Mental Process

Mental processes, often referred to as cognitive processes, are the fundamental operations by which the human brain acquires, stores, manipulates, and retrieves information. These include essential abilities such as attention, various forms of memory (e.g., working memory, verbal memory, visual memory), speed of processing, reasoning, problem-solving, and inhibitory control. These processes are critical for learning, decision-making, and navigating daily life.

Biological Basis

The biological underpinnings of mental processes involve complex interactions within neural networks and specific biochemical pathways in the brain. Genetics play a significant role in the variability of cognitive abilities among individuals. Genome-Wide Association Studies (GWAS) have identified numerous single nucleotide polymorphisms (SNPs) and genes associated with different cognitive domains. For instance, specific genetic variants have been linked to processing speed, attention, and various memory functions.^[1] The heritability of cognitive measures, such as processing speed and working memory, has been estimated through SNP-based analyses, highlighting a substantial genetic contribution to these traits.^[2] Genes like DISC1 have also been investigated for their influence on neuroanatomical and neurocognitive phenotypes.^[3]

Clinical Relevance

Deficits in mental processes are prominent features in many neurological and psychiatric disorders, impacting diagnosis, prognosis, and therapeutic strategies. In conditions such as schizophrenia, specific cognitive impairments in areas like attention/vigilance, working memory, verbal memory, visual memory, and reasoning/problem-solving are common and contribute to functional impairment.^[1]Understanding the genetic architecture of these cognitive deficits can aid in identifying biomarkers for early detection, developing targeted interventions, and personalizing treatment approaches. For example, genetic variants associated with cognitive domains in schizophrenia includers11763030 for Speed of Processing, rs75131442 and rs79963003 for Attention/Vigilance, and rs17511050 , rs148396385 , rs17396139 for Working Memory.^[1]

Social Importance

Mental processes are fundamental to an individual’s capacity to function and succeed in social, academic, and professional settings. Robust cognitive abilities are generally associated with higher educational attainment, greater career success, and an improved overall quality of life. Conversely, impairments in these processes can lead to substantial challenges in daily living, social interactions, and maintaining independence. Research into the genetic basis of mental processes not only deepens our understanding of human cognition but also has the potential to inform educational practices, enhance support systems for individuals facing cognitive challenges, and guide public health initiatives aimed at promoting cognitive well-being throughout life.

Methodological and Statistical Considerations

Genome-wide association studies (GWAS) investigating specific mental processes often face limitations related to sample size, which can result in insufficient statistical power to identify genome-wide significant associations. This constraint means that many genuine genetic influences on cognitive traits may remain undetected, leading to a less complete understanding of their complex genetic architecture.^[2] Furthermore, initial studies frequently report inflated effect sizes for associated SNPs due to sampling error, which often leads to weaker or even contradictory findings in subsequent replication efforts.^[4] The possibility of chance findings and false positives remains a concern in any association study, even with statistical adjustments like False Discovery Rate (FDR) control, underscoring the critical need for independent replication in diverse samples to validate findings and ensure their robustness.^[4]

Phenotypic Definition and Challenges

The assessment of mental processes can be confounded by factors such as practice or placebo effects, where observed improvements in neurocognitive outcomes might reflect a genetically mediated ability to benefit from these general effects rather than a direct genetic link to the underlying cognitive trait.^[4] Additionally, the manner in which phenotypes are defined and measured significantly impacts genetic findings; for instance, while latent factors of executive functions (EFs) show high heritability, individual EF tasks often yield lower heritability estimates, complicating the identification of specific genetic associations. The choice of stringent thresholds for characterizing cognitive impairments, such as a large standard deviation cutoff, may also be overly conservative, potentially obscuring subtle genetic effects and limiting the scope of identified associations.^[2]

Generalizability and Unaccounted Influences

A significant limitation in current genetic research on mental processes is the predominant reliance on cohorts of European ancestry. This lack of diversity restricts the generalizability of findings to other populations and necessitates extensive replication in ethnically varied samples to ensure broad applicability and avoid biased interpretations of genetic associations across different ancestral backgrounds.^[5] Moreover, environmental factors and complex gene-environment interactions are substantial confounders that are often not fully captured or accounted for in studies, potentially masking or modulating direct genetic effects. The concept of “missing heritability,” where the heritability explained by common SNPs is considerably lower than estimates from twin studies, suggests that current genetic models may not fully encompass the genetic architecture of mental processes, pointing to the involvement of rare variants, structural variants, or yet-to-be-identified complex genetic and environmental interactions.^[2]

