Understanding ADHD: Brain Chemistry, Neuroimaging, Genetics, and Diagnostic Boundaries
Authors: Joyeeta Hasan, Annabella Irani-Fey, Ishita Manikandan, & Nirza Mutta
Mentor: Dr. Liam Barrett. Dr. Barrett received his medical degree from the University of Birmingham. He is a member of the Royal College of Emergency Medicine, and is currently pursuing a DPhil in medical science at the University of Oxford.
Abstract
Attention-deficit/hyperactivity disorder (ADHD) is a complex neurodevelopmental condition that affects a person's attention, behavior, learning, and brain development. This literature review explores the factors that contribute to ADHD, the effects it has on brain chemistry, its treatment, and how effectively it can be diagnosed. The review draws on research on genetic and environmental influences, neurotransmitter signaling, medication and therapy, brain imaging, and cognitive testing. By comparing findings from scientific studies and reviews, several important patterns emerged suggesting that ADHD does not have a single cause; instead, genetic factors and environmental exposures interact in complex ways. Studies also show subtle structural and functional differences in brain regions involved in attention and executive function. ADHD also does not have a single treatment or diagnostic standard that can be applied to everyone. Instead, it is a highly individual condition that varies across demographic groups, individuals, and age groups. Commonly used cognitive tests can provide useful information, yet diagnosis requires multiple sources of evidence, which can include behavioral assessments and functional impairment. Evidence supports ADHD as a clinically meaningful neurodevelopmental condition rather than simply an extreme form of normal attention variation. The review also identifies important limitations in current research, including uneven diagnostic accuracy across under-represented groups and limited understanding of genetic and environmental interactions. Continuous future research on the mechanisms underlying ADHD and treatment plans across diverse populations can better help individuals get diagnosed accurately and help professionals understand ADHD better.
Introduction
Attention-deficit/hyperactivity disorder, or ADHD, is a neurodevelopmental disorder affecting the development of the brain along with social and emotional behavior (Faraone et al., 2024). It remains a central focus among neurodevelopmental disorders. A global systematic review and meta-analysis estimated that 2.58% of adults have persistent ADHD that began in childhood. When all adults with ADHD symptoms are counted, regardless of when these began, the figure rises to 6.76%. This is equivalent to approximately 139.8 million and 366.3 million adults worldwide in 2020 (Song et al., 2021).
ADHD was described by Sir Alexander Crichton as early as 1798, as “the incapacity of attending with a necessary degree of constancy to any one object.” About 100 years later, it was further described as a childhood deficit (Lange et al., 2010). ADHD remains a large topic of interest in health and science as scientists attempt to decipher its true source within the brain and the factors playing large roles in its development.
As described in the name, typical symptoms include an inability to retain full attention or stay organized, feeling restless and hyperactive, and acting on impulse (Faraone et al., 2024). As ADHD is most commonly diagnosed during childhood, such symptoms can often affect one's learning behavior and success in school. Students with ADHD often underperform in reading, writing, and mathematical standardized tests, as well as show an increase in behavioral disruptions resulting in detention or expulsion (Loe & Feldman, 2007).
Several risk factors have been associated with ADHD, including exposure to neurotoxins such as lead and maternal tobacco exposure during pregnancy (Banerjee et al., 2007). ADHD also runs in families and is highly heritable, which points to a strong genetic influence (Faraone et al., 2024). A substantial proportion of cases is thought to remain unrecognized, and individuals with ADHD face effects in their thinking patterns, attention spans, and overall brain structure throughout their lifespan (Song et al., 2021).
Researchers around the world maintain differing perspectives on ADHD's effects on the brain, continuing to question whether ADHD is a social construct, and simply diagnoses behaviors lying within normal variation. Yet, no one can say for sure what the true cause of ADHD is, as it remains largely under-researched in several demographic groups.
