ArticleProceedings of the National Academy of Sciences of the United States of America2018
Mouse maternal protein restriction during preimplantation alone permanently alters brain neuron proportion and adult short-term memory.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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37 citing papers in PubMed, 70 citations in OpenAlex.
- Review
- Maternal fasting during early gestation induces epigenetic alterations and schizophrenia-related phenotypes.Molecular psychiatry · 2026Article
- Neural stem cells as potential mediators of prenatal dietary stress through epigenetic mechanisms.Stem cell reports · 2026Article
- Poverty and caregiver mental health are related to infant and toddler resting-state brain networks: insights from fNIRS.Neurophotonics · 2026Article
- Early and long-term effects of maternal protein restriction on offspring organs and systems: insights from the developmental origins of health and disease (DOHaD).Biogerontology · 2025Review
- Murine maternal microbiome modifies adverse effects of protein undernutrition on offspring neurobehaviour.Nature microbiology · 2025Article
- The microbiome as a modulator of neurological health across the maternal-offspring interface.The Journal of clinical investigation · 2025Review
- Prenatal protein deficiency causes age-specific alteration in number and distribution of inhibitory neurons in the somatosensory cortex during early postnatal development.Journal of biosciences · 2025Article
- Unraveling the Molecular Mechanisms of the Neurodevelopmental Consequences of Fetal Protein Deficiency: Insights From Rodent Models and Public Health Implications.Biological psychiatry global open science · 2024Review
- Protein restriction during pregnancy alters Cdkn1c silencing, dopamine circuitry and offspring behaviour without changing expression of key neuronal marker genes.Scientific reports · 2024Article
- Effects of Soy Protein Isolate on Fragile X Phenotypes in Mice.Nutrients · 2024Article
- A maternal low-protein diet results in sex-specific differences in synaptophysin expression and milk fatty acid profiles in neonatal rats.Journal of nutritional science · 2024Article
- Maternal protein intake in early pregnancy and child development at age 3 years.Pediatric research · 2023Article
- Review
- Maternal Undernutrition Induces Cell Signalling and Metabolic Dysfunction in Undifferentiated Mouse Embryonic Stem Cells.Stem cell reviews and reports · 2023Article
- Characterisation of the Paternal Influence on Intergenerational Offspring Cardiac and Brain Lipid Homeostasis in Mice.International journal of molecular sciences · 2023Article
- Preimplantation or gestation/lactation high-fat diet alters adult offspring metabolism and neurogenesis.Brain communications · 2023Article
- Maternal gastrointestinal nematode infection enhances spatial memory of uninfected juvenile mouse pups.Scientific reports · 2022Article
- Perinatal exposure to synergistic multiple stressors leads to cellular and behavioral deficits mimicking Schizophrenia-like pathology.Biology open · 2022Article
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17 authors at 2 institutions in 1 country.
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Abstract
Maternal protein malnutrition throughout pregnancy and lactation compromises brain development in late gestation and after birth, affecting structural, biochemical, and pathway dynamics with lasting consequences for motor and cognitive function. However, the importance of nutrition during the preimplantation period for brain development is unknown. We have previously shown that maternal low-protein diet (LPD) confined to the preimplantation period (Emb-LPD) in mice, with normal nutrition thereafter, is sufficient to induce cardiometabolic and locomotory behavioral abnormalities in adult offspring. Here, using a range of in vivo and in vitro techniques, we report that Emb-LPD and sustained LPD reduce neural stem cell (NSC) and progenitor cell numbers at E12.5, E14.5, and E17.5 through suppressed proliferation rates in both ganglionic eminences and cortex of the fetal brain. Moreover, Emb-LPD causes remaining NSCs to up-regulate the neuronal differentiation rate beyond control levels, whereas in LPD, apoptosis increases to possibly temper neuron formation. Furthermore, Emb-LPD adult offspring maintain the increase in neuron proportion in the cortex, display increased cortex thickness, and exhibit short-term memory deficit analyzed by the novel-object recognition assay. Last, we identify altered expression of fragile X family genes as a potential molecular mechanism for adverse programming of brain development. Collectively, these data demonstrate that poor maternal nutrition from conception is sufficient to cause abnormal brain development and adult memory loss.
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