Variants

Genetic variations play a crucial role in individual differences in cognitive abilities and susceptibility to various neurological conditions. Understanding these genetic underpinnings is vital for elucidating the biological basis of complex mental processes, including learning, memory, and reasoning.^[6] For instance, the CDHR3 gene, or Cadherin Related Family Member 3, encodes a protein involved in cell adhesion, a fundamental process for tissue structure and cell-to-cell communication, particularly important in the developing and adult nervous system. The variant rs574109761 within CDHR3 may influence the efficiency of these cell adhesion processes, potentially impacting synaptic plasticity and neural network formation, which are critical for cognitive functions such as memory consolidation and information processing.^[7]Alterations in cadherin function have been implicated in neurodevelopmental disorders and cognitive impairments, suggesting that this variant could contribute to subtle differences in mental processing.

The FHITgene, or Fragile Histidine Triad, is a tumor suppressor gene known for its involvement in cellular stress responses, DNA repair, and apoptosis. While primarily studied in cancer,FHIT is also expressed in brain tissue, where its proper function is essential for maintaining genomic stability and cellular health in neurons.^[8] The variant rs766488186 in FHITcould potentially affect gene expression or protein stability, thereby influencing how neurons respond to stress or damage. Such effects might indirectly impact cognitive resilience and brain aging, as chronic cellular stress can impair neuronal function and contribute to cognitive decline over time. Variations in genes related to cellular maintenance can subtly modulate the efficiency of neural circuits, affecting functions like attention and processing speed.

Long intergenic non-coding RNA 2490, or LINC02490, represents a class of RNA molecules that do not encode proteins but play crucial regulatory roles in gene expression. These non-coding RNAs are increasingly recognized for their involvement in various biological processes, including brain development and function. LINC02490 may act by modulating the transcription of nearby genes or by interacting with proteins to influence chromatin structure, thereby affecting the expression of genes vital for neuronal differentiation, synaptic function, or neurotransmitter synthesis.^[9] The variant rs719714 could alter the structure or stability of LINC02490, potentially disrupting its regulatory functions and leading to subtle changes in gene expression patterns critical for optimal brain function. Such disruptions might manifest as individual differences in cognitive flexibility or problem-solving abilities.

The PTPROgene, Protein Tyrosine Phosphatase Receptor Type O, encodes a receptor-type protein tyrosine phosphatase that removes phosphate groups from specific proteins, a critical step in cell signaling pathways. In the brain, protein tyrosine phosphatases are involved in regulating neuronal growth, axon guidance, synaptic plasticity, and myelin formation, all of which are fundamental for proper cognitive function and information transfer.^[10] The variant rs2300290 within PTPROcould affect the enzyme’s activity or its interaction with signaling molecules, thereby altering the phosphorylation status of key proteins in neural cells. Such an alteration might impact the efficiency of neural communication or the structural integrity of neural networks, potentially influencing higher-order cognitive processes like memory recall and executive function.^[6]

Key Variants

RS ID	Gene	Related Traits
rs574109761	CDHR3	mental process
rs766488186	FHIT	mental process
rs719714	LINC02490	mental process
rs2300290	PTPRO	mental process

Biological Background of Mental Processes

Mental processes, encompassing functions like memory, reasoning, and executive functions, are complex biological phenomena rooted in intricate genetic, molecular, and cellular mechanisms within the nervous system.^[2] These processes are not static but are shaped by developmental trajectories, influenced by the brain’s molecular architecture, and can be disrupted by various pathophysiological conditions.^[11] Understanding the biological underpinnings of mental processes requires examining their foundations from the genomic level to the systemic interactions of neural circuits.

