ArticlePloS one2012
Knockdown of amyloid precursor protein in zebrafish causes defects in motor axon outgrowth.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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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.
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Who cites it
14 citing papers in PubMed, 47 citations in OpenAlex.
- Experimental modeling of Alzheimer's disease: Translational lessons from cross-taxon analyses.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Review
- Genetic and chemical disruption of amyloid precursor protein processing impairs zebrafish sleep maintenance.iScience · 2024Article
- Alzheimer's Disease: Models and Molecular Mechanisms Informing Disease and Treatments.Bioengineering (Basel, Switzerland) · 2024Review
- Studying zebrafish nervous system structure and function in health and disease with electron microscopy.Development, growth & differentiation · 2023Review
- Assessing Drug Administration Techniques in Zebrafish Models of Neurological Disease.International journal of molecular sciences · 2023Review
- Effect ofAdvances in pharmacological and pharmaceutical sciences · 2021Article
- Zebrafish as an Emerging Model for Bioassay-Guided Natural Product Drug Discovery for Neurological Disorders.Medicines (Basel, Switzerland) · 2019Review
- Reduced Abundance and Subverted Functions of Proteins in Prion-Like Diseases: Gained Functions Fascinate but Lost Functions Affect Aetiology.International journal of molecular sciences · 2017Review
- Decrease in levels of the evolutionarily conserved microRNA miR-124 affects oligodendrocyte numbers in Zebrafish, Danio rerio.Invertebrate neuroscience : IN · 2015Article
- Using the zebrafish model for Alzheimer's disease research.Frontiers in genetics · 2014Review
- Dosage of amyloid precursor protein affects axonal contact guidance in Down syndrome.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2014Article
- In vivo modeling of the morbid human genome using Danio rerio.Journal of visualized experiments : JoVE · 2013Article
- Origins of amyloid-β.BMC genomics · 2013Article
- Amyloid precursor protein is an autonomous growth cone adhesion molecule engaged in contact guidance.PloS one · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Amyloid precursor protein (APP) plays a pivotal role in Alzheimer's disease (AD) pathogenesis, but its normal physiological functions are less clear. Combined deletion of the APP and APP-like protein 2 (APLP2) genes in mice results in post-natal lethality, suggesting that APP performs an essential, if redundant, function during embryogenesis. We previously showed that injection of antisense morpholino to reduce APP levels in zebrafish embryos caused convergent-extension defects. Here we report that a reduction in APP levels causes defective axonal outgrowth of facial branchiomotor and spinal motor neurons, which involves disorganized axonal cytoskeletal elements. The defective outgrowth is caused in a cell-autonomous manner and both extracellular and intracellular domains of human APP are required to rescue the defective phenotype. Interestingly, wild-type human APP rescues the defective phenotype but APPswe mutation, which causes familial AD, does not. Our results show that the zebrafish model provides a powerful system to delineate APP functions in vivo and to study the biological effects of APP mutations.
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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.