ArticleCellular and molecular life sciences : CMLS2021
Aβ1-16 controls synaptic vesicle pools at excitatory synapses via cholinergic modulation of synapsin phosphorylation.
Article in Cellular and molecular life sciences : CMLS, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- The missing link: Piccolino is essential for tethering synaptic vesicles to rod photoreceptor ribbons.The Journal of cell biology · 2026Article
- Serotonergic Psychedelics Rapidly Modulate Evoked Glutamate Release in Cultured Cortical Neurons.Journal of neurochemistry · 2025Article
- Hydroxynorketamine, but not ketamine, acts via α7 nicotinic acetylcholine receptor to control presynaptic function and gene expression.Translational psychiatry · 2024Article
- Developmental effect of RASopathy mutations on neuronal network activity on a chip.Frontiers in cellular neuroscience · 2024Article
- Physiological Roles of β-amyloid in Regulating Synaptic Function: Implications for AD Pathophysiology.Neuroscience bulletin · 2023Review
- The Amyloid Precursor Protein Regulates Synaptic Transmission at Medial Perforant Path Synapses.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Elevated amyloid beta disrupts the nanoscale organization and function of synaptic vesicle pools in hippocampal neurons.Cerebral cortex (New York, N.Y. : 1991) · 2023Article
- Role of Cholinergic Signaling in Alzheimer's Disease.Molecules (Basel, Switzerland) · 2022Review
- Development and Application of Automatized Routines for Optical Analysis of Synaptic Activity Evoked by Chemical and Electrical Stimulation.Frontiers in bioinformatics · 2022Article
- Overexpression of wild-type human amyloid precursor protein alters GABAergic transmission.Scientific reports · 2021Article
- γ-secretase targeting in Alzheimer's disease.Journal of Alzheimer's disease reportsReview
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Amyloid beta (Aβ) is linked to the pathology of Alzheimer's disease (AD). At physiological concentrations, Aβ was proposed to enhance neuroplasticity and memory formation by increasing the neurotransmitter release from presynapse. However, the exact mechanisms underlying this presynaptic effect as well as specific contribution of endogenously occurring Aβ isoforms remain unclear. Here, we demonstrate that Aβ1-42 and Aβ1-16, but not Aβ17-42, increased size of the recycling pool of synaptic vesicles (SV). This presynaptic effect was driven by enhancement of endogenous cholinergic signalling via α7 nicotinic acetylcholine receptors, which led to activation of calcineurin, dephosphorylation of synapsin 1 and consequently resulted in reorganization of functional pools of SV increasing their availability for sustained neurotransmission. Our results identify synapsin 1 as a molecular target of Aβ and reveal an effect of physiological concentrations of Aβ on cholinergic modulation of glutamatergic neurotransmission. These findings provide new mechanistic insights in cholinergic dysfunction observed in AD.
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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.