Genetic and Epigenetic Regulation of Neural Function

The blueprint for mental processes begins at the genetic level, where specific genes and their regulatory elements dictate the development and function of neural cells. Genome-wide association studies have identified genetic variants associated with latent cognitive measures, intelligence, and memory performance, indicating a significant genetic component to these traits.^[2] For instance, the expression and regulation of genes like HDAC9, which is involved in transcriptional regulation, cell cycle progression, and neuronal development and transmission, are crucial. Similarly, NDUFS4is implicated in verbal memory, with altered expression in the prefrontal cortex and hippocampus linked to impaired cognitive function.^[1]Epigenetic modifications, such as DNA methylation and histone acetylation, further modulate gene expression without altering the underlying DNA sequence, profoundly impacting neuronal plasticity and the dynamic regulation of mental capabilities.

Heritability studies demonstrate that genomic regions with higher accessibility in the brain’s germinal zone, a critical area for neural stem cell proliferation, are enriched for cognitive traits, highlighting the importance of early brain development in shaping cognitive potential.^[11] Genes like PPM1B, a Ser/Thr protein phosphatase, play roles in cell stress response pathways, neuroprotection, and neurodegeneration, and its interactions with other putative schizophrenia susceptibility genes likeNRG1 and DTNBP1underscore the complex genetic interplay underlying mental health and cognitive function.^[1] The gene CPNE3has also been identified as moderating the association between anxiety and working memory, indicating specific genetic influences on the interaction between emotional states and cognitive performance.^[12]

Molecular and Cellular Signaling in Cognition

At the cellular level, mental processes rely on intricate molecular signaling pathways and metabolic processes that govern neuronal communication and plasticity. Key pathways associated with memory performance include themTOR signaling pathway, which is vital for synaptic plasticity and protein synthesis crucial for long-term memory formation.^[13] Other essential pathways include axon guidance, critical for establishing proper neural connections during development, and the regulation of autophagy, a cellular process that maintains neuronal health by clearing damaged components. mRNA end processing and stability, along with Ephrin receptor signaling, further contribute to the precise control of gene expression and cell-to-cell communication within neural circuits.^[13] These molecular mechanisms are mediated by a diverse array of biomolecules. Critical proteins, enzymes, and receptors facilitate neurotransmission, modulate synaptic strength, and propagate intracellular signals. For example, protein phosphatases like PPM1Bare crucial for regulating cell stress responses and neuronal survival, directly impacting cognitive function.^[1] Hormones and transcription factors also play significant roles, with transcription factors like HDAC9 regulating the expression of genes involved in neuronal development and transmission.^[1] The coordinated action of these biomolecules ensures the efficient encoding, processing, and storage of information, which are fundamental to all cognitive functions.^[13]

Neural Development and Regional Brain Specialization

The development and organization of the brain, particularly the cerebral cortex, are fundamental to the emergence of complex mental processes. The human cerebral cortex undergoes global and regional development, with its molecular architecture directly influencing occupational aptitudes and complex behaviors.^[11] This development involves highly regulated biological processes such as cell proliferation, centrosome duplication, chromosome separation, neural closure, and brain morphogenesis, which together establish the structural framework for cognition.^[11] Different brain regions specialize in distinct mental functions; for instance, the prefrontal cortex is critical for executive functions and working memory, while the hippocampus is essential for memory formation.^[2] Tissue interactions and systemic consequences further highlight the interconnectedness of brain regions. The coordinated activity of neuronal populations across different cortical areas underlies complex cognitive tasks, such as visuospatial working memory and arithmetical performance.^[14] The molecular architecture of these regions, including the accessibility of genomic regions in the germinal zone versus the cortical plate, influences their developmental trajectories and functional capabilities, ultimately contributing to individual differences in cognitive abilities.^[11]