This review looks at how genetic factors and environmental exposures affect the development of ADHD. It also looks at how well treatments work, including therapies such as cognitive behavioral therapy and medications such as Ritalin and Adderall. Next, it compares brain imaging of people with and without ADHD to look for differences in structure and function. Finally, it examines how ADHD is diagnosed, including the use of cognitive testing.
Literature Review
Research question 1: Do genetic factors and environmental exposures contribute to the development and persistence of ADHD, and if so, how do they interact?
There is a growing interest in understanding the causes of ADHD, as studies suggest that genetic and environmental factors may interact and influence the development of ADHD. For example, when DAT1 VNTR—a genetic variation in the DAT1 gene controlling how the brain regulates dopamine—interacts with prenatal smoking exposure, it may contribute to hyperactive and impulsive ADHD symptoms (Palladino et al., 2019). However, findings across studies have been inconsistent. Another genotype, DRD4 VNTR, is a variation in a gene for one of the brain’s dopamine receptors. It has also been associated with environmental factors related to ADHD, including maternal smoking (Palladino et al., 2019). Unfortunately, despite these findings, current evidence linking the influence of genetic and environmental factors with ADHD remains limited.
ADHD is a polygenic disorder where multiple genes each contribute to the development of ADHD. Researchers have found that these genes affect processes that control how neurons form connections and how gene activity is regulated during development. Some of the same genetic influences also seem to be shared with other psychological and physical traits, although much of this is still not fully understood (Folego-Temoteo et al., 2026). Additionally, three genes associated with the development of ADHD—MAP1A, ANO8, and ANK2—contain rare variants that may contribute to ADHD and other neurodevelopmental conditions. These risk genes are generally expressed and active during prenatal and postnatal brain development and affect neuronal functions (Demontis et al., 2026). In addition, another gene—FOXP1—provides instructions for producing a protein that controls the activity of other genes. Therefore, harmful FOXP1 variants can result in FOXP1 syndrome, which involves behavioral abnormalities and may include ADHD as a co-occurring condition (Rappold et al., 2023). However, it is important to recognize that the rare variants in these genes carry a high risk of ADHD. They are only present in a small number of people (Demontis et al., 2026).
Research also indicates that environmental factors may impact the development of ADHD. A developing brain is sensitive, so exposure to harmful environmental factors may contribute to various consequences such as disabilities, disorders, and long-term mental-health challenges. Environmental factors that have been associated with ADHD include diet, food additives, lead contamination, cigarette and alcohol exposure, maternal smoking during pregnancy, and low birth weight (Banerjee et al., 2007). However, many of these links are small and may be partly explained by other factors, such as shared genes, so they do not necessarily cause ADHD (Faraone et al., 2024). Besides prenatal factors, stress may also contribute to ADHD. People with ADHD may have disruptions in neural inhibitory functions, which help with balancing the electric signals in one's brain. These disruptions may interfere with developmental processes and increase sensitivity to stress stimuli, resulting in cognitive, affective, and motor impairments (Bob & Privara, 2025). Therefore, environmental exposures may influence ADHD's development, symptoms, or persistence throughout life.
Another problem in this area of research is that findings on genes and the environment have often been inconsistent and difficult to repeat (Palladino et al., 2019). One reason for this may be that studies measure environmental factors in different ways. For example, maternal smoking may be recorded through questionnaires, medical records, or biological tests, and each method can lead to different mistakes. Additionally, childhood ADHD and ADHD that continues into adulthood may not be exactly the same genetically, so combining them in one study could hide real effects. These problems do not mean that genes and the environment are unimportant, but they do mean that claims about one gene interacting with one specific exposure should be treated with caution.
