ReviewNeural regeneration research2018
Synaptic dysfunction in Alzheimer's disease: the effects of amyloid beta on synaptic vesicle dynamics as a novel target for therapeutic intervention.
Review in Neural regeneration research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 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
79 citing papers in PubMed, 1 synthesis or guideline pooled it, 162 citations in OpenAlex.
- Deregulated mitochondrial microRNAs in Alzheimer's disease: Focus on synapse and mitochondria.Ageing research reviews · 2022Pooled it
- Prodromal changes in cortical neuron physiology before amyloid pathology in a mild model of Alzheimer's disease.Scientific reports · 2026Article
- Membrane Merger Dynamics in Exocytosis and Endocytosis.Advances in experimental medicine and biology · 2026Review
- Pathological calcium influx through amyloid beta pores disrupts synaptic function.Cell calcium · 2025Article
- Therapeutic Potentials of the Seaweed-Derived Compounds for Alzheimer's Disease.Molecules (Basel, Switzerland) · 2025Review
- Integrated multi-omics analyses of synaptosomes revealed synapse-associated novel targets in Alzheimer's disease.Molecular psychiatry · 2025Article
- Adiponectin Receptor Agonist Ameliorates Synaptic Dysfunction in 3xTg Alzheimer's Disease Mouse Model by Activation of AMPK.CNS neuroscience & therapeutics · 2025Article
- Exploring the Mechanisms and Therapeutic Approaches of Mitochondrial Dysfunction in Alzheimer's Disease: An Educational Literature Review.Molecular neurobiology · 2025Review
- Astaxanthin nanoemulsion improves cognitive function and synaptic integrity in Streptozotocin-induced Alzheimer's disease model.Metabolic brain disease · 2025Article
- Astrocytic EphA4 signaling is important for the elimination of excitatory synapses in Alzheimer's disease.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Protective Effects of Bifidobacterium Breve MCC1274 as a Novel Therapy for Alzheimer's Disease.Nutrients · 2025Review
- Evolution of Alzheimer's Disease Therapeutics: From Conventional Drugs to Medicinal Plants, Immunotherapy, Microbiotherapy and Nanotherapy.Pharmaceutics · 2025Review
- Revealing excitation-inhibition imbalance in Alzheimer's disease using multiscale neural model inversion of resting-state functional MRI.Communications medicine · 2025Article
- Neuronal expression of S100B triggered by oligomeric AFrontiers in molecular neuroscience · 2025Article
- Advancing Alzheimer's Disease Modelling by Developing a Refined Biomimetic Brain Microenvironment for Facilitating High-Throughput Screening of Pharmacological Treatment Strategies.International journal of molecular sciences · 2024Review
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- A Computational Approach in the Systematic Search of the Interaction Partners of Alternatively Spliced TREM2 Isoforms.International journal of molecular sciences · 2024Article
- Tremendous Fidelity of Vitamin D3 in Age-related Neurological Disorders.Molecular neurobiology · 2024Review
19 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
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The most prevalent form of dementia in the elderly is Alzheimer's disease. A significant contributing factor to the progression of the disease appears to be the progressive accumulation of amyloid-β42 (Aβ42), a small hydrophobic peptide. Unfortunately, attempts to develop therapies targeting the accumulation of Aβ42 have not been successful to treat or even slow down the disease. It is possible that this failure is an indication that targeting downstream effects rather than the accumulation of the peptide itself might be a more effective approach. The accumulation of Aβ42 seems to affect various aspects of physiological cell functions. In this review, we provide an overview of the evidence that implicates Aβ42 in synaptic dysfunction, with a focus on how it contributes to defects in synaptic vesicle dynamics and neurotransmitter release. We discuss data that provide new insights on the Aβ42 induced pathology of Alzheimer's disease and a more detailed understanding of its contribution to the synaptic deficiencies that are associated with the early stages of the disease. Although the precise mechanisms that trigger synaptic dysfunction are still under investigation, the available data so far has enabled us to put forward a model that could be used as a guide to generate new therapeutic targets for pharmaceutical intervention.
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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.