ArticleiScience2022
Aβ-induced synaptic impairments require CaMKII activity that is stimulated by indirect signaling events.
Article in iScience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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
3 citing papers in PubMed, 7 citations in OpenAlex.
- Aβ impairs the LTP-related movement of endogenous CaMKII but not of exogenous GFP-CaMKII.Molecular biology of the cell · 2025Article
- Oxygen/glucose-deprivation causes long-term impairment of synaptic CaMKII movement.bioRxiv : the preprint server for biology · 2025Article
- CaMKII modulates memory destabilization by regulating the interaction of theta and gamma oscillations.Frontiers in cellular neuroscience · 2025Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Aβ bears homology to the CaMKII regulatory domain, and peptides derived from this domain can bind and disrupt the CaMKII holoenzyme, suggesting that Aβ could have a similar effect. Notably, Aβ impairs the synaptic CaMKII accumulation that is mediated by GluN2B binding, which requires CaMKII assembly into holoenzymes. Furthermore, this Aβ-induced impairment is prevented by CaMKII inhibitors that should also inhibit the putative direct Aβ binding. However, our study did not find any evidence for direct effects of Aβ on CaMKII: Aβ did not directly disrupt CaMKII holoenzymes, GluN2B binding, T286 autophosphorylation, or kinase activity
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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.