ArticleThe Journal of biological chemistry2010
Beta-amyloid causes depletion of synaptic vesicles leading to neurotransmission failure.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.
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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.
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Who cites it
78 citing papers in PubMed, 177 citations in OpenAlex.
- Phenserine efficacy in Alzheimer's disease.Journal of Alzheimer's disease : JAD · 2010Trial
- Widespread synaptic density loss in schizophrenia follows molecular and network architecture.Molecular psychiatry · 2026Article
- Digging Deep into Alzheimer Disease: How Electron Microscopy Helps Elucidating Its Pathogenesis.Cellular and molecular neurobiology · 2026Review
- Amyloid-β acute exposition affects the CA1 hippocampal network activity and its topological organization, evaluated with multielectrode arrays.Frontiers in dementia · 2026Article
- Pathological calcium influx through amyloid beta pores disrupts synaptic function.Cell calcium · 2025Article
- GALM Alleviates Aβ Pathology and Cognitive Deficit Through Increasing ADAM10 Maturation in a Mouse Model of Alzheimer's Disease.Neuroscience bulletin · 2025Article
- CaCell reports · 2025Article
- Unraveling the neuroprotective mechanisms of elephant black garlic extract against beta amyloid peptide-induced neurotoxicity.Frontiers in nutrition · 2025Article
- Article
- Systematic Analysis of Biological Processes Reveals Gene Co-expression Modules Driving Pathway Dysregulation in Alzheimer's Disease.bioRxiv : the preprint server for biology · 2024Article
- Physiological Roles of β-amyloid in Regulating Synaptic Function: Implications for AD Pathophysiology.Neuroscience bulletin · 2023Review
- SorCS1 inhibits amyloid-β binding to neurexin and rescues amyloid-β-induced synaptic pathology.Life science alliance · 2023Article
- Damaged mitochondria coincide with presynaptic vesicle loss and abnormalities in alzheimer's disease brain.Acta neuropathologica communications · 2023Article
- A Function of Amyloid-β in Mediating Activity-Dependent Axon/Synapse Competition May Unify Its Roles in Brain Physiology and Pathology.Journal of Alzheimer's disease : JAD · 2023Review
- Endogenous Amyloid-formed CaFunction (Oxford, England) · 2023Article
- Neuroprotective Properties of Eudesmin on a Cellular Model of Amyloid-β Peptide Toxicity.Journal of Alzheimer's disease : JAD · 2023Article
- Bioactive human Alzheimer brain soluble Aβ: pathophysiology and therapeutic opportunities.Molecular psychiatry · 2022Review
- Amyloidosis in Alzheimer's Disease: Pathogeny, Etiology, and Related Therapeutic Directions.Molecules (Basel, Switzerland) · 2022Review
- The Stimulatory Effects of Intracellular α-Synuclein on Synaptic Transmission Are Attenuated by 2-Octahydroisoquinolin-2(1H)-ylethanamine.International journal of molecular sciences · 2021Article
- Super-resolution microscopy: a closer look at synaptic dysfunction in Alzheimer disease.Nature reviews. Neuroscience · 2021Review
18 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
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer disease is a progressive neurodegenerative brain disorder that leads to major debilitating cognitive deficits. It is believed that the alterations capable of causing brain circuitry dysfunctions have a slow onset and that the full blown disease may take several years to develop. Therefore, it is important to understand the early, asymptomatic, and possible reversible states of the disease with the aim of proposing preventive and disease-modifying therapeutic strategies. It is largely unknown how amyloid beta-peptide (A beta), a principal agent in Alzheimer disease, affects synapses in brain neurons. In this study, we found that similar to other pore-forming neurotoxins, A beta induced a rapid increase in intracellular calcium and miniature currents, indicating an enhancement in vesicular transmitter release. Significantly, blockade of these effects by low extracellular calcium and a peptide known to act as an inhibitor of the A beta-induced pore prevented the delayed failure, indicating that A beta blocks neurotransmission by causing vesicular depletion. This new mechanism for A beta synaptic toxicity should provide an alternative pathway to search for small molecules that can antagonize these effects of A beta.
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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.