ReviewNeurobiology of aging2013
Amyloid β precursor protein as a molecular target for amyloid β--induced neuronal degeneration in Alzheimer's disease.
Review in Neurobiology of aging, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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
24 citing papers in PubMed, 46 citations in OpenAlex.
- Gallein-Loaded Albumin Nanoparticles Prevent Amyloid-β-Induced Amyloidogenic APP Processing, Synaptic Loss, and Dendritic Pathology.Molecular neurobiology · 2026Article
- APP-C31 pathology as a target in neurodegenerative diseases.Journal of biomedical science · 2026Review
- Amyloid-β disrupts APP-regulated protein aggregation and dissociation from recycling endosomal membranes.The EMBO journal · 2025Article
- Research Progress on Phytochemicals from Mulberry with Neuroprotective Effects: A Review.Pharmaceuticals (Basel, Switzerland) · 2025Review
- The Biological Activity ofMolecules (Basel, Switzerland) · 2024Review
- Article
- AP2S1 regulates APP degradation through late endosome-lysosome fusion in cells and APP/PS1 mice.Traffic (Copenhagen, Denmark) · 2023Article
- Aβ Assemblies Promote Amyloidogenic Processing of APP and Intracellular Accumulation of Aβ42 Through Go/Gβγ Signaling.Frontiers in cell and developmental biology · 2022Article
- Effects ofAdvanced biomedical research · 2020Article
- Non-coding RNA influences in dementia.Non-coding RNA research · 2018Review
- APP signaling in Alzheimer's disease.Aging · 2018Article
- Revolution of Resting-State Functional Neuroimaging Genetics in Alzheimer's Disease.Trends in neurosciences · 2017Review
- Phosphoinositides: Two-Path Signaling in Neuronal Response to Oligomeric Amyloid β Peptide.Molecular neurobiology · 2017Article
- Amyloid-Beta and Phosphorylated Tau Accumulations Cause Abnormalities at Synapses of Alzheimer's disease Neurons.Journal of Alzheimer's disease : JAD · 2017Review
- The Role of Retromer in Alzheimer's Disease.Molecular neurobiology · 2016Review
- Role ofFrontiers in molecular neuroscience · 2016Review
- APP overexpression in the absence of NPC1 exacerbates metabolism of amyloidogenic proteins of Alzheimer's disease.Human molecular genetics · 2015Article
- Proteomic Profiling of Cranial (Superior) Cervical Ganglia Reveals Beta-Amyloid and Ubiquitin Proteasome System Perturbations in an Equine Multiple System Neuropathy.Molecular & cellular proteomics : MCP · 2015Article
- Evaluation of the amyloid beta-GFP fusion protein as a model of amyloid beta peptides-mediated aggregation: a study of DNAJB6 chaperone.Frontiers in molecular neuroscience · 2015Article
- Protective Effects of Dietary Supplementation with a Combination of Nutrients in a Transgenic Mouse Model of Alzheimer's Disease.PloS one · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
A role of amyloid β (Aβ) peptide aggregation and deposition in Alzheimer's disease (AD) pathogenesis is widely accepted. Significantly, abnormalities induced by aggregated Aβ have been linked to synaptic and neuritic degeneration, consistent with the "dying-back" pattern of degeneration that characterizes neurons affected in AD. However, molecular mechanisms underlying the toxic effect of aggregated Aβ remain elusive. In the last 2 decades, a variety of aggregated Aβ species have been identified and their toxic properties demonstrated in diverse experimental systems. Concurrently, specific Aβ assemblies have been shown to interact and misregulate a growing number of molecular effectors with diverse physiological functions. Such pleiotropic effects of aggregated Aβ posit a mayor challenge for the identification of the most cardinal Aβ effectors relevant to AD pathology. In this review, we discuss recent experimental evidence implicating amyloid β precursor protein (APP) as a molecular target for toxic Aβ assemblies. Based on a significant body of pathologic observations and experimental evidence, we propose a novel pathologic feed-forward mechanism linking Aβ aggregation to abnormalities in APP processing and function, which in turn would trigger the progressive loss of neuronal connectivity observed early in AD.
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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.