ReviewMolecular neurobiology2022
The amyloid precursor protein: a converging point in Alzheimer's disease.
Review in Molecular neurobiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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
31 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.
- Re-evaluation of the efficacy and safety of anti-Aβ monoclonal antibodies (lecanemab/donanemab) in the treatment of early Alzheimer's disease.Frontiers in pharmacology · 2025Pooled it
- Cell-specific expression of APP and GABABrain research · 2026Article
- Autophagy and selective autophagy receptors: Key players against Alzheimer's disease.Neural regeneration research · 2026Article
- Article
- MicroRNA and Alzheimer's disease: Diagnostic biomarkers and potential therapeutic targets.Neural regeneration research · 2026Article
- Tagged and untagged amyloid precursor protein E2 domain have comparable thermal stability and metal-ion binding propensity.BMC research notes · 2026Article
- Article
- A perspective for alzheimer disease from gut microbiota-associated NMR-based fecal metabolomics: a study with 5XFAD mice.Metabolic brain disease · 2026Article
- APP-C31 pathology as a target in neurodegenerative diseases.Journal of biomedical science · 2026Review
- Co-expression-wide association studies link genetically regulated interactions with complex traits.Nature communications · 2025Article
- Oligodendrocytes show enriched expression of amyloid precursor protein and GABA B receptor isoform 1a.bioRxiv : the preprint server for biology · 2025Article
- Multidomain therapy for Alzheimer's disease: a scoping review of cognitive decline trials.Molecular neurodegeneration · 2025Article
- Central Nervous System-Derived Extracellular Vesicles as Biomarkers in Alzheimer's Disease.International journal of molecular sciences · 2025Review
- Copper homeostasis and cuproptosis: implications for neurodegenerative diseases.Frontiers in aging neuroscience · 2025Review
- The Link Between Matrix Metalloproteinases and Alzheimer's Disease Pathophysiology.Molecular neurobiology · 2025Review
- Promising neuroprotective potential of naringenin against trimethyltin-induced cognitive deficits and hippocampal neurodegeneration in rats.Frontiers in neuroscience · 2025Article
- Understanding the Molecular Impact of Physical Exercise on Alzheimer's Disease.International journal of molecular sciences · 2024Review
- The Azalea Hypothesis of Alzheimer Disease: A Functional Iron Deficiency Promotes Neurodegeneration.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2024Review
- Tetramethylpyrazine Nitrone (TBN) Reduces Amyloid β Deposition in Alzheimer's Disease Models by Modulating APP Expression, BACE1 Activity, and Autophagy Pathways.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Potential Application of MicroRNAs and Some Other Molecular Biomarkers in Alzheimer's Disease.Current issues in molecular biology · 2024Review
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
Abstract
The decades of evidence that showcase the role of amyloid precursor protein (APP), and its fragment amyloidβ (Aβ), in Alzheimer's disease (AD) pathogenesis are irrefutable. However, the absolute focus on the single APP metabolite Aβ as the cause for AD has resulted in APP and its other fragments that possess toxic propensity, to be overlooked as targets for treatment. The complexity of its processing and its association with systematic metabolism suggests that, if misregulated, APP has the potential to provoke an array of metabolic dysfunctions. This review discusses APP and several of its cleaved products with a particular focus on their toxicity and ability to disrupt healthy cellular function, in relation to AD development. We subsequently argue that the reduction of APP, which would result in a concurrent decrease in Aβ as well as all other toxic APP metabolites, would alleviate the toxic environment associated with AD and slow disease progression. A discussion of those drug-like compounds already identified to possess this capacity is also included.
Indexed as
Identifiers
What Socratic 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 Socratic graph.