Numerous studies have examined these genetic and environmental influences through research, statistics, and experiments. One longitudinal twin study used data from the Minnesota Twin Family Study, a study involving 2,764 twins. Throughout this study, researchers examined patterns and relationships between socioeconomic status (SES) and ADHD. They found that childhood ADHD was linked to both lower family SES while growing up and lower educational attainment in adulthood. When one twin had ADHD and the other did not, the twin with ADHD still reached lower levels of education. This means the link could not be fully explained by shared genes and family background. In contrast, ADHD that appeared to begin in adulthood showed no significant link with childhood family SES, although this group was small (Mohan et al., 2026). Overall, genetic factors, environmental factors, and numerous other factors all contribute to the development of ADHD. Therefore, there is not a prevailing factor in terms of genetics and environmental exposures that directly causes ADHD. Yet, more integrated research is needed to claim the interaction between environmental and genetic factors that contribute to the development of ADHD.
Research question 2: To what extent does neurotransmitter signaling underlie ADHD, and what does the effectiveness of medication and other therapies add to the picture?
ADHD is linked to changes in dopamine and norepinephrine signaling, especially in the prefrontal cortex and the areas connected to it. These chemical systems are important for attention, working memory, and controlling behavior (Curatolo et al., 2010; Faraone et al., 2024). Working memory is one of the areas most affected by ADHD. Research shows that most children with ADHD have difficulties with central executive working memory, which is the part of memory used to manage and work with information. However, short-term memory for simply storing information seems to be less affected (Kofler et al., 2020). Adults with ADHD also often experience anxiety and depression at the same time, which can make both diagnosis and treatment more difficult (Fu et al., 2025).
Stimulant medications, mainly methylphenidate (Ritalin) and amphetamines (Adderall), are considered the most effective medications for ADHD, and they work by acting on dopamine and norepinephrine (Curatolo et al., 2010). However, stimulants have some limitations. One review reported that 24.7% of patients developed tolerance to their medication within days to weeks, meaning it became less effective over time (Handelman & Sumiya, 2022). Non-stimulants are used as a second option. Atomoxetine is a selective norepinephrine reuptake inhibitor, which increases the amount of norepinephrine available in the brain. It can cause side effects such as nausea, fatigue, and a higher heart rate and blood pressure (Fedder et al., 2023). Guanfacine works on alpha-2A adrenergic receptors, a type of receptor in the brain that responds to norepinephrine. It can be used when stimulants do not work well or cause too many side effects (Strange, 2008).
For adults, using medication together with psychological therapy is usually more helpful than using either one alone (Kolar et al., 2008). Other than medication, new treatments are also being tested, such as digital therapy apps, new forms of medication, and devices that stimulate the nerves (Baweja et al., 2024). Moreover, there is growing evidence that adults with ADHD may have a higher risk of cognitive decline later in life. This may be linked to problems with dopamine, oxidative stress, and long-term inflammation in the brain (Golimstok & Berrios, 2025).
Research question 3: What do brain imaging studies show about structural and functional differences in ADHD, and how consistent are these findings?
There has been interest in whether ADHD involves altered dopamine signaling and structural differences that affect brain function. However, researchers debate whether ADHD is associated with consistent structural differences because findings vary. Brain imaging, particularly magnetic resonance imaging (MRI), suggests subtle differences in interconnected regions involved in attention, executive function, inhibition, and behavioral control. The frontostriatal circuitry connects the frontal cortex with the striatum and basal ganglia and supports attention, working memory, motivation, reward, and behavioral control (Mizuno et al., 2025). MRI studies have found differences in the frontal cortex, basal ganglia, and cerebellum, suggesting changes across multiple regions rather than one specific area (Mizuno et al., 2025).
Studies have found differences in gray matter volume and cortical development. Mizuno et al. (2025) reported reduced gray matter volume in the frontal cortex, basal ganglia, and cerebellum, along with delayed cortical maturation. Chen et al. (2025), in a meta-analysis of gray matter studies, found decreased volume in regions including the orbitofrontal cortex, putamen, and frontal gyri. Yu et al. (2023) also identified differences in the left superior frontal gyrus and corpus callosum. However, findings vary in location and size, suggesting that structural differences may contribute to ADHD but do not represent one specific cause.
