manifests as a memory decline. Understanding the role of APP in normal cognition is fundamental in understanding the progression of AD, and mammalian studies have pointed to a role of secreted APPα in memory. In Drosophila, we recently showed that APPL, the fly APP ortholog, is required for associative memory. In the present study, we aimed to characterize which form of APPL is involved in this process. We show that expression of a secreted-APPL form in the mushroom bodies, the center for olfactory memory, is able to rescue the memory deficit caused by APPL partial loss of function. We next assessed the impact on memory of the Drosophila α-secretase kuzbanian (KUZ), the enzyme initiating the nonamyloidogenic pathway that produces secreted APPLα. Strikingly, KUZ overexpression not only failed to rescue the memory deficit caused by APPL loss of function, it exacerbated this deficit. We further show that in addition to an increase in secreted-APPL forms, KUZ overexpression caused a decrease of membrane-bound full-length species that could explain the memory deficit. Indeed, we observed that transient expression of a constitutive membrane-bound mutant APPL form is sufficient to rescue the memory deficit caused by APPL reduction, revealing for the first time a role of full-length APPL in memory formation. Our data demonstrate that, in addition to secreted APPL, the noncleaved form is involved in memory, raising the possibility that secreted and full-length APPL act together in memory processes.
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