Pathophysiology and Cognitive Impairment

Disruptions to the intricate biological processes underlying mental functions can lead to pathophysiological conditions and cognitive deficits. Diseases such as schizophrenia are often characterized by cognitive domain deficits, including impairments in reasoning, problem-solving, working memory, and verbal memory.^[1] These impairments can be linked to specific genetic variants and altered gene expression patterns, such as lower prefrontal cortex and hippocampal expression of NDUFS4.^[1] Animal models, such as Ndufs4conditional knockout mice, further demonstrate that such genetic disruptions can lead to impaired cognitive function and increased anxiety-like behaviors, mirroring aspects of human psychiatric conditions.^[1]Homeostatic disruptions, including those affecting cellular stress response pathways, can have profound effects on neuronal health and cognitive function. Proteins likePPM1B, which are negative regulators of cell stress pathways, are involved in both neuroprotection and neurodegeneration, illustrating how imbalances in these cellular functions can contribute to cognitive decline and disease.^[1] Deficits in the brain’s ability to encode, process, and store information, whether due to genetic predispositions, developmental anomalies, or molecular pathway dysregulation, can result in severe cognitive dysfunctions, impacting an individual’s daily life and overall well-being.^[13]

Genetic and Epigenetic Regulation of Neural Architecture

Mental processes are profoundly influenced by the intricate molecular architecture of the human cerebral cortex, which is shaped by complex genetic and epigenetic regulatory mechanisms.^[11] Gene regulation, including the activity of transcription factors, dictates the expression profiles of proteins essential for neuronal development, differentiation, and connectivity. For instance, epigenetic modifications like H3K4 methylation, influenced by enzymes such as KDM5B, play a critical role in focusing methylation near promoters and enhancers during embryonic stem cell self-renewal and differentiation, thereby influencing the developmental trajectory of neural cells.^[8] These regulatory processes ensure the proper formation and regional specialization of brain structures, which are fundamental for cognitive functions and overall mental health.

Protein modification, including post-translational regulation and allosteric control, further refines the function of proteins involved in neural signaling and structural integrity. The precise control over gene expression and protein activity, achieved through these regulatory layers, is crucial for establishing the sophisticated networks that underlie complex mental processes. Dysregulation in these fundamental genetic and epigenetic pathways can lead to altered brain architecture and function, contributing to various neuropsychiatric conditions.^{[1], [15]}

Neurobiological Signaling and Network Dynamics

The dynamic nature of mental processes relies on robust neurobiological signaling pathways and their integration into functional brain networks. Although specific intracellular signaling cascades are not detailed in research, the presence of various neuroscience and psychiatry research centers highlights the importance of neuronal communication through receptor activation, neurotransmitter release, and subsequent intracellular responses.^{[1], [11]} These cascades often involve feedback loops that modulate the strength and duration of signals, ensuring adaptive responses within neural circuits. Such intricate signaling underlies various cognitive domains, from basic sensory processing to higher-order executive functions.

At a systems level, these signaling pathways engage in extensive crosstalk, forming complex network interactions across different brain regions, such as those involved in cerebral integration.^[11] The coordinated activity within these networks, which can be observed during tasks like exploratory eye movements, is essential for coherent mental function.^[15]Disruptions in the precise balance of these network interactions can manifest as cognitive deficits or behavioral dysfunctions, as seen in conditions like schizophrenia, where specific brain regions and their connectivity are affected.^{[1], [15]}

Metabolic Underpinnings of Cognitive Function

The brain’s high metabolic demand necessitates efficient metabolic pathways to support continuous neural activity, which is fundamental for mental processes. Energy metabolism, including glucose utilization and ATP production, provides the fuel for ion pumps, neurotransmitter synthesis, and synaptic transmission. While specific brain metabolic pathways are not extensively detailed, research indicates a relationship between systemic metabolic factors, such as body mass index and plasma lipids, and cognitive health, suggesting that broader metabolic regulation impacts brain function.^{[8], [16]}Nutritional factors, including dietary fat and fiber, also influence systemic inflammation and C-reactive protein levels, which can indirectly affect brain health and cognitive integrity.^[17]Beyond energy, biosynthesis pathways are critical for producing essential neurotransmitters, lipids, and structural components of neurons, while catabolism ensures the breakdown of waste products and recycling of molecular components. Metabolic regulation and flux control maintain cellular homeostasis, which is vital for sustained mental processes. Dysregulation in these metabolic pathways can impair neuronal function, contributing to cognitive impairment and increasing the risk for neurological and psychiatric disorders.^[8]

