Infant White Matter Volume
Introduction
Section titled “Introduction”White matter, a critical component of the human brain, consists primarily of myelinated axons that form the communication highways connecting different brain regions. This intricate network is essential for rapid information processing, supporting complex cognitive functions, motor skills, and emotional regulation. In infants, the development of white matter during the prenatal and early postnatal periods is a foundational phase, marked by rapid growth and myelination, which are crucial for lifelong neurological health and developmental trajectories This limitation impacts statistical power, potentially hindering the detection of variants with smaller effect sizes and affecting the stability of SNP-based heritability estimates.[1]Given that this is a novel investigation into infant brain volumes, independent replication of the identified genetic associations is critically important, particularly for single-nucleotide polymorphisms (SNPs) like the intronic variant inIGFBP7 (rs114518130 ), which has a low minor allele frequency and thus requires robust validation in additional cohorts.[1] Furthermore, comparisons with genetic data from adolescent and adult populations reveal minimal overlap in the common genetic variants influencing brain volumes across different developmental stages.[1] This finding suggests that the genetic architecture underlying global brain volumes is highly distinct at varying ages, implying that genetic determinants for neonatal brain volumes are likely involved in foundational prenatal processes, while those for later life stages target postnatal neurodevelopment.[1] Consequently, findings from this infant cohort may not be directly generalizable to other age groups, underscoring the need for age-specific genetic studies and potentially indicating that observed effects in this unique developmental window might not persist or manifest similarly later in life.
Generalizability and Phenotype Specificity
Section titled “Generalizability and Phenotype Specificity”The generalizability of the findings is partially limited by the demographic composition of the study cohort, where 63% of subjects are of European ancestry, with the remainder primarily of African ancestry.[1] While population stratification was assessed, this predominant ancestry distribution means that the identified genetic associations may not be universally applicable across all global populations, potentially overlooking population-specific genetic variants or effect modifications. Future studies with more diverse cohorts are essential to ensure the broad applicability of these genetic insights into infant brain development.
Moreover, the focus on global brain volumes (white matter, gray matter, cerebrospinal fluid, and intracranial volume) as phenotypes may not fully capture the complexity of neurodevelopmental processes. The resolution of current MRI techniques might not be sufficient to detect subtle but critical genetic influences on brain development, and other neuroimaging phenotypes, such as cortical thickness, surface area, ventricular volume, or diffusion tensor imaging, could be more relevant for specific genetic associations or psychiatric risks.[1] Additionally, reliance on cross-sectional measurements at approximately 5 weeks of age provides a snapshot rather than a dynamic view of brain development, potentially missing critical longitudinal changes or trajectories that are crucial for understanding the unfolding nature of psychiatric disorders.
Developmental and Etiological Complexities
Section titled “Developmental and Etiological Complexities”A significant finding from this study is that genetic predisposition scores for schizophrenia and autism spectrum disorders (ASD) did not predict global brain volumes in neonates.[1]This suggests that the genetic risk for these complex psychiatric conditions may influence neurodevelopmental processes at a resolution not captured by global brain volumes, or that the manifestation of these genetic effects on brain structure occurs at later developmental stages.[1] These null findings highlight a critical knowledge gap regarding the early etiological pathways of psychiatric disorders and imply that alternative neuroimaging phenotypes or longitudinal assessments may be more sensitive indicators of genetic risk in infancy.
Furthermore, while the study accounted for several demographic and medical covariates and incorporated common environmental effects within its statistical models, the intricate interplay of genetic and environmental factors remains a complex area. The “missing heritability” in complex traits often points to unmeasured environmental confounders, gene-environment interactions, or rare genetic variants not fully captured in common variant GWAS.[1]Understanding the full spectrum of genetic influences on infant white matter volume requires disentangling these complex interactions and addressing how they contribute to neurodevelopmental trajectories across infancy and childhood.
Variants
Section titled “Variants”Genetic variations play a critical role in shaping early brain development, including the formation and volume of white matter. A genome-wide association study (GWAS) identified several common single-nucleotide polymorphisms (SNPs) influencing infant brain volumes, highlighting genes involved in foundational prenatal processes like neurogenesis and axonogenesis.[1]These variants offer insights into the genetic architecture underlying infant white matter volume and its potential implications for neurodevelopmental trajectories.