Structural MRI (sMRI) examines brain structure, such as gray matter volume, while functional MRI (fMRI) measures brain activity during tasks or at rest. Studies have found both structural and functional differences in ADHD, particularly in frontal, subcortical, and cingulate regions. Chen et al. (2025) found increased activity in the right parahippocampal gyrus and in the orbitofrontal cortex on both sides of the brain, but decreased activity in parts of the cingulate cortex. Mizuno et al. (2025) also reported structural differences and delayed cortical maturation. These findings show that ADHD is not associated with one consistent pattern of brain differences.
Most MRI studies compare people with ADHD to neurotypical or healthy controls who do not meet ADHD diagnostic criteria. Parlatini et al. (2024), for example, compared 60 adults with ADHD to 23 neurotypical controls. These comparisons allow researchers to identify brain differences associated with ADHD. However, the findings are not fully consistent. Studies repeatedly identify differences in the frontal regions, basal ganglia, cingulate cortex, orbitofrontal cortex, and limbic regions, but the exact location, direction, and size of these differences vary. Mizuno et al. (2025) note that large studies often report relatively small effects, suggesting that ADHD-related brain differences are subtle and vary between individuals. This variation may reflect ADHD's heterogeneity, differences in MRI methods and sample sizes, and variation in participants' age, developmental stage, presentation, and medication status. The evidence therefore supports measurable group-level differences, but no single brain abnormality appears in everyone with ADHD.
There are several reasons why brain imaging studies may not agree with each other. The number of participants varies greatly between studies, and smaller studies often report bigger but less reliable differences. Participants are also different in ways that are hard to control. Age and stage of development matter because the brain matures along a different timeline in people with ADHD. Whether participants are taking medication at the time of the scan may also affect the results. Researchers also make different choices when analyzing their data, such as how they divide the brain into regions and which statistical thresholds they use. Therefore, comparing studies is not simple, even when they seem to look at the same brain structures. Mizuno et al. (2025) suggest that larger studies with more consistent methods are needed before researchers can say which differences are truly reliable.
Pan et al. (2026) found that ADHD is heterogeneous at the brain-network level. Using morphometric similarity networks, a method that maps how similar different brain regions are in their structure, the researchers identified different structural patterns, or “biotypes,” among children with ADHD. Their discovery dataset included 446 participants with ADHD and 708 controls, supporting the idea that ADHD does not have one universal pattern of brain structure. Overall, MRI research has improved our understanding of ADHD, but there is still a lot of uncertainty about how these group differences relate to the symptoms of each individual.
Research question 4: Is ADHD a distinct condition or the extreme end of normal variation in attention, and what does data about the ADHD diagnosis and cognitive testing suggest?
There has been growing interest and controversy in recent years surrounding ADHD and the effects it has on cognition. While some commentators describe it as an extreme end of normal variation in attention, others treat it as a distinct medical condition. Unlike most medical conditions, research on diagnosis and cognitive testing suggests that ADHD cannot be identified through one single medical test (Musullulu, 2025). And unlike a personality trait, ADHD cannot be identified through a self-assessment (Harrison & Edwards, 2023). The question, however, has a complicated answer. Diagnosing ADHD depends on a full evaluation of symptoms, behavior, and difficulties in daily life across different settings. The lack of studies across different demographic groups also makes it harder to give ADHD a clear definition and list of symptoms (National Academies of Sciences, Engineering, and Medicine, 2024). Health professionals currently use the Diagnostic and Statistical Manual of Mental Disorders (DSM-5-TR) as the formal diagnostic criteria (American Psychiatric Association, 2022). Although the DSM-5 took nearly two decades to develop, it is mainly intended to give clinicians a shared way of describing and diagnosing symptoms. It does not explain what causes them or how they should be treated (Lasalvia, 2015).
