ArticleThe European journal of neuroscience2019
Kalirin-7 prevents dendritic spine dysgenesis induced by amyloid beta-derived oligomers.
Article in The European journal of neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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.
The trial behind it
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Rare and novel genetic variants in sporadic and familial Alzheimer's disease: insights from the first Saudi cohort.Frontiers in aging · 2026Article
- Are Methylation Patterns in theInternational journal of molecular sciences · 2024Article
- Cognitive synaptopathy: synaptic and dendritic spine dysfunction in age-related cognitive disorders.Frontiers in aging neuroscience · 2024Review
- The Labyrinthine Landscape of APP Processing: State of the Art and Possible Novel Soluble APP-Related Molecular Players in Traumatic Brain Injury and Neurodegeneration.International journal of molecular sciences · 2023Article
- Review
- Role of Kalirin and mouse strain in retention of spatial memory training in an Alzheimer's disease model mouse line.Neurobiology of aging · 2020Article
- Rapid 3D Enhanced Resolution Microscopy Reveals Diversity in Dendritic Spinule Dynamics, Regulation, and Function.Neuron · 2020Article
- Kalirin and Trio: RhoGEFs in Synaptic Transmission, Plasticity, and Complex Brain Disorders.Trends in neurosciences · 2020Review
- The Toxicity and Polymorphism of β-Amyloid Oligomers.International journal of molecular sciences · 2020Review
- Early-Occurring Dendritic Spines Alterations in Mouse Models of Alzheimer's Disease Inform on Primary Causes of Neurodegeneration.Frontiers in synaptic neuroscience · 2020Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Synapse degeneration and dendritic spine dysgenesis are believed to be crucial early steps in Alzheimer's disease (AD), and correlate with cognitive deficits in AD patients. Soluble amyloid beta (Aβ)-derived oligomers, also termed Aβ-derived diffusible ligands (ADDLs), accumulate in the brain of AD patients and play a crucial role in AD pathogenesis. ADDLs bind to mature hippocampal neurons, induce structural changes in dendritic spines and contribute to neuronal death. However, mechanisms underlying structural and toxic effects are not fully understood. Here, we report that ADDLs bind to cultured mature cortical pyramidal neurons and induce spine dysgenesis. ADDL treatment induced the rapid depletion of kalirin-7, a brain-specific guanine-nucleotide exchange factor for the small GTPase Rac1, from spines. Kalirin-7 is a key regulator of dendritic spine morphogenesis and maintenance in forebrain pyramidal neurons and here we show that overexpression of kalirin-7 prevents ADDL-induced spine degeneration. Taken together, our results suggest that kalirin-7 may play a role in the early events leading to synapse degeneration, and its pharmacological activation may prevent or delay synapse pathology 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 Socratic graph.