One significant variant identified is rs10514437 , an intronic SNP located within the WWOX(WW domain-containing oxidoreductase) gene, which neared genome-wide significance for its association with infant white matter volume.[1] The WWOX gene functions as a tumor suppressor and is integral to cell growth and apoptosis, processes critical for proper brain development.[1] Mutations in WWOXare associated with severe neurological phenotypes, including autosomal recessive spinocerebellar ataxia-12, epilepsy, mental retardation, and microcephaly, often presenting with imaging findings such as hypomyelination and structural abnormalities in white matter tracts like the corpus callosum.[1] The protein encoded by WWOX, WOX1, is abundantly expressed in neuronal axons and nerve bundles, such as the corpus callosum and striatal fascicles, reinforcing its direct relevance to white matter formation and integrity.[1] Other variants, while not reaching genome-wide significance for white matter specifically, are located near genes with plausible roles in brain development. The variant rs117068934 is associated with the SLC13A3(Solute Carrier Family 13 Member 3) gene, which encodes a sodium-dependent dicarboxylate transporter vital for metabolic processes in the brain, indirectly supporting the energy demands of myelination and neuronal function.[1] Similarly, rs138549714 is located near MYOM1 (Myomesin 1), a gene whose expression strongly increases from prenatal to postnatal life, suggesting a developmental role, possibly in cellular structural integrity or migration critical for neuronal and glial development.[1] Another important variant is rs9361254 , which is near HTR1B (5-hydroxytryptamine receptor 1B), a serotonin receptor gene with strong biological plausibility for influencing neurodevelopment.[1] Serotonin signaling is crucial for various aspects of brain development, including neurogenesis, neuronal migration, and differentiation, processes that indirectly impact white matter organization and volume.[1] Several other identified variants are associated with pseudogenes, which are typically non-coding copies of functional genes, but can sometimes play regulatory roles. The variant rs200193477 is located near SLC6A6P1 and RNU1-139P, both pseudogenes related to genes involved in taurine transport and RNA splicing, respectively.[1] While pseudogenes themselves may not encode proteins, their genomic location or potential non-coding RNA functions could influence the expression of nearby functional genes critical for brain development. Similarly, rs11834561 is associated with PGAM1P5, a pseudogene of PGAM1 (Phosphoglycerate Mutase 1), an enzyme central to glycolysis.[1] Given the high metabolic demands of brain development, especially for the lipid synthesis required for myelination, any regulatory influence from such pseudogenes on energy metabolism could indirectly affect white matter volume.[1]
Key Variants
Section titled “Key Variants”Defining Infant White Matter Volume
Section titled “Defining Infant White Matter Volume”Infant white matter (WM) volume refers to the quantifiable amount of white matter tissue present within the brain of an infant, typically measured within the first 24 weeks of life, often around 5 weeks of age.[1] This trait represents a critical aspect of early neurodevelopment, as white matter facilitates communication between different gray matter regions through myelinated axons. The study of infant WM volume provides insights into the foundational phase of human brain development, which is intricately linked to the origins of psychiatric disorders and offers a promising target for early therapeutic interventions.[1] Conceptually, WM volume is part of the total intracranial volume (ICV), which is the sum of gray matter (GM), white matter, and cerebrospinal fluid (CSF) volumes.[1]
Methodologies and Criteria
Section titled “Methodologies and Criteria”The operational definition of infant white matter volume relies on advanced neuroimaging techniques and computational analyses. is typically achieved through high-resolution T1- and T2-weighted magnetic resonance imaging (MRI) scans.[1] Following image acquisition, an atlas-based expectation-maximization segmentation algorithm is employed to automatically delineate and quantify white matter tissue, distinguishing it from gray matter and cerebrospinal fluid.[1] Critical criteria include the use of specific scanner types, such as Siemens Allegra head-only 3T or Siemens TIM Trio 3T scanners, with platform type being a significant covariate in analyses to account for potential impacts on brain volume measurements.[1]Additional covariates, such as birth weight, gestational age at birth, sex, and age at MRI, are also incorporated into statistical models to refine volume estimations and account for demographic and medical factors.[1]
Genetic Terminology and Classification of Variants
Section titled “Genetic Terminology and Classification of Variants”Understanding infant white matter volume often involves genetic terminology, particularly within the context of genome-wide association studies (GWAS) that investigate common genetic variants, known as single-nucleotide polymorphisms (SNPs), influencing brain structure.[1]A key term, “infant white matter volume,” is often analyzed alongside related measures such as gray matter (GM), cerebrospinal fluid (CSF), and intracranial volume (ICV), which represents the total brain volume.[1] Genetic associations are evaluated against thresholds like genome-wide significance, defined as P = 1.25 × 10 −8 after Bonferroni correction for multiple phenotypes, to identify significant SNPs.[1] For instance, an intronic SNP in WWOX (rs10514437 ) neared this significance for white matter volume.[1] Further classification involves distinguishing linkage disequilibrium (LD)-independent SNPs, defined as those with low LD (r2 < 0.1) to more significant SNPs within a 500 kb window, and considering minor allele frequency (MAF).[1] The study also utilizes polygenic scores to assess the collective effect of multiple genetic variants, revealing that genetic determinants of global brain volumes can be highly distinct across different developmental ages, such as neonates, adolescents, and adults.[1]This distinction suggests a developmental classification of genetic influence, rather than a fixed disease classification for white matter volume itself.
