ReviewCell research2012
APP physiological and pathophysiological functions: insights from animal models.
Review in Cell research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 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
56 citing papers in PubMed, 105 citations in OpenAlex.
- Article
- Negative correlation between microRNA and insulin sensitivity gene expression in adipose tissue: potential implications for diabetes and neurodegenerative diseases.Nutrition & metabolism · 2026Article
- APP E590D mutation increases generation of Aβ and Aη peptides and exacerbates tauopathy.NPJ dementia · 2026Article
- Article
- Multi-omics delineate growth factor network underlying exercise effects in an Alzheimer's mouse model.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Astrocyte-to-neuron HNature metabolism · 2025Article
- A Novel Missense Variant in SORBS2 Is Causative With Familial Alzheimer's Disease.CNS neuroscience & therapeutics · 2025Article
- Roles of the Receptor for Advanced Glycation End Products and Its Ligands in the Pathogenesis of Alzheimer's Disease.International journal of molecular sciences · 2025Review
- The Role of Hydrogen Sulfide in iNOS and APP Localization and Expression in Neurons and Glial Cells Under Traumatic Effects: An Experimental Study with Bioinformatics Analysis and Biomodeling.International journal of molecular sciences · 2024Article
- Diverse signaling mechanisms and heterogeneity of astrocyte reactivity in Alzheimer's disease.Journal of neurochemistry · 2024Review
- Protein modification in neurodegenerative diseases.MedComm · 2024Review
- Multi-omics delineate growth factor network underlying exercise effects in an Alzheimer's mouse model.bioRxiv : the preprint server for biology · 2024Article
- Neuropathogenesis-on-chips for neurodegenerative diseases.Nature communications · 2024Review
- Aberrant palmitoylation caused by a ZDHHC21 mutation contributes to pathophysiology of Alzheimer's disease.BMC medicine · 2023Article
- Article
- DYRK1a Inhibitor Mediated Rescue ofFrontiers in pharmacology · 2022Article
- Metformin activates chaperone-mediated autophagy and improves disease pathologies in an Alzheimer disease mouse model.Protein & cell · 2021 · on this mapArticle
- Copper, Iron, Selenium and Lipo-Glycemic Dysmetabolism in Alzheimer's Disease.International journal of molecular sciences · 2021Review
- Nutraceutical and Probiotic Approaches to Examine Molecular Interactions of the Amyloid Precursor Protein APP inInternational journal of molecular sciences · 2021Review
- Alternative Targets to Fight Alzheimer's Disease: Focus on Astrocytes.Biomolecules · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The amyloid precursor protein (APP) has been under intensive study in recent years, mainly due to its critical role in the pathogenesis of Alzheimer's disease (AD). β-Amyloid (Aβ) peptides generated from APP proteolytic cleavage can aggregate, leading to plaque formation in human AD brains. Point mutations of APP affecting Aβ production are found to be causal for hereditary early onset familial AD. It is very likely that elucidating the physiological properties of APP will greatly facilitate the understanding of its role in AD pathogenesis. A number of APP loss- and gain-of-function models have been established in model organisms including Caenorhabditis elegans, Drosophila, zebrafish and mouse. These in vivo models provide us valuable insights into APP physiological functions. In addition, several knock-in mouse models expressing mutant APP at a physiological level are available to allow us to study AD pathogenesis without APP overexpression. This article will review the current physiological and pathophysiological animal models of APP.
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.