1. Introduction

Autism spectrum disorder (ASD) is a neurodevelopmental disorder classified by deficits and repetitive patterns of interests, activities and behaviour (Liu et al., 2025). Autism is defined in the psychiatric literature as a neurodevelopmental disorder characterised by failure to communicate and interact socially (Alpert, 2021). Current data highlights ASD’s high prevalence, with the condition present in approximately one in 36 children, with diagnoses occurring four times more commonly in males than in females (Alpert, 2021; Liu et al., 2025). Furthermore, ASD is a heterogeneous group of neurodevelopmental disorders that affects up to 2.6% of the worldwide population (Dunalska et al., 2021). Diagnostic traits are identified early in childhood, with impaired eye contact and social interactions observed (Alpert, 2021). The term “weak central coherence” is commonly used to refer to the detail-focused processing technique used to characterise ASD characteristics (Happé & Frith, 2006). 

For an individual to be diagnosed with ASD, they must show difficulties, either in the past or present, in each of the three subdomains of social communication: deficits in social-emotional reciprocity; deficits in developing, maintaining and understanding relationships; and deficits in non-verbal communication behaviour while socially interacting (Lord et al., 2018; Hirota & King, 2023). There must also be difficulties, either past or present, in two out of the four repetitive, restricted sensory-motor behaviours: hyper/hypo-reactivity to unusual sensory interests or inputs; highly restricted and fixated interests which are abnormal in intensity and focus; repetitive or stereotyped motor movements in speech or uses of objects; and an insistence and obstinate adherence to fixed patterns or routines (American Psychiatric Association, 2022). For instance, autistic individuals may continue to handle or play with objects repetitively rather than engage in social interaction. These behaviours are often called “stimming”, meaning self-stimulating behaviours that primarily involve repetitive vocalizations and movements (Alpert, 2021). ASD is often defined by a broad range of severity, hence the term “spectrum”. In its most severe form, this disorder can require supportive care in a chronic healthcare institution. Meanwhile, in milder forms, autistic individuals may develop coping strategies to live independent lives (Alpert, 2021).

Though ASD diagnoses are dependent on behavioural symptoms, research driven by neuroimaging and molecular advances indicates that behavioural features result from underlying neurological differences and not a lack of functioning in one brain region (Lord et al., 2018). Nevertheless, although there has been significant progress in understanding brain differences, little is known about how neurological processes and cognitive features are linked in autism spectrum disorder (Liu et al., 2025). Specifically, it is not known how differences in neural connectivity and brain development lead to deficits in social communication, executive function, sensory processing and restrictive or repetitive behaviours (Uddin et al., 2017). Understanding this link would help further our understanding of the pathophysiology of ASD and lead to more effective interventions. Therefore, this review aims to assess the relationship between neurological mechanisms and cognitive function involved in autism spectrum disorder, with an emphasis on how differences in brain organisation influence behavioural and cognitive outcomes.

2. Psychological Aspects

2.1 Social Cognition and Communication

Theory of mind is the ability to assign mental states, including beliefs, desires, knowledge and intentions, to predict and explain human behaviour (Beaudoin et al., 2020). Models like the self to other model of empathy distinguish theory of mind from other parts of social cognition (Beaudoin et al., 2020). Theory of mind lacks the emotional caring and sharing aspects of empathy, focusing on mentalising internal cognitive states of third parties. Additionally, theory of mind differs from more basic social abilities, such as identifying motion through facial expression or tone of voice (Beaudoin et al., 2020; Wang et al., 2022). These processes involve being able to recognise emotional cues, whereas theory of mind requires deeper reasoning about another individual’s mental state and perspective (Beaudoin et al., 2020).

Explicit false-belief understanding, which lets children realise that others can hold beliefs that differ from reality, starts at around four-years-old in typical development (Carlsson et al., 2018). Language acts as a vital framework for theory of mind, providing a mental-state lexicon and complex linguistic structures, such as sentence complements, that support reasoning about false beliefs (Carlsson et al., 2018). However, children with ASD follow a different mental path with theory of mind. Autistic individuals face challenges in standard explicit false-belief understanding by relying on language and conscious reasoning instead of intuition (Carlsson et al., 2018). Furthermore, affective empathy is often preserved in children with autism, but differences in theory of mind abilities are more significantly connected to performance on structured social tasks, such as resource allocation, where understanding a different person’s perspective includes prosocial decision-making (Wang et al., 2022). Overall, theory of mind is complex, developing through language, reasoning and experience, and differences in how it develops may help explain variation in social understanding in individuals with autism.