Cognitive testing may also be used alongside questionnaires and clinical interviews. One common measure is the Continuous Performance Test (CPT), which assesses sustained attention, vigilance, and response inhibition (Levy et al., 2018). CPT is done on a computer and measures how well a person can focus their attention and stop impulsive actions over a sustained period of time. One study of 458 children aged 6–12 used a machine-learning model, which is a computer program that learns patterns from data. The model combined MOXO-CPT scores with each child’s age, sex, and the time the test was taken. This model identified ADHD with 87% accuracy, but this accuracy belongs to the model rather than to the test alone (Slobodin et al., 2020). Research shows that CPTs themselves can identify only modest to moderate differences in children and adolescents with ADHD. Nevertheless, cognitive testing can be useful in diagnosis but has many limitations; researchers advise using CPTs as one supportive part of a broader clinical evaluation (Arrondo et al., 2024). Other cognitive and neuropsychological measures include questionnaires such as the Behavior Rating Inventory of Executive Function (BRIEF), which measures executive functions in children. These measures can give useful information about an individual’s specific difficulties. However, a recent review warned that the BRIEF’s ability to tell apart children with and without ADHD may be overestimated, partly because many of its questions overlap with ADHD symptoms (Bunford et al., 2026).
In young people, ADHD symptoms are measured through interviews, symptom rating scales, and impairment rating scales (Bunford et al., 2026). The criteria these scales are based on are known as the DSM-5-TR; it evaluates behavioral signs and functional impairments across academic, occupational, or social domains. While the DSM-5-TR can be effective, it has been criticized for child-centric and male-centric biases and for an orientation toward outwardly observable signs rather than internal difficulty (Melo & Franca, 2026). This makes diagnosis less accurate for some groups, such as women, who tend to mask their physical ADHD symptoms. Studies show that females with ADHD may develop better coping strategies that hide their symptoms, and anxiety and depression are also common in females with ADHD, which can lead to misdiagnosis. Females are also more likely to show inattentive and internalizing symptoms rather than hyperactive ones, which can contribute to underdiagnosis (Quinn & Madhoo, 2014). Research has also found structural inequalities across sex and ethnicity in who receives an ADHD diagnosis (Warburton et al., 2025). Adults may maintain academic or occupational success while experiencing significant internal difficulties, meaning that externally observable behavior alone does not show a person's struggles with ADHD (Milioni et al., 2017). Timing matters too: a population-based study found that a later first diagnosis was associated with poorer educational outcomes, underlining the cost of delayed recognition (Volotinen et al., 2026).
However, asking whether ADHD is a distinct condition or just the extreme end of normal attention may not be the most useful question. Many medical conditions, such as high blood pressure and type 2 diabetes, are also found at the far end of a normal range, yet they are still treated as real conditions. What matters more is whether the ADHD label identifies people who share important difficulties, and whether diagnosing them leads to better support and outcomes. Based on the studies in this review, the diagnosis does seem to be useful. People with ADHD show measurable differences in thinking and brain structure, face difficulties across many areas of life, and respond to specific treatments. Therefore, the bigger question may not be whether ADHD is real, but where the line for diagnosis should be drawn, and who is being missed by the criteria used today.
Looking at these modern studies and diagnostic methods, ADHD is extremely complicated and remains largely under-researched. While it may seem to be an extreme end of attention, it is also linked to neurodevelopmental conditions with symptoms that are unique to common demographics and to an individual level. With further research and development, this individualistic medical condition can be better understood, helping more people find effective ways to succeed in life.
Discussion
The findings across the studies reviewed suggest that ADHD is influenced by a combination of genetic, environmental, neurological, and cognitive factors. Regarding genetic and environmental interactions, numerous findings highlighted their contributions to ADHD development across the studies and research referenced above. More evidence is currently available on environmental contributions than on genetic ones. Topics such as the different genotypes linked to ADHD and the rare gene variants affecting its development need to be studied further to clearly understand genetic influences. Longitudinal and family-based designs are likely to be the most informative here. The weight of evidence suggests that ADHD does not arise from a single factor but rather from complex interactions between genetic and environmental influences.