Genetic Regulation of Early Brain Development
Section titled “Genetic Regulation of Early Brain Development”The development of infant white matter volume is profoundly influenced by genetic mechanisms, which orchestrate the precise spatiotemporal regulation of gene expression during prenatal and early postnatal life.[1]Common genetic variants, such as single-nucleotide polymorphisms (SNPs), have been identified as influencing global brain tissue volumes in infants, suggesting that individual genetic differences contribute to variations in white matter development.[1] For instance, an intronic SNP, rs10514437 , located in the WWOX gene, has been associated with white matter volume, indicating its potential role in regulating the formation and maturation of white matter tracts.[1] Genes like RBFOX1 and TOX3also show elevated prenatal expression, highlighting their importance in foundational neurodevelopmental processes that lay the groundwork for white matter structure.[1] These genetic factors influence a range of cellular functions and regulatory networks essential for building the infant brain.
Cellular and Molecular Foundations of White Matter
Section titled “Cellular and Molecular Foundations of White Matter”White matter, critical for rapid communication between brain regions, is primarily composed of myelinated axons, and its development relies on complex molecular and cellular pathways. These include neurogenesis, neuronal migration, differentiation, programmed cell death, dendritogenesis, and axonogenesis.[1] These processes involve intricate signaling pathways and metabolic activities that guide the formation of neurons and glial cells, particularly oligodendrocytes, which are responsible for producing myelin. Key biomolecules, such as proteins and enzymes encoded by genes like WWOX, play structural and regulatory roles in these developmental stages, ensuring the proper insulation and connectivity of neural circuits.[1] Aberrations in these foundational cellular functions can impact the overall volume and integrity of white matter, potentially leading to neurological or psychiatric conditions later in life.
Developmental Trajectories and Brain Plasticity
Section titled “Developmental Trajectories and Brain Plasticity”The infant brain is characterized by immense plasticity and undergoes rapid, distinct developmental processes compared to later life stages.[1] Genetic determinants influencing neonatal white matter have detectable effects in adolescence and are primarily involved in foundational prenatal processes like neurogenesis, neuronal migration, and axonogenesis.[1] As individuals age, the genetic influences on brain volumes shift, with adolescent brain volumes being more impacted by genes involved in synaptogenesis and synaptic/dendritic pruning, and adult volumes reflecting further pruning and potential neurodegenerative events.[1] This suggests that white matter development is a dynamic, age-dependent process, where gene expression patterns and their regulatory networks evolve, shaping the tissue and organ-level biology of the brain throughout the lifespan. The early postnatal period, specifically, represents a critical window for brain development and potential therapeutic interventions due to its high plasticity.[1]
Pathophysiological Insights and Clinical Relevance
Section titled “Pathophysiological Insights and Clinical Relevance”Variations in infant white matter volume can have significant pathophysiological implications, potentially serving as early indicators for neurodevelopmental disorders. Early aberrations in neurodevelopment, detectable via MRI in infants, have been linked to psychiatric disorders such as schizophrenia and autism spectrum disorders (ASD).[1]While genetic predisposition scores for schizophrenia and ASD did not directly predict global brain volumes in neonates in one study, the overall understanding is that early life brain structural differences can be relevant to these conditions.[1] Additionally, the burden of rare copy number variants (CNVs) has been investigated for its association with brain volumes, highlighting how significant genetic alterations can disrupt homeostatic processes and lead to structural changes. Understanding the genetic and developmental underpinnings of infant white matter is crucial for identifying early risk factors and developing targeted interventions for psychiatric illnesses with origins in fetal life.[1]
Early Life Neurodevelopmental Insights and Risk Stratification
Section titled “Early Life Neurodevelopmental Insights and Risk Stratification”Measuring infant white matter volume provides crucial insights into the foundational phase of human brain development, which is highly influenced by precise spatiotemporal gene regulation.[1] Imaging-genetic studies in infants, utilizing high-resolution MRI scans around 5 weeks of age, can identify early aberrations in neurodevelopment, offering a window into the origins of psychiatric disorders where many associated genes show elevated expression in early life.[1]The identification of common genetic variants, such as an intronic single-nucleotide polymorphism (SNP) inWWOX (rs10514437 ) associated with white matter volume, provides a genetic basis for understanding individual differences in early brain structure.[1]This foundational understanding is critical for future clinical applications, including identifying infants at higher risk for neurodevelopmental conditions, thereby enabling more personalized medicine approaches and the potential for targeted prevention strategies during this period of high brain plasticity.
