Clinically-probed mechanisms of action in fragile-X syndrome fail to normalize translational EEG phenotypes in Fmr1 knockout mice
Open accessAbstract
Fragile X syndrome (FXS) is a neurodevelopmental disorder caused by Fragile X Messenger Ribonucleoprotein (FMRP) deficiency. Electroencephalogram (EEG) changes in FXS include alterations of oscillatory activity and responses to sensory stimuli, some of which have been back-translated into rodent models by knocking-out the Fragile X messenger ribonucleoprotein 1 gene (Fmr1-KO). However, the validity of these EEG phenotypes as objective biomarkers requires further investigation. Potential pharmacotherapies such as mGluR5 inhibitors (e.g. CTEP; 2-chloro-4-((2,5-dimethyl-1-(4-(trifluoromethoxy)phenyl)-1H-imidazole-4-yl)ethynyl)pyridine), GABA B R agonists (e.g. arbaclofen) and δ-containing GABA A R agonists (e.g. gaboxadol) have not translated into clinical success despite rescuing many phenotypes in the Fmr1-KO model. Yet none of these treatments have been assessed on EEG phenotypes in the Fmr1-KO model. Therefore, we set out to discover new EEG phenotypes in Fmr1-KO mice, using "task-free" and auditory-evoked (AEPs) and visually-evoked potential (VEP) paradigms, and probe their modulation by CTEP, arbaclofen and gaboxadol, using within-subjects designs. First, we report Fmr1-KO-associated EEG abnormalities that closely resemble those observed in FXS, including elevated gamma-band power, reduced alpha/beta-band coherence, increased AEPs and delayed VEPs. Secondly, we found that pharmacological treatment, at best, only partially normalized EEG phenotypes. CTEP restored alpha/beta…
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These opposing changes converge on abnormal oscillatory dynamics, including altered gamma and theta rhythms, which are critical for hippocampal functions such as cognitive mapping and social memory.
“These opposing changes converge on abnormal oscillatory dynamics, including altered gamma and theta rhythms, which are critical for hippocampal functions such as cognitive mapping and social memory (Janz et al., 2025).”
From Biological hierarchy from genotype to phenotype in syndromic and non-syndromic autism spectrum disorder (2026) · cites this paper as Janz et al., 2025
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- Authors
- Janz, P., Bainier, M., Marashli, S., Gross, S., & Redondo, R. L.
- Affiliations
- F. Hoffmann-La Roche AG (CH)
- Corresponding author
- Janz, Philipp
- Venue
- Neuropharmacology
- Publisher
- Elsevier BV
- Published
- 2025-01
- Volume
- 262
- Pages
- 110182
- ISSN
- 0028-3908 (ISSN-L)
- OpenAlex
- W4403332370
- Cited by
- 11
- References
- 63
- Citations by year
- 2026: 7 · 2025: 4
- FWCI
- 2.91
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Neuropharmacology (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Funders
- F. Hoffmann-La Roche Ltd
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cognitive Neuroscience › Autism Spectrum Disorder Research
- Keywords
- fragile X syndrome, Fmr1 knockout mice, gamma power, auditory evoked potentials, visual evoked potentials, CTEP, gaboxadol, FMRP
- MeSH terms
- Animals, Baclofen, Disease Models, Animal, Electroencephalography, Fragile X Syndrome, Imidazoles, Isoxazoles, Male, Mice, Inbred C57BL, Phenotype, Pyridines, Mice, Knockout, Mice, Fragile X Messenger Ribonucleoprotein 1, GABA-B Receptor Agonists, Receptor, Metabotropic Glutamate 5
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