ReviewMolecular brain2011
APP processing in Alzheimer's disease.
Review in Molecular brain, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 462 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
462 citing papers in PubMed, 1 synthesis or guideline pooled it, 939 citations in OpenAlex.
- Systematic review and meta-analysis of randomized controlled trials on the effects of exercise interventions on amyloid beta levels in humans.Experimental brain research · 2024Pooled it
- A new era of genome-wide association studies in the field of Alzheimer's disease and overlapping co-pathologies: lessons learned from a neuropathology-centered approach.Acta neuropathologica · 2026Review
- Tuberostemonine ameliorates Alzheimer's disease pathology by suppression of the p38 MAPK signaling pathway.iScience · 2026Article
- The interplay between gut microbiota and Alzheimer's disease: mechanistic insights from dysbiosis to disease modulation.Metabolic brain disease · 2026Review
- Molecular Mechanisms of Neurodegenerative Diseases: Emerging Biomarkers and Therapeutic Targets.Brain sciences · 2026Review
- Omega-3 Fatty Acids and Alzheimer's Disease: Toward a New Understanding of Neuroprotective Mechanisms and Intervention Strategies.Marine drugs · 2026Review
- A human telomerase reverse transcriptase-derived peptide GV1001 rescues neurodegeneration in a mouse model of Alzheimer disease.Experimental & molecular medicine · 2026Article
- Molecular Mechanisms Underlying Alzheimer's Disease Pathogenesis: Comprehensive Overview.International journal of molecular sciences · 2026Review
- Engineered APP C-terminus Alters Its Native Transcript Dynamics in Differentiated SH-SY5Y-Derived Neurons.Molecular neurobiology · 2026Article
- Solvent-free synthesis of quinazolinone-chalcone hybrids and their evaluation as dual inhibitors of AChE and BuChE for alzheimer's disease.Die Naturwissenschaften · 2026Article
- Multi-Target-Directed Ligands (MTDLs) as Potential Therapeutic Candidates Targeting Multiple Pathogenic Factor of Alzheimer's Disease.CNS neuroscience & therapeutics · 2026Review
- Amyloid-β 1-42 fibrils regulate SH-SY5Y cell adhesion in a delayed manner.Journal of Alzheimer's disease : JAD · 2026Article
- Astrocytoma-Specific Prognostic Associations of Amyloid-Related Biological Processes.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026Article
- Small Molecule Therapeutics Targeting Amyloid-β in Alzheimer's Disease: Mechanisms, Clinical Progress, and Future Strategies.Experimental neurobiology · 2026Review
- Small-Molecule Targeting of the Iron-Responsive Element in the APP mRNA 5'-UTR to Control Amyloid Translation in Alzheimer's Disease.International journal of molecular sciences · 2026Review
- The exocyst is an insulin-sensitive regulator of amyloid precursor protein trafficking and amyloid-beta generation in neurons.bioRxiv : the preprint server for biology · 2026Article
- Comparative analyses of regional and temporal transcriptomics of early human and mouse central nervous systems.iScience · 2026Article
- Platelet proteomic signatures of amyloid β-positive mild cognitive impairment and Alzheimer's disease.Molecular brain · 2026Article
- The microtubule nexus linking amyloid beta and tau: A simple and unifying theory for the underlying cause of Alzheimer's disease.PNAS nexus · 2026Article
- APP-C31 pathology as a target in neurodegenerative diseases.Journal of biomedical science · 2026Review
402 more citing papers are in PubMed but not listed here.
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 2 institutions in 2 countries.
Funding
Abstract
An important pathological feature of Alzheimer's disease (AD) is the presence of extracellular senile plaques in the brain. Senile plaques are composed of aggregations of small peptides called β-amyloid (Aβ). Multiple lines of evidence demonstrate that overproduction/aggregation of Aβ in the brain is a primary cause of AD and inhibition of Aβ generation has become a hot topic in AD research. Aβ is generated from β-amyloid precursor protein (APP) through sequential cleavages first by β-secretase and then by γ-secretase complex. Alternatively, APP can be cleaved by α-secretase within the Aβ domain to release soluble APPα and preclude Aβ generation. Cleavage of APP by caspases may also contribute to AD pathologies. Therefore, understanding the metabolism/processing of APP is crucial for AD therapeutics. Here we review current knowledge of APP processing regulation as well as the patho/physiological functions of APP and its metabolites.
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.