ArticleThe EMBO journal2011
APP and APLP2 are essential at PNS and CNS synapses for transmission, spatial learning and LTP.
Article in The EMBO journal, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 103 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
103 citing papers in PubMed, 1 synthesis or guideline pooled it, 183 citations in OpenAlex.
- Pooled it
- IntelliCage protocols using incentive-disincentive dual motivation work with male as well as female mice and reveal sex differences in motivated behavior.Frontiers in behavioral neuroscience · 2026Article
- Amyloid Beta in Alzheimer's Disease: Mechanisms, Biomarker Potential, and Therapeutic Targets.CNS neuroscience & therapeutics · 2025Review
- Amyloid precursor protein modulates cerebellar Purkinje cell activity and motor function through regulation of Nav1.6 currents.PLoS biology · 2025Article
- A multi-omic atlas of human autonomic and sensory ganglia implicates cell types in peripheral neuropathies.bioRxiv : the preprint server for biology · 2025Article
- Mid-life exposure to chronic stress accelerates cerebrovascular dysfunction and upregulates oxidative stress in Alzheimer's disease mice.Journal of Alzheimer's disease : JAD · 2025Article
- Immunohistochemical profile of non-invasive follicular thyroid neoplasm with papillary-like nuclear features (NIFTP) versus other thyroid follicular lesions.Diagnostic pathology · 2025Article
- A comprehensive and standardized pipeline for automated profiling of higher cognition in mice.Cell reports methods · 2025Article
- The AICD interactome: implications in neurodevelopment and neurodegeneration.Biochemical Society transactions · 2024Review
- IER3IP1-mutations cause microcephaly by selective inhibition of ER-Golgi transport.Cellular and molecular life sciences : CMLS · 2024Article
- APP family member dimeric complexes are formed predominantly in synaptic compartments.Cell & bioscience · 2023Article
- APP in the Neuromuscular Junction for the Development of Sarcopenia and Alzheimer's Disease.International journal of molecular sciences · 2023Review
- The Pathology of Primary Familial Brain Calcification: Implications for Treatment.Neuroscience bulletin · 2023Review
- IntelliCage: the development and perspectives of a mouse- and user-friendly automated behavioral test system.Frontiers in behavioral neuroscience · 2023Review
- APPsα rescues CDK5 and GSK3β dysregulation and restores normal spine density in Tau transgenic mice.Frontiers in cellular neuroscience · 2023Article
- APPsα Rescues Tau-Induced Synaptic Pathology.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Finding New Ways How to Control BACE1.The Journal of membrane biology · 2022Article
- Single cell transcriptomics reveals dysregulated cellular and molecular networks in a fragile X syndrome model.PLoS genetics · 2022Article
- Effects of amyloid precursor protein peptide APP96-110, alone or with human mesenchymal stromal cells, on recovery after spinal cord injury.Neural regeneration research · 2022Article
- Lack of APLP1 leads to subtle alterations in neuronal morphology but does not affect learning and memory.Frontiers in molecular neuroscience · 2022Article
43 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
18 authors at 6 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Despite its key role in Alzheimer pathogenesis, the physiological function(s) of the amyloid precursor protein (APP) and its proteolytic fragments are still poorly understood. Previously, we generated APPsα knock-in (KI) mice expressing solely the secreted ectodomain APPsα. Here, we generated double mutants (APPsα-DM) by crossing APPsα-KI mice onto an APLP2-deficient background and show that APPsα rescues the postnatal lethality of the majority of APP/APLP2 double knockout mice. Surviving APPsα-DM mice exhibited impaired neuromuscular transmission, with reductions in quantal content, readily releasable pool, and ability to sustain vesicle release that resulted in muscular weakness. We show that these defects may be due to loss of an APP/Mint2/Munc18 complex. Moreover, APPsα-DM muscle showed fragmented post-synaptic specializations, suggesting impaired postnatal synaptic maturation and/or maintenance. Despite normal CNS morphology and unaltered basal synaptic transmission, young APPsα-DM mice already showed pronounced hippocampal dysfunction, impaired spatial learning and a deficit in LTP that could be rescued by GABA(A) receptor inhibition. Collectively, our data show that APLP2 and APP are synergistically required to mediate neuromuscular transmission, spatial learning and synaptic plasticity.
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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.