ArticleMolecular psychiatry2023
An IGFBP2-derived peptide promotes neuroplasticity and rescues deficits in a mouse model of Phelan-McDermid syndrome.
Article in Molecular psychiatry, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- Neuronal Igfbp2 deficiency in the prefrontal cortex impairs cognition through synaptic dysfunction in male mice.iScience · 2026Article
- Astrocytic Igfbp2 Promotes Spontaneous Seizures in a Mouse Model of Mesial Temporal Lobe Epilepsy.Glia · 2026Article
- Igfbp2 Downregulation in PVT-CeA Glutamatergic Circuits Drives Neonatal Anesthesia-Induced Fear Memory Deficits.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Impact of Heat Stress on Gene Expression in the Hypothalamic-Pituitary-Ovarian Axis of Hu Sheep.Animals : an open access journal from MDPI · 2025Article
- IGFBP-2 and IGF-II: Key Components of the Neural Stem Cell Niche? Implications for Glioblastoma Pathogenesis.International journal of molecular sciences · 2025Review
- Syngap1 promotes cognitive function through regulation of cortical sensorimotor dynamics.Nature communications · 2025Article
- Article
- Disease-relevant upregulation of P2YNature communications · 2024Article
- Insulin-like growth factor binding protein-2 in at-risk adults and autopsy-confirmed Alzheimer brains.Brain : a journal of neurology · 2024Article
- Article
- Disrupted extracellular matrix and cell cycle genes in autism-associated Shank3 deficiency are targeted by lithium.Molecular psychiatry · 2024Article
- Neuroplasticity of children in autism spectrum disorder.Frontiers in psychiatry · 2024Review
- A prefrontal cortex alpha/delta switch controls the transition from positive to negative affective states.Discover mental health · 2023Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
We developed an IGFBP2-mimetic peptide fragment, JB2, and showed that it promotes basal synaptic structural and functional plasticity in cultured neurons and mice. We demonstrate that JB2 directly binds to dendrites and synapses, and its biological activity involves NMDA receptor activation, gene transcription and translation, and IGF2 receptors. It is not IGF1 receptor-dependent. In neurons, JB2 induced extensive remodeling of the membrane phosphoproteome. Synapse and cytoskeletal regulation, autism spectrum disorder (ASD) risk factors, and a Shank3-associated protein network were significantly enriched among phosphorylated and dephosphorylated proteins. Haploinsufficiency of the SHANK3 gene on chromosome 22q13.3 often causes Phelan-McDermid Syndrome (PMS), a genetically defined form of autism with profound deficits in motor behavior, sensory processing, language, and cognitive function. We identified multiple disease-relevant phenotypes in a Shank3 heterozygous mouse and showed that JB2 rescued deficits in synaptic function and plasticity, learning and memory, ultrasonic vocalizations, and motor function; it also normalized neuronal excitability and seizure susceptibility. Notably, JB2 rescued deficits in the auditory evoked response latency, alpha peak frequency, and steady-state electroencephalography response, measures with direct translational value to human subjects. These data demonstrate that JB2 is a potent modulator of neuroplasticity with therapeutic potential for the treatment of PMS and ASD.
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Registered trials
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