ArticleExperimental neurology2011
A selective role for ARMS/Kidins220 scaffold protein in spatial memory and trophic support of entorhinal and frontal cortical neurons.
Article in Experimental neurology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
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Who cites it
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.
- Extended genome-wide association study employing the African genome resources panel identifies novel susceptibility loci for Alzheimer's disease in individuals of African ancestry.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Pooled it
- Evidence that cholinergic mechanisms contribute to hyperexcitability at early stages in Alzheimer's disease.Frontiers in dementia · 2025Review
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- Choline supplementation in early life improves and low levels of choline can impair outcomes in a mouse model of Alzheimer's disease.bioRxiv : the preprint server for biology · 2024Article
- Article
- Phospholipase D3 degrades mitochondrial DNA to regulate nucleotide signaling and APP metabolism.Nature communications · 2023Article
- ARMS-NF-κB signaling regulates intracellular ROS to induce autophagy-associated cell death upon oxidative stress.iScience · 2023Article
- Kidins220/ARMS modulates brain morphology and anxiety-like traits in adult mice.Cell death discovery · 2022Article
- Rapid Aging in the Perforant Path Projections to the Rodent Dentate Gyrus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- SINO Syndrome Causative KIDINS220/ARMS Gene Regulates Adipocyte Differentiation.Frontiers in cell and developmental biology · 2021Article
- Kidins220/ARMS controls astrocyte calcium signaling and neuron-astrocyte communication.Cell death and differentiation · 2020Article
- Adult neurogenesis in the mouse dentate gyrus protects the hippocampus from neuronal injury following severe seizures.Hippocampus · 2019Article
- PARK14 (D331Y) PLA2G6 Causes Early-Onset Degeneration of Substantia Nigra Dopaminergic Neurons by Inducing Mitochondrial Dysfunction, ER Stress, Mitophagy Impairment and Transcriptional Dysregulation in a Knockin Mouse Model.Molecular neurobiology · 2019Article
- Increased gyrification and aberrant adult neurogenesis of the dentate gyrus in adult rats.Brain structure & function · 2017Article
- Neurotrophin signalling: novel insights into mechanisms and pathophysiology.Clinical science (London, England : 1979) · 2017Review
- Prefrontal neuronal integrity predicts symptoms and cognition in schizophrenia and is sensitive to genetic heterogeneity.Schizophrenia research · 2016Article
- Phenotypically distinct subtypes of psychosis accompany novel or rare variants in four different signaling genes.EBioMedicine · 2016Article
- The carbonic anhydrase inhibitor methazolamide prevents amyloid beta-induced mitochondrial dysfunction and caspase activation protecting neuronal and glial cells in vitro and in the mouse brain.Neurobiology of disease · 2016Article
- Stepping Out of the Shade: Control of Neuronal Activity by the Scaffold Protein Kidins220/ARMS.Frontiers in cellular neuroscience · 2016Review
- Interictal spike frequency varies with ovarian cycle stage in a rat model of epilepsy.Experimental neurology · 2015Article
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
Progressive cortical pathology is common to several neurodegenerative and psychiatric disorders. The entorhinal cortex (EC) and frontal cortex (FC) are particularly vulnerable, and neurotrophins have been implicated because they appear to be protective. A downstream signal transducer of neurotrophins, the ankyrin repeat-rich membrane spanning scaffold protein/Kidins 220 (ARMS) is expressed in the cortex, where it could play an important role in trophic support. To test this hypothesis, we evaluated mice with a heterozygous deletion of ARMS (ARMS(+/-) mice). Remarkably, the EC and FC were the regions that demonstrated the greatest defects. Many EC and FC neurons became pyknotic in ARMS(+/-) mice, so that large areas of the EC and FC were affected by 12 months of age. Areas with pyknosis in the EC and FC of ARMS(+/-) mice were also characterized by a loss of immunoreactivity to a neuronal antigen, NeuN, which has been reported after insult or injury to cortical neurons. Electron microscopy showed that there were defects in mitochondria, myelination, and multilamellar bodies in the EC and FC of ARMS(+/-) mice. Although primarily restricted to the EC and FC, pathology appeared to be sufficient to cause functional impairments, because ARMS(+/-) mice performed worse than wild-type on the Morris water maze. Comparisons of males and females showed that female mice were the affected sex in all comparisons. Taken together, the results suggest that the expression of a prominent neurotrophin receptor substrate normally protects the EC and FC, and that ARMS may be particularly important in females.
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