ReviewCNS neuroscience & therapeutics2012
The upside of APP at synapses.
Review in CNS neuroscience & therapeutics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
52 citing papers in PubMed, 1 synthesis or guideline pooled it, 82 citations in OpenAlex.
- Dissecting Complex and Multifactorial Nature of Alzheimer's Disease Pathogenesis: a Clinical, Genomic, and Systems Biology Perspective.Molecular neurobiology · 2016Pooled it
- Insulin Signaling in Alzheimer's Disease: Association with Brain Insulin Resistance.International journal of molecular sciences · 2026Review
- Amyloid Beta in Alzheimer's Disease: Mechanisms, Biomarker Potential, and Therapeutic Targets.CNS neuroscience & therapeutics · 2025Review
- Gene-Exercise Interactions in Amyloid Metabolism and Clearance: Implications for Alzheimer's Disease.International journal of molecular sciences · 2025Review
- Genome-Wide Identification of Microglia-Related RNA-Binding Proteins and Regulated Alternative Splicing in Spinal Cord Injury.ACS omega · 2025Article
- Decoding the Role of Neurotrophins in Glycogen Synthase Kinase 3-Beta Regulation in Alzheimer's Disease.Molecular neurobiology · 2025Review
- Conditioned Generative Modeling of Molecular Glues: A Realistic AI Approach for Synthesizable Drug-like Molecules.Biomolecules · 2025Article
- Insulin resistance in Alzheimer's disease: signalling mechanisms and therapeutics strategies.Inflammopharmacology · 2025Review
- Coupling of Alzheimer's Disease Genetic Risk Factors with Viral Susceptibility and Inflammation.Aging and disease · 2024Review
- Pathways linking microbiota-gut-brain axis with neuroinflammatory mechanisms in Alzheimer's pathophysiology.Microbiome research reports · 2024Review
- The Drosophila homolog of APP promotes Dscam expression to drive axon terminal growth, revealing interaction between Down syndrome genes.Disease models & mechanisms · 2023Article
- Organ and cell-specific biomarkers of Long-COVID identified with targeted proteomics and machine learning.Molecular medicine (Cambridge, Mass.) · 2023Article
- Interactions of amyloidogenic proteins with mitochondrial protein import machinery in aging-related neurodegenerative diseases.Frontiers in physiology · 2023Review
- Article
- Insulin and Insulin Resistance in Alzheimer's Disease.International journal of molecular sciences · 2021Review
- 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
- Insulin-like growth factor-1 improves postoperative cognitive dysfunction following splenectomy in aged rats.Experimental and therapeutic medicine · 2021Article
- Presynaptic APP levels and synaptic homeostasis are regulated by Akt phosphorylation of huntingtin.eLife · 2020Article
- Insulin Resistance at the Crossroad of Alzheimer Disease Pathology: A Review.Frontiers in endocrinology · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The memory dysfunctions that characterize Alzheimer's disease (AD) are strongly correlated with synapse loss. The amyloid precursor protein (APP) and its cleavage product Aβ play central roles in synapse and memory loss, and thus are strongly implicated in the pathogenesis of AD. Numerous in vitro and transgenic AD mouse model studies have shown that overexpression of APP leads to Aβ accumulation, which causes decreased synaptic activity and dendritic spine density. However, the normal synaptic function of APP itself is not fully understood. Several recent studies have found that full-length APP promotes synaptic activity, synapse formation, and dendritic spine formation. These findings cast APP as a potential key player in learning and memory. It is of interest that the synaptic functions of full-length APP are opposite to the effects associated with pathological Aβ accumulation. In this review, we will summarize the normal functions of APP at synapses and spines along with other known functions of APP, including its role in cell motility, neuronal migration, and neurite outgrowth. These studies shed light on the physiological actions of APP, independent of Aβ effects, and thus lead to a better understanding of the synaptic dysfunctions associated with AD.
Indexed as
Identifiers
What OpenQuestion holds
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.