ArticleFrontiers in molecular neuroscience2024
Development of KCC2 therapeutics to treat neurological disorders.
Article in Frontiers in molecular neuroscience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Solute carrier membrane transporters: emerging targets in CNS disorders.Nature reviews. Drug discovery · 2026Review
- The Mechanism of Long Non-coding RNA GABPB1-AS1/SLC12A5 Regulating Neuronal Ferroptosis in Epileptic Seizures.Neurochemical research · 2026Article
- Small extracellular vesicle-integrated by herbal hydrogels for spatiotemporal immunomodulation and neurovascular repair following traumatic brain injury.Bioactive materials · 2026Article
- Article
- When the gatekeeper falls: developmental vulnerability of the thalamic reticular nucleus in neonatal and pediatric hypoxic-ischemic brain injury.Frontiers in systems neuroscience · 2026Review
- Excitability-margin narrowing as a candidate gating mechanism for maladaptive circuit reactivation: a ventral CA1-centered model.Frontiers in behavioral neuroscience · 2026Article
- Do Glioma Cells Rewire Neural Circuits through Epigenetic Changes? DNA Methylation Analysis of Genes Involved in Neuron-Glioma Communication in the Human Frontal Cortex.Journal of molecular neuroscience : MN · 2025Article
- KCC2 enhancers normalize reflex responses and improve locomotor function after chronic spinal cord injury.The Journal of physiology · 2025Article
- Altered GABAergic signaling and chloride homeostasis in eye movement circuits during late neurodevelopment: implications for Alzheimer's disease therapy.Frontiers in pharmacology · 2025Review
- Daphnetin Ameliorates the Amyloid β-Induced Alzheimer Disease via Restoring Potassium-Chloride Co-Transporter 2 (KCC2) Ion Channel Functions in Mice.Iranian journal of pharmaceutical research : IJPRArticle
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2 authors.
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Abstract
KCC2 is CNS neuron-specific chloride extruder, essential for the establishment and maintenance of the transmembrane chloride gradient, thereby enabling synaptic inhibition within the CNS. Herein, we highlight KCC2 hypofunction as a fundamental and conserved pathology contributing to neuronal circuit excitation/inhibition (E/I) imbalances that underly epilepsies, chronic pain, neuro-developmental/-traumatic/-degenerative/-psychiatric disorders. Indeed, downstream of both acquired and genetic factors, multiple pathologies (e.g., hyperexcitability and inflammation) converge to impair KCC2-dependent inhibition in CNS. When KCC2 hypofunction occurs, affected neurons are disinhibited due to impaired inhibitory responses to GABA/glycine. This causes neuronal hyperexcitability, disinhibition within neuron circuits, and disrupted neurological functions. More recently, KCC2 was identified as a genetically-validated target for epilepsy, intellectual disability, and autism spectrum disorder, and pathogenic mutations in human SLC12A5 gene were linked to psychiatric/mood disorders. The broad therapeutic utility of KCC2-upmodulating drugs relates to its critical role in determining inhibitory activity of GABAergic neurotransmission, a mechanism widely targeted by several drugs. However, in cases of KCC2 hypofunction GABAergic neurotransmission can be depolarizing/excitatory, thereby impairing endogenous neuronal inhibition while also limiting the effectiveness of existing therapeutics targeting/requiring GABAergic pathway inhibition. Several preclinical reports have shown that KCC2 upmodulating treatments rescue and increase the efficacy of anti-seizure and analgesic medications. Thus, a first-in-class KCC2-potentiating therapy would provide a novel mechanism for restoring physiological CNS inhibition and addressing drug resistance in patients with E/I imbalance pathologies. Herein, we discuss progress toward and further work needed to develop the first-in-class KCC2 therapeutics to treat neurological disorder patients.
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