Perinatal supplementation with omega-3 fatty acids corrects the aberrant social and cognitive traits observed in a genetic model of autism based on FMR1 deletion in rats
Abstract
Background and objective: Autism spectrum disorder (ASD) is a complex neurodevelopmental disorder for which no treatments exist. Fragile X syndrome (FXS) is the most common form of inherited mental retardation and the most frequent monogenic cause of ASD. Given the lack of pharmacological treatments for ASD, increasing interest is devoted to non-pharmacological approaches, including dietary interventions. Omega-3 polyunsaturated fatty acids (PUFAs) are critical for neurobehavioraldevelopment. This study had two aims: 1. To validatethe recently developed Fmr1- Δ exon 8 rat model of FXS; 2. To assess the impact of omega-3 PUFAs dietary supplementation during pregnancy and lactation on the altered behavior displayed by Fmr1- Δ exon 8 rats. Methods: Female Fmr1- Δ exon 8 and wild-type Sprague-Dawley rats were fed with either an omega-3 PUFAs enriched diet or with an isocaloric control diet during pregnancy and lactation. Behavioral experiments were carried out on the infant (Postnatal days (PNDs) 9 and 13), juvenile (PND 35) and adult (PND 90) male offspring. Results: Fmr1- Δ exon 8 pups showed hypolocomotion, reduced ultrasonic vocalizations (USVs) emission and impaired social discrimination compared to wild-type controls. Juvenile and adult Fmr1- Δ exon 8 rats showed deficits in the social and cognitive domains, that were counteracted by perinatal omega-3 PUFAs supplementation. Conclusion: Our results support the validity of the Fmr1- Δ exon 8 rat model to mimic key autistic-li…
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The deletion of exon 8 in the Fmr1-Δexon 8 rat is sufficient to cause FXS-like traits, such as deficits in sustained visuospatial attention, altered patterns of social interaction, cognitive impairment, and abnormal synaptic plasticity.
“Such deletion is sufficient to cause FXS-like traits, such as deficits in sustained visuospatial attention [34], altered patterns of social interaction, and cognitive impairment [28], together with abnormal synaptic plasticity [32,35,36].”
From Brain Cholesterol Biosynthetic Pathway Is Altered in a Preclinical Model of Fragile X Syndrome (2022) · cites this paper as [28]
Cites
Hagerman, R. J., Berry-Kravis, E., Hazlett, H. C., Bailey, D. B., Moine, H., Kooy, R. F., Tassone, F., Gantois, I., Sonenberg, N., Mandel, J. L., et al. (2017) · Nature Reviews Disease Primers · doi:10.1038/nrdp.2017.65 · Cited by 838 · see citing works
Till, S. M., Asiminas, A., Jackson, A. D., Katsanevaki, D., Barnes, S. A., Osterweil, E. K., Bear, M. F., Chattarji, S., Wood, E. R., Wyllie, D. J. A., et al. (2015) · Human Molecular Genetics · doi:10.1093/hmg/ddv299 · Cited by 109 · see citing works
Loss of FMRP Impaired Hippocampal Long-Term Plasticity and Spatial Learning in Rats
Tian, Y., Yang, C., Shang, S., Cai, Y., Deng, X., Zhang, J., Shao, F., Zhu, D., Liu, Y., Chen, G., et al. (2017) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2017.00269 · Cited by 82 · see citing works
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Psilocybin mitigates the cognitive deficits observed in a rat model of Fragile X syndrome
Buzzelli, V., Carbone, E., Manduca, A., Schiavi, S., Feo, A., Perederiy, J. V., Ambert, K. H., Hausman, M., & Trezza, V. (2023) · Psychopharmacology · doi:10.1007/s00213-022-06286-3 · Cited by 22 · see citing works
Self-citationBrain Cholesterol Biosynthetic Pathway Is Altered in a Preclinical Model of Fragile X Syndrome
Parente, M., Tonini, C., Buzzelli, V., Carbone, E., Trezza, V., & Pallottini, V. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23063408 · Cited by 11 · see citing works
“Here, we used the recently developed Fmr1-∆exon 8 rat model of FXS [28] to study the involvement of the cholesterol biosynthetic pathway, the socalled MVA pathway, in FXS.”
BackgroundMethodSelf-citation
- Authors
- Schiavi, S., Carbone, E., Melancia, F., Buzzelli, V., Manduca, A., Campolongo, P., Pallottini, V., & Trezza, V.
- Affiliations
- Roma Tre University (IT)
- Fondazione Santa Lucia (IT)
- Corresponding author
- Schiavi, Sara
- Trezza, Viviana
- Venue
- Nutritional Neuroscience
- Publisher
- Informa UK Limited
- Published
- 2020-09-11
- Volume
- 25
- Issue
- 5
- Pages
- 898-911
- ISSN
- 1028-415X (ISSN-L)
- 1476-8305
- OpenAlex
- W3085458292
- Cited by
- 34
- References
- 3
- Citations by year
- 2026: 2 · 2025: 4 · 2024: 7 · 2023: 5 · 2022: 10 · 2021: 4 · 2020: 2
- FWCI
- 3.07
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Nutritional Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- IRIS Research product catalog (Sapienza University of Rome) (submittedVersion)
- Iris (Roma Tre University) (submittedVersion)
- Funders
- Marie Curie (PCIG09-GA-2011-293589)
- Jerome Lejeune Foundation Research (1674)
- MIUR (Grant/Award Numbers: ARTICOLO 1, COMMI 314-337 LEGGE 232/2016, ARTICOLO 1)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Health Sciences › Nursing › Nutrition and Dietetics › Fatty Acid Research and Health
- Life Sciences › Neuroscience › Cognitive Neuroscience › Autism Spectrum Disorder Research
- Keywords
- autism spectrum disorder, omega-3 polyunsaturated fatty acids, dietary supplementation, fragile X syndrome, perinatal nutrition, social behavior, cognitive impairment, ultrasonic vocalizations, hypolocomotion, social discrimination, brain development
- MeSH terms
- Autism Spectrum Disorder, Animals, Autistic Disorder, Cognition, Female, Fragile X Syndrome, Humans, Male, Models, Genetic, Pregnancy, Fatty Acids, Omega-3, Rats, Sprague-Dawley, Dietary Supplements, Rats, Fragile X Messenger Ribonucleoprotein 1
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