ReviewJournal of Alzheimer's disease : JAD2018
The Unexpected Role of Aβ1-42 Monomers in the Pathogenesis of Alzheimer's Disease.
Review in Journal of Alzheimer's disease : JAD, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.
- Regulatory role of the endocannabinoid system on glial cells toward cognitive function in Alzheimer's disease: A systematic review and meta-analysis of animal studies.Frontiers in pharmacology · 2023Pooled it
- Rhamnazin attenuates Amyloid β-Peptide (1-42) induced spatial memory impairments by modulation of BDNF-ERK signaling pathway.3 Biotech · 2026Article
- Overexpression of PGRMC2 in astrocytes improved cognitive function in a mouse model of Alzheimer's disease by modulating neuroinflammation.Journal of translational medicine · 2026Article
- Bornyl Acetate and Menthol Provide Neuroprotection Against Lipopolysaccharide-Induced Alzheimer's Disease-Like Condition in C57BL/6 Mice by Downregulating NARC-1 Lipid Antagonist.Molecular neurobiology · 2025Article
- Optimal control of monomers and oligomers degradation in an Alzheimer's disease model.Journal of mathematical biology · 2025Article
- Mapping the hippocampal spatial proteomic signature in male and female mice of an early Alzheimer's disease model.Biology of sex differences · 2025Article
- Expanding horizons in theragnostics: from oncology to multidisciplinary applications.La Radiologia medica · 2025Review
- Photobiomodulation modulates mitochondrial energy metabolism and ameliorates neurological damage in an APP/PS1 mousmodel of Alzheimer's disease.Alzheimer's research & therapy · 2025Article
- Passive Anti-amyloid Beta Monoclonal Antibodies: Lessons Learned over Past 20 Years.Neurology and therapy · 2024Review
- Exploring the therapeutic efficacy ofHeliyon · 2023Article
- Lecanemab (BAN2401): an anti-beta-amyloid monoclonal antibody for the treatment of Alzheimer disease.Expert opinion on investigational drugs · 2023Review
- Unveiling the Potential of Polyphenols as Anti-Amyloid Molecules in Alzheimer's Disease.Current neuropharmacology · 2023Review
- A how-to guide for a precision medicine approach to the diagnosis and treatment of Alzheimer's disease.Frontiers in aging neuroscience · 2023Review
- Europium-Doped Cerium Oxide Nanoparticles for Microglial Amyloid Beta Clearance and Homeostasis.ACS chemical neuroscience · 2022Article
- The Dynamics of β-Amyloid Proteoforms Accumulation in the Brain of a 5xFAD Mouse Model of Alzheimer's Disease.International journal of molecular sciences · 2021Article
- Multiple-Coated PLGA Nanoparticles Loading Triptolide Attenuate Injury of a Cellular Model of Alzheimer's Disease.BioMed research international · 2021Article
- Review
- The English (H6R) Mutation of the Alzheimer's Disease Amyloid-β Peptide Modulates Its Zinc-Induced Aggregation.Biomolecules · 2020Article
- Combining Virtual Screening Protocol and In Vitro Evaluation towards the Discovery of BACE1 Inhibitors.Biomolecules · 2020Article
- Osmolytes: A Possible Therapeutic Molecule for Ameliorating the Neurodegeneration Caused by Protein Misfolding and Aggregation.Biomolecules · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Amyloid-β (Aβ) has been proposed as a biomarker and a drug target for the therapy of Alzheimer's disease (AD). The neurotoxic entity and relevance of each conformational form of Aβ to AD pathology is still under debate; Aβ oligomers are considered the major killer form of the peptide whereas monomers have been proposed to be involved in physiological process. Here we reviewed some different effects mediated by monomers and oligomers on mechanisms involved in AD pathogenesis such as autophagy and tau aggregation. Data reported in this review demonstrate that Aβ monomers could have a major role in sustaining the pathogenesis of AD and that AD therapy should be focused not only in the removal of oligomers but also of monomers.
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.