ArticleActa neuropathologica communications2014
Comparative analysis of single and combined APP/APLP knockouts reveals reduced spine density in APP-KO mice that is prevented by APPsα expression.
Article in Acta neuropathologica communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 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
58 citing papers in PubMed, 97 citations in OpenAlex.
- APP SUMOylation prevents BACE1 cleavage of APP and increases BACE1 degradation to promote the nonamyloidogenic pathway.Molecular medicine (Cambridge, Mass.) · 2025Article
- Diazinon-induced Cognitive Impairment: Alternations in Amyloid Precursor Proteins, and TNF-α Expression in the Hippocampus of Adult Rats.Current topics in medicinal chemistry · 2025Article
- CNTN4 modulates neural elongation through interplay with APP.Open biology · 2024Article
- Engineering memory with an extrinsically disordered kinase.Science advances · 2023Article
- Amyloid precursor protein and its interacting proteins in neurodevelopment.Biochemical Society transactions · 2023Review
- APP family member dimeric complexes are formed predominantly in synaptic compartments.Cell & bioscience · 2023Article
- 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
- Lack of APLP1 leads to subtle alterations in neuronal morphology but does not affect learning and memory.Frontiers in molecular neuroscience · 2022Article
- Fe65: A Scaffolding Protein of Actin Regulators.Cells · 2021Review
- Amyloid-Beta Mediates Homeostatic Synaptic Plasticity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Loss of all three APP family members during development impairs synaptic function and plasticity, disrupts learning, and causes an autism-like phenotype.The EMBO journal · 2021Article
- Amyloid Beta-Mediated Changes in Synaptic Function and Spine Number of Neocortical Neurons Depend on NMDA Receptors.International journal of molecular sciences · 2021Article
- The β-Secretase BACE1 in Alzheimer's Disease.Biological psychiatry · 2021Review
- Effect of a Cognitive Training Program on the Platelet APP Ratio in Patients with Alzheimer's Disease.International journal of molecular sciences · 2020Article
- Amyloid, APP, and Electrical Activity of the Brain.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2020Review
- Presynaptic APP levels and synaptic homeostasis are regulated by Akt phosphorylation of huntingtin.eLife · 2020Article
- PhIP exposure in rodents produces neuropathology potentially relevant to Alzheimer's disease.Toxicology · 2020Article
- Hebbian and Homeostatic Synaptic Plasticity-Do Alterations of One Reflect Enhancement of the Other?Frontiers in cellular neuroscience · 2020Article
- Is brain iron trafficking part of the physiology of the amyloid precursor protein?Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2019Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Synaptic dysfunction and synapse loss are key features of Alzheimer's pathogenesis. Previously, we showed an essential function of APP and APLP2 for synaptic plasticity, learning and memory. Here, we used organotypic hippocampal cultures to investigate the specific role(s) of APP family members and their fragments for dendritic complexity and spine formation of principal neurons within the hippocampus. Whereas CA1 neurons from APLP1-KO or APLP2-KO mice showed normal neuronal morphology and spine density, APP-KO mice revealed a highly reduced dendritic complexity in mid-apical dendrites. Despite unaltered morphology of APLP2-KO neurons, combined APP/APLP2-DKO mutants showed an additional branching defect in proximal apical dendrites, indicating redundancy and a combined function of APP and APLP2 for dendritic architecture. Remarkably, APP-KO neurons showed a pronounced decrease in spine density and reductions in the number of mushroom spines. No further decrease in spine density, however, was detectable in APP/APLP2-DKO mice. Mechanistically, using APPsα-KI mice lacking transmembrane APP and expressing solely the secreted APPsα fragment we demonstrate that APPsα expression alone is sufficient to prevent the defects in spine density observed in APP-KO mice. Collectively, these studies reveal a combined role of APP and APLP2 for dendritic architecture and a unique function of secreted APPs for spine density.
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