Systems-Level Integration and Emergent Mental Properties

Complex mental processes, such as personality traits, cognitive aptitudes, and emotional regulation, emerge from the highly integrated activity of distributed brain networks, reflecting systems-level integration. Pathway crosstalk among different neural circuits allows for the sophisticated coordination of information processing across the cerebral cortex, which exhibits distinct molecular architecture and regional development.^[11] Hierarchical regulation governs how simpler neural operations combine to form increasingly complex functions, leading to emergent properties that characterize human cognition and behavior. For example, studies on temperament scales and occupational aptitudes suggest that these complex traits are not attributable to single genes or pathways but arise from the interplay of many genetic and environmental factors across integrated brain systems.^{[11], [18]}The functional integrity of these integrated networks is essential for cognitive performance, with studies examining cognitive domain deficits in conditions like schizophrenia highlighting the importance of network interactions.^[1] Alterations in brain structures, such as ventricular volume, can reflect broader disruptions in these integrated systems, impacting overall mental function.^[19] Understanding these network dynamics is key to unraveling the biological basis of mental processes.

Dysregulation in Neurological and Psychiatric Conditions

Dysregulation within these molecular and cellular pathways is a hallmark of various neurological and psychiatric conditions, impacting mental processes significantly. Genetic studies have identified numerous loci and polygenic risk scores associated with conditions like major depression, alcoholism risk, and schizophrenia, indicating specific pathway dysregulation as underlying mechanisms.^{[1], [15], [20], [21]}For instance, specific polymorphisms on chromosome 5q21.3 have been linked to exploratory eye movement dysfunction in schizophrenia, pointing to discrete genetic influences on neural circuits involved in cognitive control.^[15]In response to pathway dysregulation, the brain often employs compensatory mechanisms to maintain function, though these may eventually become insufficient. Identifying these dysfunctional pathways and compensatory responses is crucial for developing therapeutic targets. For example, understanding the genetic associations with cognitive impairment or brain structural changes like ventricular volume can inform strategies for intervention.^{[8], [19]} Research into the molecular architecture of the cerebral cortex and its development provides a framework for pinpointing vulnerabilities and developing targeted therapies for disorders affecting mental processes.^[11]

Diagnostic and Prognostic Utility of Mental Functional Impairment

Assessing mental processes, particularly in the context of functional impairment, offers significant diagnostic and prognostic utility in clinical practice. The Mental Component Summary (MCS), which encompasses aspects like sadness, fatigue, and calmness, serves as an important indicator of functional status in psychiatric disorders such as major depressive disorder, bipolar disorder, and schizophrenia.^[22] While psychiatric symptom severity and demographic variables predict some functional impairment, they account for less than one-third of the variance in MCS scores, indicating that MCS captures distinct and crucial aspects of a patient’s overall health beyond core symptoms.^[22] This suggests that evaluating mental functional impairment can provide a more comprehensive understanding of a patient’s condition, complementing traditional diagnostic criteria.

Furthermore, the quantification of mental functional impairment holds prognostic value for anticipating disease progression and long-term outcomes. The residual variance in functional impairment, after controlling for psychiatric symptoms and demographic factors, can identify individuals at higher risk for persistent functional limitations.^[22] This “index of functional risk/resilience” allows clinicians to predict potential challenges in recovery and to implement early interventions aimed at mitigating long-term disability, thereby improving patient care planning and resource allocation.^[22]

Personalized Risk Stratification and Treatment Selection

Understanding the specific contributions of mental processes to functional impairment is vital for personalized risk stratification and tailoring treatment approaches. By analyzing the deviation of an individual’s functional impairment from an expected score given their symptom severity, clinicians can identify those with heightened functional risk or resilience.^[22]This stratification facilitates the development of targeted prevention strategies for high-risk individuals, aiming to prevent further functional decline and promote recovery across various psychiatric conditions.

