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Tag: Neurogenesis

  • Environmental stressors linked to fetal brain development challenges

    Environmental stressors linked to fetal brain development challenges

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    In a recent review article published in the journal Antioxidants, researchers explored how environmental factors impact the brain development of fetuses and neonates, emphasizing inflammation and oxidation stress as common denominators across various stressors.

    Their conclusions highlight the critical role of healthy intrauterine environments for promoting fetal brain development and stress the importance of interventions that aim to reduce modifiable stress factors during pregnancy.

    Review: Impact of Maternal Environment and Inflammation on Fetal Neurodevelopment. Image Credit: Sebastian Kaulitzki / ShutterstockReview: Impact of Maternal Environment and Inflammation on Fetal Neurodevelopment. Image Credit: Sebastian Kaulitzki / Shutterstock

    Background

    The development of the human brain, which commences during the second to third week of gestation and continues through childhood, is influenced by a combination of genetic, epigenetic, and environmental factors.

    Key developmental milestones occur during specific gestational periods, such as cellular migration in the neocortex and extensive neurogenesis between the eighth and eighteenth weeks.

    Maternal environmental exposures during the prenatal and antenatal periods can impact intrauterine development and the short—and long-term health of the offspring, potentially raising the risks of developing non-communicable diseases in adulthood.

    These exposures can epigenetically modify placental and fetal phenotypes, affecting organ structure, metabolism, and physiology. However, understanding the precise molecular mechanisms linking external factors to neurodevelopmental alterations remains challenging.

    In this review, researchers aimed to explore the effects of various maternal environmental exposures, including nutrition, lifestyle, stress, and pollution, on fetal brain development and neonatal neurodevelopment-related outcomes, drawing from a comprehensive literature search that encompassed human and animal studies published within the last 15 years.

    External stimuli, through inflammation and reduced micronutrient supply, impact on fetal neurodevelopment. SES: socioeconomic status.External stimuli, through inflammation and reduced micronutrient supply, impact on fetal neurodevelopment. SES: socioeconomic status.

    Maternal environmental exposures

    Maternal nutrition plays a crucial role in fetal neurodevelopment, with evidence suggesting that both insufficient and unhealthy dietary patterns during pregnancy can affect fetal brain development.

    For example, the Mediterranean diet, characterized by nutrient-rich foods, has been associated with positive neurodevelopmental outcomes in offspring.

    However, deficiencies in micronutrients like docosahexaenoic acid (DHA), folate, and iodine and excessive intake of macronutrients have been linked to adverse neurodevelopmental effects.

    The Western diet, in particular, is known to be high in macronutrients but poor in micronutrients. Affordable but low-quality foods characterize it. Mouse models suggest that pow-protein diets may also be associated with neurodevelopmental delays.

    Alterations in maternal gut microbiota during pregnancy have been linked to worse behavioral outcomes in offspring, potentially mediated through inflammation and metabolic endotoxemia.

    Maternal obesity and a high-fat diet have also been implicated, with animal models and epidemiological studies suggesting associations with cognitive deficits, attention deficit hyperactivity disorder (ADHD), autism, and psychoses in offspring.

    Additionally, maternal depression, anxiety, and stress can lead to disturbed fetal neurodevelopment, potentially resulting in altered brain structure and function, as evidenced by investigations using human and animal models.

    Smoking and alcohol consumption during pregnancy have well-documented detrimental effects on fetal neurodevelopment, including increased risks of ADHD, autism, schizophrenia, and behavioral issues.

    Exposure to air pollution, mainly particulate matter, and polycyclic aromatic hydrocarbons, has been linked to neurodevelopmental disorders in offspring, with oxidative stress and inflammatory responses implicated as underlying mechanisms.

    Socioeconomic status also plays a role, with disadvantaged conditions associated with adverse pregnancy outcomes and poorer neurodevelopmental outcomes in children.

    Underlying mechanisms

    Numerous studies have linked pathological pregnancy conditions like fetal growth restriction (FGR) and preterm birth (PTB) with neurodevelopmental issues in offspring. Two main mechanisms are implicated: altered fetal nutrient supply and intrauterine inflammation involving placental factors.

    FGR, often due to placental dysfunction, leads to chronic fetal hypoxia and undernutrition, impacting fetal brain development despite adaptive responses like brain sparing.

    PTB, often linked to maternal inflammation or infection, presents various neurodevelopmental challenges, including disruptions in axonal and neuronal development and brain abnormalities like cerebral palsy.