Expanding on these principles of social cognition, identifying emotions through facial expressions involves more than simply looking at a person’s face. Individuals must first notice and comprehend different facial features, such as changes in expression, before linking those cues to what another individual might be feeling (Barrett et al., 2019). This process involves quickly recognising major emotional signals, including signs of fear or distress, while considering the context of the situation to determine the expression’s meaning (Barrett, 2022; Barrett et al., 2019). For example, the same facial expression may convey various other emotions depending on the social surroundings (Barrett, 2022). Individuals also rely on somatic simulation, where they use their own experiences to better understand and relate to another individual’s feelings (Wood et al., 2016).

Effective social communication entails the integration of three key language domains: expressive language, receptive language and pragmatic language, in which autistic individuals may struggle to utilise these skills (Sterling, 2014). Expressive language allows someone to share their emotions, intentions and thoughts through words. Some autistic individuals find it challenging to translate their internal experience using speech (Sterling, 2014). Receptive language is the ability to grasp spoken and written language, and difficulties in this area can affect how autistic individuals follow complex language, especially in fast-paced environments. These challenges may be mistaken for disinterest or inattention when they instead reflect variances in comprehension (Sterling, 2014). Pragmatic language involves the use of communication in social situations, and those with autism may experience differences in this area. Autistic individuals might interpret language more literally and have more difficulty recognising hidden meaning, like sarcasm (Sterling, 2014). There is distinctiveness across these linguistic fields, showing how everyone’s unique style of processing information and talking to people shapes how neurodivergent demographics connect with the world.

2.2 Executive Function and Processing

The term “executive function” refers to an individual’s ability to facilitate functions such as planning, working memory, impulse control, inhibition and mental flexibility (Hill, 2004). Autistic individuals with average intellectual functioning demonstrate deficits in cognitive flexibility, phonological fluency and working memory (St. John et al., 2021). However, autistic individuals also display strengths in planning, decision-making and semantic verbal fluency (St. John et al., 2021). The prevalence of executive dysfunction remains a topic of debate due to implications of the frontal lobe (Hill, 2004). Direct evidence of executive dysfunction within ASD throughout cognitive development and its significance for guiding interventional techniques remains unresearched (Demetriou et al., 2018). 

Cognitive flexibility defines the multifaceted fundamental process that underlies the capacity to shift behaviour, mental tasks or strategies in response to environmental changes (Lage et al., 2024). Most complex variations of cognitive flexibility rely on set-shifting abilities (Lage et al., 2024). In autistic individuals, cognitive flexibility deficits have been linked to increased social difficulties (Lage et al., 2024). Executive functional deficits provide evidence for repetitive behaviours and restricted interests seen in autistic individuals (Hedvall et al., 2013). According to preexisting research, poor mental flexibility is correlated with rigidity and concrete-bound behaviour with occasional perseverations (Hedvall et al., 2013). Further evidence also suggests the critical role of cognitive flexibility in academic achievement and adaptive behaviour (Lage et al., 2024).

Intellectual disability (ID) is one of the most common co-occurring disorders in ASD. Among these, processing speed proves the most prevalent (Hedvall et al., 2013). This deficit shows a tendency of “invisibility” within children with ASD with “normal” IQs; however, derecognition often leads to errors in the expected execution of daily tasks (Hedvall et al., 2013). Processing speed is analogous to the operating speed of a computer and is often linked to higher-order cognition (Hedvall et al., 2013). Processing speed was found to be the weakest relative to other indicators on the Wechsler Intelligence Scale for Children (WISC-IV UK) within groups of high-functioning children aged ten (IQ >70) diagnosed with ASD (Hedvall et al., 2013). Deficits in processing speed create hardships in learning rates, comprehension, and mental fatigue (Hedvall et al., 2013).

In addition to intellectual disabilities, atypical sensory processing remains a critical topic for autistic individuals (Neklyudova et al., 2022). Defined behaviourally, sensory abnormalities present as hypo- and hyperreactivity (Neklyudova et al., 2022). Hyper-sensitivity refers to an autistic individual’s overreactiveness towards sensory stimulation (Balasco et al., 2020). In contrast, hypo-sensitivity is characterised by reduced reactivity to sensory stimulation and sensory-seeking behaviours (Balasco et al., 2020). The DSM-5 recognises both hypo- and hypersensitivity to stimulation as unusual sensory interests in sensory aspects of the surrounding environment in the criteria for ASD (Neklyudova et al., 2022). Some of these abnormalities influence higher-order functioning processes, including language and social inference (Neklyudova et al., 2022). 