The detailed assessment of mental functional impairment also supports a more refined approach to treatment selection and monitoring. Moving beyond symptom-focused interventions, clinicians can leverage insights into specific functional deficits to personalize treatment plans, ensuring that interventions address both symptomatic and functional recovery.^[22] While studies investigating genetic pathways (e.g., KEGG) related to functional risk and resilience indicate a future direction for genetically informed precision medicine, the current understanding of mental functional impairment already allows for more individualized and effective monitoring of treatment efficacy.^[22]

Cross-Disorder Implications and Comorbidities

The investigation of mental functional impairment across multiple psychiatric disorders highlights shared underlying mechanisms and overlapping phenotypes, crucial for understanding comorbidities and broader clinical presentations. The use of standardized residuals allows for a uniform comparison of functional impairment across major depressive disorder, bipolar disorder, and schizophrenia, demonstrating commonalities in how mental processes contribute to overall disability despite distinct diagnostic labels.^[22] This cross-disorder perspective is essential for recognizing functional impairment as a pervasive complication that transcends specific diagnostic boundaries.

Given that psychiatric symptom severity accounts for only a portion of mental functional impairment, research suggests that other factors, including genetic predispositions, significantly contribute to the complex clinical picture.^[22] This supports a model of psychiatric disorders as syndromic presentations where mental processes are influenced by a multifaceted interplay of symptomatic and non-symptomatic elements. Reliable of such sub-phenotypes, with reported intraclass correlation values for age at onset between 0.68 and 0.97 and rater agreement for psychotic symptoms at 0.91, is critical for accurately characterizing these complex presentations and guiding integrated care models that address both core symptoms and comprehensive functional recovery.^[23]

Frequently Asked Questions About Mental Process

These questions address the most important and specific aspects of mental process based on current genetic research.

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1. Why do some people learn new things faster than I do?

Genetic factors significantly influence processing speed and other cognitive abilities. Heritability estimates show a substantial genetic contribution to these traits, meaning some individuals naturally process information faster due to their unique genetic makeup.

2. My parents have great memories; will mine be too?

Yes, various forms of memory, like working memory, show substantial genetic contributions. You might inherit similar cognitive strengths from your parents, as genetics play a significant role in the variability of these abilities among individuals.

3. Is it true my genes influence how well I can focus?

Yes, your genes do influence your ability to focus. Genome-Wide Association Studies have identified specific genetic variants linked to attention and vigilance, which can impact how well you maintain concentration.

4. Why do I sometimes struggle to solve problems at work?

Genetic factors contribute to individual differences in reasoning and problem-solving abilities. While these are critical for daily tasks, variations in your genetic makeup can influence your natural aptitude and efficiency in these areas.

5. Can my family history of mental illness explain my memory issues?

Yes, a family history of psychiatric disorders can be linked to your cognitive abilities. In conditions like schizophrenia, specific genetic variants, such asrs17511050 for Working Memory, are associated with cognitive impairments that can run in families.

6. Does my ethnic background affect my brain’s abilities?

Yes, your ethnic background can be relevant, though research is still developing. Most current genetic studies on mental processes have predominantly focused on cohorts of European ancestry, meaning genetic associations and risks might vary in other populations.

7. Can I really improve my memory if it feels genetically weak?

Yes, you absolutely can improve your memory, even with genetic predispositions. While genetics play a significant role, understanding the genetic architecture of cognitive deficits can aid in developing targeted interventions and personalized approaches to strengthen your abilities.

8. My sibling is so quick-witted, but I’m not. Why?

Individual differences in cognitive abilities, like processing speed, are significantly influenced by genetics. Each person inherits a unique combination of genetic variants that contribute to the variability in how quickly and efficiently their brain functions.

9. Does stress actually make my thinking slower because of my genes?

While environmental factors like stress are known to impact cognition, the complex interplay between stress and your specific genetic predispositions is not yet fully understood. Current genetic models often do not completely capture these intricate gene-environment interactions.

10. Why do scientists still find some aspects of my brain’s abilities a mystery?

Even with advanced research, a portion of the genetic influences on mental processes remains unexplained, a concept known as “missing heritability.” This suggests that rare variants, structural variants, or other complex genetic and environmental interactions are still to be identified.

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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

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[2] Donati, G. et al. “Genome-Wide Association Study of Latent Cognitive Measures in Adolescence: Genetic Overlap With Intelligence and Education.”Mind Brain Educ, 2019.

[3] Carless, M. A. et al. “Impact of DISC1 variation on neuroanatomical and neurocognitive phenotypes.” Mol Psychiatry, vol. 17, no. 5, 2012, pp. 477-85.

