ReviewExperimental neurology2010
Signaling effect of amyloid-beta(42) on the processing of AbetaPP.
Review in Experimental neurology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 64 citations in OpenAlex.
- The dysregulation of innate immunity by Porphyromonas gingivalis in the etiology of Alzheimer's disease.Journal of internal medicine · 2026Review
- Amyloid Beta in Alzheimer's Disease: Mechanisms, Biomarker Potential, and Therapeutic Targets.CNS neuroscience & therapeutics · 2025Review
- Mitochondrial Damage and Autophagy Dysregulation in Alzheimer's Disease: Mechanisms and Therapeutic Opportunities.Neurochemical research · 2025Review
- Older Amyloid Beta as a Candidate Blood Biomarker of Early Cognitive Decline in the Elderly-A Preliminary Study.Current issues in molecular biology · 2025Article
- Are mitophagy enhancers therapeutic targets for Alzheimer's disease?Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2022Review
- Structural Features and Toxicity of α-Synuclein Oligomers Grown in the Presence of DOPAC.International journal of molecular sciences · 2021Article
- Secernin-1 is a novel phosphorylated tau binding protein that accumulates in Alzheimer's disease and not in other tauopathies.Acta neuropathologica communications · 2019Article
- Oxidative DNA Damage Signalling in Neural Stem Cells in Alzheimer's Disease.Oxidative medicine and cellular longevity · 2019Review
- Caenorhabditis elegans hub genes that respond to amyloid beta are homologs of genes involved in human Alzheimer's disease.PloS one · 2019Article
- Tyrosine Rotamer States in Beta Amyloid: Signatures of Aggregation and Fibrillation.ACS omega · 2018Article
- Insight into the Molecular Imaging of Alzheimer's Disease.International journal of biomedical imaging · 2016Review
- Aβ Influences Cytoskeletal Signaling Cascades with Consequences to Alzheimer's Disease.Molecular neurobiology · 2015Review
- Alzheimer's disease: Unique markers for diagnosis & new treatment modalities.The Indian journal of medical research · 2015Review
- Successful therapies for Alzheimer's disease: why so many in animal models and none in humans?Frontiers in pharmacology · 2014Review
- Increased inflammatory response in cytomegalovirus seropositive patients with Alzheimer's disease.PloS one · 2014Article
- Wild type TDP-43 induces neuro-inflammation and alters APP metabolism in lentiviral gene transfer models.Experimental neurology · 2012Article
- Article
- Article
- Article
- Amyloid-β-induced amyloid-β secretion: a possible feed-forward mechanism in Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2011Article
Corrections and comments
- Commented on by
Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
Abstract
The effects of amyloid-beta are extremely complex. Current work in the field of Alzheimer disease is focusing on discerning the impact between the physiological signaling effects of soluble low molecular weight amyloid-beta species and the more global cellular damage that could derive from highly concentrated and/or aggregated amyloid. Being able to dissect the specific signaling events, to understand how soluble amyloid-beta induces its own production by up-regulating BACE1 expression, could lead to new tools to interrupt the distinctive feedback cycle with potential therapeutic consequences. Here we describe a positive loop that exists between the secretases that are responsible for the generation of the amyloid-beta component of Alzheimer disease. According to our hypothesis, in familial Alzheimer disease, the primary overproduction of amyloid-beta can induce BACE1 transcription and drive a further increase of amyloid-beta precursor protein processing and resultant amyloid-beta production. In sporadic Alzheimer disease, many factors, among them oxidative stress and inflammation, with consequent induction of presenilins and BACE1, would activate a loop and proceed with the generation of amyloid-beta and its signaling role onto BACE1 transcription. This concept of a signaling effect by and feedback on the amyloid-beta precursor protein will likely shed light on how amyloid-beta generation, oxidative stress, and secretase functions are intimately related in sporadic Alzheimer disease.
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.