N-Methyl-D-Aspartate Receptors, Ketamine, and Rett Syndrome: Something Special on the Road to Treatments?
D. M. Katz, F. Menniti, R. J. Mather
Biological Psychiatry May 1, 2016 DOI: 10.1016/j.biopsych.2016.03.1045 (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Commentary Peer reviewed |
|---|---|
| Topics | Esketamine Ketamine |
| Key points | The commentary describes a 2007 mouse study in which reactivating the Mecp2 gene in severely ill animals reversed neurological dysfunction to a significant degree, indicating that Rett syndrome symptoms are reversible in this model. |
Abstract
In 2007, Adrian Bird and his colleagues at the University of Edinburgh published a groundbreaking study demonstrating that Rett syndrome (RTT), a severe genetic neurodevelopmental disorder, is reversible in mouse models of the disease (1). Using Cre-Lox technology, the Bird group engineered a mouse in which the disease-causing gene, Mecp2, could be reversibly inactivated. Animals born with the gene switched off —a condition that mimics the loss of MECP2 function that underlies the human disease—developed full-blown symptoms of murine RTT. However, when the gene was reactivated in these severely ill mice, neurological dysfunction was reversed to a significant degree.
Citations in the library
Cited by 3
- Ketamine: A Review for Clinicians FOCUS: The Journal of Lifelong Learning in Psychiatry July 1, 2018
- Intravenous esketamine in pediatric Rett syndrome: An open-label, early phase 1 pilot study. Molecular therapy. Methods & clinical development March 13, 2025
- Autistic-like social deficits in hippocampal MeCP2 knockdown rat models are rescued by ketamine. BMB reports May 2022