While current genetic predisposition scores for adolescent or adult brain volumes, or for complex disorders like schizophrenia and Autism Spectrum Disorder (ASD), do not strongly predict global brain volumes in neonates, the ability to detect genetic influences on neonatal white matter volume points to its potential for refined risk stratification.[1]Understanding how specific genetic variants contribute to white matter volume in infancy can help clinicians develop more precise risk assessment tools, especially when integrated with other clinical and environmental factors. Such early identification of genetic predispositions influencing white matter development could pave the way for early interventions, potentially mitigating the severity or altering the trajectory of various neurodevelopmental challenges before overt symptoms emerge.
Prognostic Indicators for Neuropsychiatric Outcomes
Section titled “Prognostic Indicators for Neuropsychiatric Outcomes”Infant white matter volume measurements hold potential as prognostic indicators for long-term neurodevelopmental outcomes, given that genetic variants influencing neonatal white matter have detectable, albeit small, effects extending into adolescence.[1]This suggests that early life white matter development, shaped by common genetic variation, may contribute to the trajectory of brain maturation and subsequent neuropsychiatric health. Exploring these early genetic influences on white matter volume could lead to the development of predictive markers for the progression of neurodevelopmental conditions or for assessing an individual’s response to early therapeutic interventions.
The finding that genetic determinants of global brain volumes are highly distinct at different ages, with neonatal variants implicated in foundational prenatal processes like neurogenesis and axonogenesis, highlights the unique prognostic value of infant white matter measurements.[1]Although direct predictive power for specific psychiatric disorders like schizophrenia or ASD was not established in this particular study, the identification of several individual genetic loci relevant to intellectual disability and mental illness underscores the broader prognostic utility of these early brain volume assessments.[1]Longitudinal studies are essential to fully elucidate how these genetic influences on infant white matter volume translate into long-term implications for patient care and to integrate them into comprehensive prognostic models for diverse neurodevelopmental challenges.
Complexities in Comorbidity and Phenotype Associations
Section titled “Complexities in Comorbidity and Phenotype Associations”Despite the relevance of individual genetic loci to intellectual disability and mental illness, the study found that genetic predisposition scores for schizophrenia and Autism Spectrum Disorder (ASD) did not predict global brain volumes in neonates.[1]This suggests a complex relationship where the genetic architecture influencing global brain volumes in infancy may be largely distinct from the polygenic risk for these specific psychiatric conditions at such an early developmental stage. Similarly, while rare copy number variations (CNVs) are implicated in ASD and schizophrenia, the overall CNV burden did not significantly predict global infant brain volumes, indicating that gross volumetric changes may not be the primary early manifestation of these genetic risks.[1]These findings suggest that early neurodevelopmental aberrations relevant to psychiatric disorders might manifest through mechanisms not fully captured by global white matter volume alone, potentially involving finer-resolution neuroimaging phenotypes such as cortical thickness, surface area, or diffusion tensor imaging, or through functional connectivity patterns.[1] Furthermore, differences in global brain volumes related to psychiatric risk might emerge later in life, as evidenced by reports of generalized brain enlargement in older children with ASD, which is not typically observed in high-risk infants at 6 months of age.[1]Future research with larger cohorts is crucial to investigate the intricate interplay between genetic predisposition, CNV burden, sex, and specific neurodevelopmental trajectories across infancy and childhood, moving beyond cross-sectional global volume measures to fully understand comorbidities and overlapping phenotypes.
