ArticleCell reports2019
Simultaneous Live Imaging of Multiple Endogenous Proteins Reveals a Mechanism for Alzheimer's-Related Plasticity Impairment.
Article in Cell reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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, 52 citations in OpenAlex.
- CaMKII monomers are sufficient for GluN2B binding, co-condensation, and synaptic potentiation.Molecular cell · 2026Article
- Article
- Aβ impairs the LTP-related movement of endogenous CaMKII but not of exogenous GFP-CaMKII.Molecular biology of the cell · 2025Article
- The neuroprotective γ-hydroxybutyrate analog 3-hydroxycyclopent-1-enecarboxylic acid does not directly affect CaMKIIα autophosphorylation at T286 or binding to GluN2B.Molecular pharmacology · 2025Article
- Oxygen/glucose-deprivation causes long-term impairment of synaptic CaMKII movement.bioRxiv : the preprint server for biology · 2025Article
- Discovery of FO-4-15, a novel 1,2,4-oxadiazole derivative, ameliorates cognitive impairments in 3×Tg mice by activating the mGluR1/CaMKIIα pathway.Acta pharmacologica Sinica · 2025Article
- miRNA-mediated control of gephyrin synthesis drives sustained inhibitory synaptic plasticity.EMBO reports · 2024Article
- Induction of LTP mechanisms in dually innervated dendritic spines.Scientific reports · 2024Article
- Article
- Studying CaMKII: Tools and standards.Cell reports · 2024Review
- Article
- miRNA-mediated control of gephyrin synthesis drives sustained inhibitory synaptic plasticity.bioRxiv : the preprint server for biology · 2023Article
- Physiological Roles of β-amyloid in Regulating Synaptic Function: Implications for AD Pathophysiology.Neuroscience bulletin · 2023Review
- Decreased nitrosylation of CaMKII causes aging-associated impairments in memory and synaptic plasticity in mice.Science signaling · 2023Article
- Distinct synaptic pools of DAPK1 differentially regulate activity-dependent synaptic CaMKII accumulation.iScience · 2023Article
- Short-term CaMKII inhibition with tatCN19o does not erase pre-formed memory and is neuroprotective in non-rodents.bioRxiv : the preprint server for biology · 2023Article
- CaMKII: a central molecular organizer of synaptic plasticity, learning and memory.Nature reviews. Neuroscience · 2022Review
- Review
- Aβ-induced synaptic impairments require CaMKII activity that is stimulated by indirect signaling events.iScience · 2022Article
- Genetically encoded intrabodies as high-precision tools to visualize and manipulate neuronal function.Seminars in cell & developmental biology · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
CaMKIIα is a central mediator of bidirectional synaptic plasticity, including long-term potentiation (LTP) and long-term depression (LTD). To study how CaMKIIα movement during plasticity is affected by soluble amyloid-β peptide oligomers (Aβ), we used FingR intrabodies to simultaneously image endogenous CaMKIIα and markers for excitatory versus inhibitory synapses in live neurons. Aβ blocks LTP-stimulus-induced CaMKIIα accumulation at excitatory synapses. This block requires CaMKII activity, is dose and time dependent, and also occurs at synapses without detectable Aβ; it is specific to LTP, as CaMKIIα accumulation at inhibitory synapses during LTD is not reduced. As CaMKII movement to excitatory synapses is required for normal LTP, its impairment can mechanistically explain Aβ-induced impairment of LTP. CaMKII movement during LTP requires binding to the NMDA receptor, and Aβ induces internalization of NMDA receptors. However, surprisingly, this internalization does not cause the block in CaMKIIα movement and is observed for extrasynaptic, but not synaptic, NMDA receptors.
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.