[4] McClay, J. L. “Genome-wide pharmacogenomic study of neurocognition as an indicator of antipsychotic treatment response in schizophrenia.”Neuropsychopharmacology, 2010.

[5] Mukherjee, S. “Genetic data and cognitively defined late-onset Alzheimer’s disease subgroups.”Molecular Psychiatry, 2018.

[6] Nakahara S. Polygenic risk score, genome-wide association, and gene set analyses of cognitive domain deficits in schizophrenia. Schizophr Res. 2018;199:21-27.

[7] Lahti J. Genome-wide meta-analyses reveal novel loci for verbal short-term memory and learning. Mol Psychiatry. 2022;27(10):4137-4148.

[8] Lutz MW. Analysis of pleiotropic genetic effects on cognitive impairment, systemic inflammation, and plasma lipids in the Health and Retirement Study. Neurobiol Aging. 2019;83:136-144.

[9] Gialluisi A. Genome-wide association scan identifies new variants associated with a cognitive predictor of dyslexia. Transl Psychiatry. 2019;9(1):65.

[10] Clifford RE. Genetic architecture distinguishes tinnitus from hearing loss. Nat Commun. 2024;15(1):686.

[11] Shin, J. et al. “Global and Regional Development of the Human Cerebral Cortex: Molecular Architecture and Occupational Aptitudes.” Cerebral Cortex, vol. 30, no. 7, 2020, PMID: 32198502.

[12] Chen, C., et al. “CPNE3 moderates the association between anxiety and working memory.”Sci Rep, vol. 11, no. 1, 2021, p. 6965.

[13] Zhu, Z., et al. “Multi-level genomic analyses suggest new genetic variants involved in human memory.” Eur J Hum Genet, vol. 27, no. 1, 2019, pp. 142–153.

[14] Dumontheil, I., and T. Klingberg. “Brain activity during a visuospatial working memory task predicts arithmetical performance 2 years later.” Cerebral Cortex, vol. 22, no. 5, 2012, pp. 1078–1085.

[15] Ma, Y. et al. “Association of chromosome 5q21.3 polymorphisms with the exploratory eye movement dysfunction in schizophrenia.”Scientific Reports, vol. 5, 2015, PMID: 26242244.

[16] Speliotes, E. K. et al. “Association analyses of 249,796 individuals reveal 18 new loci associated with body mass index.”Nature Genetics, vol. 42, no. 11, 2010, PMID: 20935630.

[17] King, D. E. et al. “Relation of dietary fat and fiber to elevation of C-reactive protein.”American Journal of Cardiology, vol. 92, no. 11, 2003, PMID: 14636916.

[18] Verweij, K. J. et al. “A genome-wide association study of Cloninger’s temperament scales: implications for the evolutionary genetics of personality.” Biological Psychology, vol. 85, no. 2, 2010, PMID: 20691247.

[19] Vojinovic, D. et al. “Genome-wide association study of 23,500 individuals identifies 7 loci associated with brain ventricular volume.” Nature Communications, vol. 9, no. 1, 2018, PMID: 30258056.

[20] Shyn, S. I. et al. “Novel loci for major depression identified by genome-wide association study of Sequenced Treatment Alternatives to Relieve Depression and meta-analysis of three studies.” Molecular Psychiatry, vol. 15, no. 1, 2010, PMID: 20038947.

[21] Heath, A. C. et al. “A quantitative-trait genome-wide association study of alcoholism risk in the community: findings and implications.” Biological Psychiatry, vol. 72, no. 12, 2012, PMID: 21529783.

[22] McGrath, L. M. et al. “Genetic predictors of risk and resilience in psychiatric disorders: a cross-disorder genome-wide association study of functional impairment in major depressive disorder, bipolar disorder, and schizophrenia.”Am J Med Genet B Neuropsychiatr Genet, vol. 165B, no. 8, 2014, pp. 627-37.

[23] Belmonte Mahon, P., et al. “Genome-wide association analysis of age at onset and psychotic symptoms in bipolar disorder.” American Journal of Medical Genetics - Neuropsychiatric Genetics, vol. 156B, no. 3, 2011, pp. 328-336.