Genetic Architecture and Developmental Trajectories of Infant White Matter Volume
Section titled “Genetic Architecture and Developmental Trajectories of Infant White Matter Volume”Population studies investigating infant white matter volume reveal a complex genetic architecture distinct from later life stages. A genome-wide association study (GWAS) involving 561 infants, aged 0 to 24 weeks, identified common genetic variants influencing global brain tissue volumes, including white matter. Specifically, an intronic single-nucleotide polymorphism (SNP) in theWWOX gene, rs10514437 , neared genome-wide significance for white matter volume, suggesting its role in early brain development.[1]This research utilized advanced methodologies, including linear mixed effects models and ACE-based models for twin data, to account for genetic and environmental factors, alongside covariates such as gestational age, birth weight, sex, and age at MRI.[1] The findings underscore the importance of studying early life brain development to understand the foundational genetic processes, such as neurogenesis and axonogenesis, that shape the infant brain.[1] Further longitudinal comparisons with large-scale neuroimaging GWAS cohorts of adolescents (PNC) and adults (ENIGMA2) suggest that the genetic determinants of global brain volumes are largely distinct across different developmental periods. While sign tests indicated some overlap between common variants impacting white matter in neonates and adolescents, the overall pattern suggests minimal shared genetic influence.[1] Polygenic score analyses, however, showed that genetic variants influencing neonatal white matter volume had detectable, albeit small, effects in adolescence, indicating some continuity.[1] This differentiation highlights that genes impacting infant brain volumes are likely involved in prenatal developmental processes, whereas variants influencing adolescent and adult volumes might relate to later processes like synaptogenesis, synaptic pruning, or even neurodegenerative events.[1]
Population Diversity and Methodological Considerations
Section titled “Population Diversity and Methodological Considerations”Understanding the population-level implications of infant white matter volume requires rigorous study design and consideration of population diversity. The infant GWAS cohort of 561 subjects included a diverse sample, with 63% of European ancestry and the remainder primarily of African ancestry, allowing for some assessment of population-specific effects.[1] To mitigate potential confounding by population stratification, researchers employed principal component analysis (PCA) and included the first three genotypic principal components as covariates in their models.[1] Imputation of genetic variants was performed using the 1000 Genomes Project reference panel, further enhancing the genomic coverage and generalizability of findings across ancestral backgrounds.[1] The study’s methodology also addressed critical factors affecting brain volume measurements, such as the use of different MRI scanner types, which were included as a covariate to account for potential technical variability.[1] The inclusion of a significant number of twins (monozygotic and dizygotic) and sibling pairs allowed for the application of ACE-based linear mixed effects models, which effectively distinguished genetic, common environmental, and unique environmental effects on brain volumes.[1] Despite these strengths, the study acknowledges limitations, such as the need for independent replication, particularly for findings involving SNPs with low minor allele frequencies.[1]Larger, more diverse cohorts are essential for calculating stable SNP-sense heritability estimates and exploring potential interactions with demographic factors like sex and rare copy number variations (CNVs) in influencing neurodevelopmental trajectories.[1]
Epidemiological Associations and Clinical Relevance
Section titled “Epidemiological Associations and Clinical Relevance”Epidemiological investigations into infant white matter volume aim to uncover prevalence patterns and demographic associations, particularly concerning early life risk factors for neurodevelopmental and psychiatric disorders. While the studied infant cohort provided insights into genetic influences, it did not find a significant association between genetic predisposition scores for schizophrenia or autism spectrum disorders (ASD) and global brain volumes in neonates.[1] This suggests that while many psychiatric risk genes show elevated expression in early life, differences in global brain volumes relevant to these conditions may not manifest until later developmental stages or require more granular neuroimaging phenotypes than global volume.[1]Furthermore, the study found no significant association between the burden of copy number variations (CNVs) and global brain volumes in neonates, despite known increases in rare genic CNVs in conditions like ASD and schizophrenia.[1] These null findings highlight the complexity of early neurodevelopment and the potential for genetic variants to influence processes at a resolution not captured by global MRI measures.[1]Future epidemiological studies with larger sample sizes and longitudinal designs are crucial to investigate how genetic predisposition and CNV burden interact with other demographic and socioeconomic correlates to influence neurodevelopmental trajectories across infancy and childhood, ultimately informing early intervention strategies for psychiatric disorders.[1]
Frequently Asked Questions About Infant White Matter Volume
Section titled “Frequently Asked Questions About Infant White Matter Volume”These questions address the most important and specific aspects of infant white matter volume based on current genetic research.