    Inflammation during pregnancy, exacerbated by factors like obesity, stress, and environmental pollutants, influences insulin and neurotransmitter signaling, affecting synaptic plasticity and neurotrophic factor expression.

    The activation of maternal immune systems contributes to mitochondrial dysfunction and oxidative stress, perpetuating a cycle of oxidative stress and inflammation that disrupts fetal brain development.

    These conditions and exposure to chemicals can compromise the blood-brain barrier and lead to additional impairments in fetal brain development.

    Overall, maternal health conditions and external factors collectively contribute to increased maternal inflammation, which impacts fetal neurodevelopment and potentially leads to long-term neurological consequences in offspring.

    Conclusions

    The review emphasizes how external factors during pregnancy affect fetal growth and brain development, impacting long-term neurodevelopment.

    Conditions like PTB and FGR alter brain morphometry, often due to inflammation and changes in nutrient supply. Evidence suggests they are influenced by maternal health and environmental factors like air pollution and stress.

    Understanding and addressing these modifiable risk factors is crucial for improving both individual and public health outcomes. This highlights the importance of preventive measures and further longitudinal research.

    Journal reference:

    • Impacts of maternal environment and inflammation on fetal neurodevelopment. Lubrano, C., Parisi, F., Cetin, I. Antioxidants (2024). DOI: 10.3390/antiox13040453, https://www.mdpi.com/2076-3921/13/4/453

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  • Mitochondrial fusion critical for adult neurogenesis and brain circuit refinement

    Mitochondrial fusion critical for adult neurogenesis and brain circuit refinement

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    Nerve cells (neurons) are amongst the most complex cell types in our body. They achieve this complexity during development by extending ramified branches called dendrites and axons and establishing thousands of synapses to form intricate networks. The production of most neurons is confined to embryonic development, yet few brain regions are exceptionally endowed with neurogenesis throughout adulthood. It is unclear how neurons born in these regions successfully mature and remain competitive to exert their functions within a fully formed organ. However, understanding these processes holds great potential for brain repair approaches during disease.

    A team of researchers led by Professor Dr. Matteo Bergami at the University of Cologne’s CECAD Cluster of Excellence in Aging Research addressed this question in mouse models, using a combination of imaging, viral tracing and electrophysiological techniques. They found that, as new neurons mature, their mitochondria (the cells’ power houses) along dendrites undergo a boost in fusion dynamics to acquire more elongated shapes. This process is key in sustaining the plasticity of new synapses and refining pre-existing brain circuits in response to complex experiences. The study ‘Enhanced mitochondrial fusion during a critical period of synaptic plasticity in adult-born neurons’ has been published in the journal Neuron.

    Mitochondrial fusion grants new neurons a competitive advantage

    Adult neurogenesis takes place in the hippocampus, a brain region controlling aspects of cognition and emotional behavior. Consistently, altered rates of hippocampal neurogenesis have been shown to correlate with neurodegenerative and depressive disorders. While it is known that the newly produced neurons in this region mature over prolonged periods of time to ensure high levels of tissue plasticity, our understanding of the underlying mechanisms is limited. The findings of Bergami and his team suggest that the pace of mitochondrial fusion in the dendrites of new neurons controls their plasticity at synapses rather than neuronal maturation per se.

    We were surprised to see that new neurons actually develop almost perfectly in the absence of mitochondrial fusion, but that their survival suddenly dropped without obvious signs of degeneration. This argues for a role of fusion in regulating neuronal competition at synapses, which is part of a selection process new neurons undergo while integrating into the network.”


    Professor Dr. Matteo Bergami, University of Cologne’s CECAD Cluster of Excellence in Aging Research

    The findings extend the knowledge that dysfunctional mitochondrial dynamics (such as fusion) cause neurological disorders in humans and suggest that fusion may play a much more complex role than previously thought in controlling synaptic function and its malfunction in diseases such as Alzheimer’s and Parkinson’s.

    Besides revealing a fundamental aspect of neuronal plasticity in physiological conditions, the scientists hope that these results will guide them towards specific interventions to restore neuronal plasticity and cognitive functions in conditions of disease.

    Source:

    Journal reference:

    Kochan, S. M. V., et al. (2024) Enhanced mitochondrial fusion during a critical period of synaptic plasticity in adult-born neurons. Neuron. doi.org/10.1016/j.neuron.2024.03.013.

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