These factors are also reflected in the neurological differences associated with ADHD. Brain imaging studies showed that ADHD is associated with subtle differences in brain structure, activity, and connectivity. Across the studies, many findings recurred, especially those involving the frontal cortex, basal ganglia, and limbic regions. This suggests that ADHD involves multiple interconnected brain regions related to attention, executive functioning, inhibition, and behavioral control, rather than a single specific area. However, it is still unclear how specific brain differences relate to individual ADHD symptoms or why people with ADHD show different brain patterns. Larger, long-term studies are therefore needed to examine how brain structure and connectivity change with age. Together, the genetic and brain imaging evidence supports ADHD as a complex neurodevelopmental condition, while also showing that more research is needed to understand why its effects vary between individuals.
The findings on brain chemistry and treatment show a similar pattern. Dopamine and norepinephrine are consistently linked to ADHD, and stimulant medication is still the most effective treatment. However, tolerance, side effects, and different responses between patients mean that no single treatment works for everyone. Future studies should aim to find out which treatments work best for which patients, and what the long-term effects of treatment are across different ages and levels of severity. This research is necessary to ensure that treatment recommendations are based on long-term evidence and can be safely applied across different individuals.
It is also important to recognize the limitations of this review. This is a narrative review rather than a systematic review. This means the studies were chosen by the authors rather than found through a fixed search method, so some relevant research may have been missed. The research itself also has gaps. Much of the brain imaging and genetic research comes from high-income countries, and many participants are recruited from clinics, which may not represent people whose ADHD has never been diagnosed. There are also far fewer studies on adults than on children, even though many adults live with ADHD. Additionally, several of the studies discussed only looked at participants at one point in time. These studies can show differences between groups, but they cannot show whether these differences cause ADHD symptoms, result from them, or share another cause. Longitudinal studies are starting to answer these questions, but there are still very few. Finally, studies with positive results are more likely to be published, so the brain imaging findings may appear more consistent than they really are. Overall, these limitations do not change the main conclusions of this review, but they show that our understanding of ADHD is still developing.
Finally, the evidence surrounding diagnosis and cognitive variability demonstrates why ADHD should not be viewed as simply an extreme form of normal attention variation. Although ADHD symptoms exist on a large spectrum, there are connections between these symptoms, cognitive differences, and functional impairment that support ADHD as a clinically meaningful neurodevelopmental condition. Diagnosis requires multiple sources of evidence, including behavioral assessments and symptom evaluations. Additionally, differences across sex and ethnicity reveal weaknesses in current diagnostic methods and standards. ADHD is a unique and largely individualistic condition, and forcing it to fit into one simple standard causes misdiagnosis or underdiagnosis. Therefore, policy and clinical recommendations should support more individualized diagnostic standards and ensure that assessment methods are effective across different demographic groups. Overall, the evidence from studies on genetics, brain imaging, brain chemistry, treatment, and cognitive testing supports ADHD as a distinct and clinically meaningful condition. It also shows the need for larger, longer-term, and more diverse research to improve diagnosis, treatment, and policy.
Conclusion
Overall, ADHD cannot be traced back to a single cause. Instead, it may develop from many small genetic effects, a few rarer high-risk variants, and environmental influences, which together affect how the brain develops and how it uses dopamine and norepinephrine. This helps explain why no single brain difference, test, or medication fits every person with ADHD. It also helps answer the question of whether ADHD is simply the extreme end of normal attention. Although its symptoms lie on a spectrum, the measurable differences in the brain, the real difficulties in daily life, and the response to treatment show that it is a meaningful condition. The biggest challenge now is not proving that ADHD exists, but recognizing it earlier and more fairly, especially in girls, adults, and other groups that are often missed. Getting this right could make a real difference to people's education and lives.
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