1. Does my family history influence my baby’s brain wiring?
Section titled “1. Does my family history influence my baby’s brain wiring?”Yes, absolutely. Your baby’s brain volumes, including white matter, are highly influenced by genetics passed down through families. Common genetic variations, such as those in genes like WWOX, are thought to play a role in shaping these foundational prenatal processes that build the brain.
2. Why do some babies’ brains grow bigger than others?
Section titled “2. Why do some babies’ brains grow bigger than others?”It’s largely due to a combination of genetic and environmental factors. Research shows that infant brain volumes are highly heritable, meaning there are common genetic differences among babies that influence how their brains, including white matter, develop and grow in size.
3. Can we tell early if my baby might have future brain issues?
Section titled “3. Can we tell early if my baby might have future brain issues?”Early measurements of infant brain volumes are increasingly seen as relevant to the origins of various psychiatric and neurodevelopmental disorders. While it’s a complex picture, understanding these early brain markers and their genetic underpinnings can offer crucial insights into potential risks, guiding early diagnostic efforts.
4. If there’s a brain difference, can we do anything about it?
Section titled “4. If there’s a brain difference, can we do anything about it?”Yes, there’s hope! The infant brain is highly plastic, meaning it’s very adaptable and responsive to its environment. This period is considered a promising target for therapeutic interventions. Understanding early differences can help guide strategies to optimize neurological outcomes for your child.
5. Do things I do impact my baby’s brain development?
Section titled “5. Do things I do impact my baby’s brain development?”Yes, while genetics are a major factor, environmental influences also play a role in your baby’s white matter development. The intricate interplay of genetic and environmental factors contributes to neurodevelopmental trajectories, shaping how your baby’s brain forms.
6. Is my baby’s brain development like an older child’s or adult’s?
Section titled “6. Is my baby’s brain development like an older child’s or adult’s?”Not exactly. The genetic factors influencing brain volumes are quite distinct at different ages. What shapes your baby’s brain in infancy primarily involves foundational prenatal processes, which are different from the genetic influences on brain development later in childhood or adulthood.
7. Does my family’s ethnic background affect my baby’s brain?
Section titled “7. Does my family’s ethnic background affect my baby’s brain?”Your family’s background can matter because genetic associations might vary across different populations. Current research often focuses on specific ancestries, so it’s important for future studies to include more diverse groups to understand how genetic influences might apply universally or in population-specific ways.
8. Can early brain scans predict my baby’s risk for autism or schizophrenia?
Section titled “8. Can early brain scans predict my baby’s risk for autism or schizophrenia?”Interestingly, current research suggests that genetic risk scores for conditions like autism spectrum disorder and schizophrenia do not predict global brain volumes in neonates. This implies that the genetic effects for these disorders might influence brain development in ways not captured by overall volume, or manifest at later stages.
9. Is measuring my baby’s brain volume really that important?
Section titled “9. Is measuring my baby’s brain volume really that important?”Yes, it’s very important. Measuring infant white matter volume helps us understand the earliest stages of brain development. It can provide insights into potential neurological vulnerabilities, inform public health, and contribute to personalized medicine approaches to optimize brain health from infancy onward.
10. Can my child’s brain development be unique, even from their sibling?
Section titled “10. Can my child’s brain development be unique, even from their sibling?”Absolutely. Even within the same family, genetic variations and unique environmental experiences contribute to individual differences in brain development. While siblings share many genes, the specific combination and the unique environmental interactions mean each child’s brain development will have its own distinct trajectory.
This FAQ was automatically generated based on current genetic research and may be updated as new information becomes available.
Disclaimer: This information is for educational purposes only and should not be used as a substitute for professional medical advice. Always consult with a healthcare provider for personalized medical guidance.
References
Section titled “References”[1] Xia K, Zhang J, Ahn M, et al. Genome-wide association analysis identifies common variants influencing infant brain volumes. Transl Psychiatry. 2017;7(8):e1195.