ReviewInternational journal of molecular sciences2021
An Unbalanced Synaptic Transmission: Cause or Consequence of the Amyloid Oligomers Neurotoxicity?
Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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
36 citing papers in PubMed, 1 synthesis or guideline pooled it, 68 citations in OpenAlex.
- Genetic and environmental risk factors for dementia in African adults: A systematic review.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Pooled it
- Presynaptic accumulation of APP-CTFβ may contribute to synaptic dysfunction in Alzheimer's disease.The EMBO journal · 2026Article
- Unknotting the Role of circRNAs and IGF2BP3 in Alzheimer's Disease.Cellular and molecular neurobiology · 2026Review
- A Multi-Axis Framework for Late-Life Alzheimer's Disease Interpretation.Journal of personalized medicine · 2026Review
- Neuronal hyperexcitability: A key to unraveling hippocampal synaptic dysfunction in Lafora disease.Epilepsia · 2026Article
- Cognitive dysfunction in type 1 diabetes: role of TREM2 in microglial activation and Aβ pathology.Journal of neuroinflammation · 2026Article
- Subregional Functional Connectivity of the Precuneus as a Preclinical Biomarker in Alzheimer's Disease.Neurology research international · 2026Article
- Natural Chiral Scaffolds in Alzheimer's Disease: Therapeutic Potential, Mechanism, and Clinical Aspects.BioMed research international · 2026Review
- Mitochondrial ecosystem restoration in Alzheimer's disease: from mechanisms to multi-target therapeutic strategies.Frontiers in cell and developmental biology · 2026Review
- The association between gamma-aminobutyric acid levels and suicidal behavior in depression.BMC psychiatry · 2025Article
- Multi-target approach to Alzheimer's disease prevention and treatment: antioxidant, anti-inflammatory, and amyloid- modulating mechanisms.Neurogenetics · 2025Review
- Acupuncture Ameliorates Alzheimer's-Like Cognitive Impairment and Pathological Changes via Regulating the Intestinal Fungal Community in APP/PS1 Mice.Neuropsychiatric disease and treatment · 2025Article
- Magnetic stirring with iron oxide nanospinners accretes neurotoxic AβMaterials today. Bio · 2024Article
- Effects of Dietary Fiber, Phenolic Compounds, and Fatty Acids on Mental Health: Possible Interactions with Genetic and Epigenetic Aspects.Nutrients · 2024Review
- Understanding the mechanisms of green tea EGCG against amyloid β oligomer neurotoxicity through computational studies.RSC advances · 2024Article
- The probable role of tissue plasminogen activator/neuroserpin axis in Alzheimer's disease: a new perspective.Acta neurologica Belgica · 2024Review
- Locally Synthetized 17-β-Estradiol Reverses Amyloid-β-42-Induced Hippocampal Long-Term Potentiation Deficits.International journal of molecular sciences · 2024Article
- Neprilysin inhibitors and risk of Alzheimer's disease: A future perspective.Journal of cellular and molecular medicine · 2024Review
- Early Astrocytic Dysfunction Is Associated with Mistuned Synapses as well as Anxiety and Depressive-Like Behavior in the AppNL-F Mouse Model of Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2024Article
- Correlation of brain tissue volume loss with inflammatory biomarkers IL1β, P-tau, T-tau, and NLPR3 in the aging cognitively impaired population.Frontiers in aging neuroscience · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Amyloid-β (Aβ) 1-40 and 1-42 peptides are key mediators of synaptic and cognitive dysfunction in Alzheimer's disease (AD). Whereas in AD, Aβ is found to act as a pro-epileptogenic factor even before plaque formation, amyloid pathology has been detected among patients with epilepsy with increased risk of developing AD. Among Aβ aggregated species, soluble oligomers are suggested to be responsible for most of Aβ's toxic effects. Aβ oligomers exert extracellular and intracellular toxicity through different mechanisms, including interaction with membrane receptors and the formation of ion-permeable channels in cellular membranes. These damages, linked to an unbalance between excitatory and inhibitory neurotransmission, often result in neuronal hyperexcitability and neural circuit dysfunction, which in turn increase Aβ deposition and facilitate neurodegeneration, resulting in an Aβ-driven vicious loop. In this review, we summarize the most representative literature on the effects that oligomeric Aβ induces on synaptic dysfunction and network disorganization.
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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.