ArticleJournal of cell science2010
CHMP2B mutants linked to frontotemporal dementia impair maturation of dendritic spines.
Article in Journal of cell science, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.
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Who cites it
42 citing papers in PubMed, 1 synthesis or guideline pooled it, 71 citations in OpenAlex.
- Functional validation of CHMP7 as an ADHD risk gene.Translational psychiatry · 2020Pooled it
- Astrocytes mobilize a broader repertoire of lysosomal repair mechanisms than neurons.iScience · 2026Article
- ESCRT-III function in membrane fission and repair.Nature reviews. Molecular cell biology · 2026Review
- Mislocalization of FTD3-associated mutant CHMP2B to the nucleus of human neurons due to loss of a nuclear export signal.Acta neuropathologica communications · 2026Article
- Dysregulation of the endosomal sorting complex III is linked to neurodegeneration in progressive multiple sclerosis.Brain pathology (Zurich, Switzerland) · 2026Article
- Review
- Astrocyte dysfunction and neuronal network hyperactivity in a CRISPR engineered pluripotent stem cell model of frontotemporal dementia.Brain communications · 2023Article
- Alteration of the Neuromuscular Junction and Modifications of Muscle Metabolism in Response to Neuron-Restricted Expression of the CHMP2BBiomolecules · 2022Article
- Biomarkers and molecular mechanisms of Amyotrophic Lateral Sclerosis.AIMS neuroscience · 2022Review
- Synaptic dysfunction in ALS and FTD: anatomical and molecular changes provide insights into mechanisms of disease.Frontiers in molecular neuroscience · 2022Review
- Neuroprotective activity of ursodeoxycholic acid in CHMP2BNeurobiology of disease · 2020Article
- Expression of a human variant of CHMP2B linked to neurodegeneration in Drosophila external sensory organs leads to cell fate transformations associated with increased Notch activity.Developmental neurobiology · 2020Article
- Granulovacuolar degeneration bodies are neuron-selective lysosomal structures induced by intracellular tau pathology.Acta neuropathologica · 2019Article
- ESCRT Proteins Control the Dendritic Morphology of Developing and Mature Hippocampal Neurons.Molecular neurobiology · 2019Article
- Frontotemporal dementia causative CHMP2B impairs neuronal endolysosomal traffic-rescue by TMEM106B knockdown.Brain : a journal of neurology · 2018Article
- Molecular Genetics of Frontotemporal Dementia Elucidated byInternational journal of molecular sciences · 2018Review
- Amyloid precursor protein products concentrate in a subset of exosomes specifically endocytosed by neurons.Cellular and molecular life sciences : CMLS · 2018Article
- The role of CHMP2BBrain research · 2016Review
- RNA Imaging with Dimeric Broccoli in Live Bacterial and Mammalian Cells.Current protocols in chemical biology · 2016Article
- α-Synuclein interferes with the ESCRT-III complex contributing to the pathogenesis of Lewy body disease.Human molecular genetics · 2016Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The highly conserved ESCRT-III complex is responsible for deformation and cleavage of membranes during endosomal trafficking and other cellular activities. In humans, dominant mutations in the ESCRT-III subunit CHMP2B cause frontotemporal dementia (FTD). The decade-long process leading to this cortical degeneration is not well understood. One possibility is that, akin to other neurodegenerative diseases, the pathogenic protein affects the integrity of dendritic spines and synapses before any neuronal death. Using confocal microscopy and 3D reconstruction, we examined whether expressing the FTD-linked mutants CHMP2B(intron5) and CHMP2B(Delta10) in cultured hippocampal neurons modified the number or structure of spines. Both mutants induced a significant decrease in the proportion of large spines with mushroom morphology, without overt degeneration. Furthermore, CHMP2B(Delta10) induced a drop in frequency and amplitude of spontaneous excitatory postsynaptic currents, suggesting that the more potent synapses were lost. These effects seemed unrelated to changes in autophagy. Depletion of endogenous CHMP2B by RNAi resulted in morphological changes similar to those induced by mutant CHMP2B, consistent with dominant-negative activity of pathogenic mutants. Thus, CHMP2B is required for spine growth. Taken together, these results demonstrate that a mutant ESCRT-III subunit linked to a human neurodegenerative disease can disrupt the normal pattern of spine development.
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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.