These deficits and differences in cognition and functioning highlight the sensory abnormalities and executive functioning characterised by autism spectrum disorder. Thus, current studies in these areas remain elusive and inconsistent, and future psychological research must be conducted to effectively link sensory abnormalities and social features of ASD, in addition to the multifaceted stability of cognitive profiles and adaptive outcomes (Hedvall et al., 2013; Balasco et al., 2020).

3. Neurological Aspects

3.1 Micro-level neurological mechanisms

Glutamate is one of the most abundant excitatory neurotransmitters in the brain and is responsible for transmitting information between neurons (Cleveland Clinic, 2022). Alternatively, gamma-aminobutyric acid (GABA) is the major inhibitory neurotransmitter, which counters glutamate by lessening a neuron’s ability to receive messages (Leon & Tadi, 2023). These neurotransmitters work together to maintain balance in neural activity. According to a literature review by Liu et al. (2025), “shifts in neural circuit connections are at the heart of ASD”, and an imbalance in these neurotransmitters, typically reduced GABAergic activity and excess glutamatergic activity, is one of the leading biological explanations for cognition in ASD (Liu et al., 2025). Lee et al. (2017) explain how “a tight balance between excitation and inhibition (E/I balance) in synaptic inputs to a neuron and in neural circuits is important for normal brain development and function. Accordingly, disturbed E/I balances have been implicated in various brain disorders, including autism spectrum disorders (ASDs)” (Lee et al., 2017).

The same article by Lee et al. (2017) found that “results collectively suggest that an increased neocortical E/I ratio caused by malfunctions of PV-expressing interneurons induces excessive gamma oscillations and autistic-like behaviours” (Lee et al., 2017). Parvalbumin (PV or PA) is a small, calcium-binding protein that is often found in inhibitory interneurons. It regulates neuronal excitability, synaptic transmission and prevents neurons from calcium overload or oxidative stress by buffering intracellular calcium (Permyakov & Uversky, 2022). “Gamma oscillation is the synchronisation with a frequency of 30-90 Hz of neural oscillations, which are rhythmic electric processes of neuron groups in the brain” (Guan et al., 2022). The purpose of these oscillations is to connect the different brain regions, which is extremely important for memory, movement, perception and emotion (Guan et al., 2022). If there are excessive gamma oscillations, it can lead to the kind of “autistic-like behaviours” that are mentioned throughout the article. Behaviours associated with excessive oscillation include: social deficits, repetitive behaviours, intellectual disability, cognitive deficits (including learning, memory and cognitive flexibility), emotional deficits, multisensory integration deficits, epilepsy/seizure susceptibility, motor deficits, hyperactivity and anxiety.

According to de Lahunta and Glass (2009), cortical minicolumns are “vertical arrays of interconnected neurons within the cerebral cortex, structured in a laminar organisation that facilitates specific functional roles” (de Lahunta & Glass, 2009). They are part of the elaborate neural structure that allows perception and motor control. Minicolumn abnormalities are one of the biological pathologies found in ASD. In autistic individuals, minicolumns in areas of the frontal cortex are smaller, meaning they are less developed. These minicolumns contribute to “deficient neuronal insulation” and serve as the structural basis for increased neuronal “cross-talk” and overstimulation. Using this information, we can see how abnormalities in cortical minicolumns could be one of the main drivers for sensory gating difficulties that autistic individuals experience. A different source explains that sensory gating is an automatic process that prevents overstimulation by filtering sensory input (Heckman et al., 2015). Disruptions in this process are associated with clinical disorders, including ASD.

3.2 Macro-level neurological mechanisms

Cortical thickness refers to the distance between the white matter and the outer surface of the cerebral cortex (Fischl, 2012), whereas cortical folding (gyrification) describes the pattern of folds that increases cortical surface area and supports efficient neural connectivity (Llinares-Benadero & Borrell, 2019). Both measures are indicators of brain maturation and neurodevelopment (Ronan & Fletcher, 2015).

Individuals with ASD often exhibit atypical cortical thickness and altered gyrification, suggesting differences in cortical development (Khundrakpam et al., 2017; Ni et al., 2020). Ni et al. (2020) report that there is dysregulation of cortical folding, which is observed in the right middle frontal (dorsolateral prefrontal cortex) and right lateral orbitofrontal regions (Ni et al., 2020). The right middle frontal cortex is involved in top-down executive control through the frontoparietal network, while the right lateral orbitofrontal regions regulate emotion through the affective processing intrinsic network (Ochsner et al., 2004; Yeo et al., 2011). Increased cortical thickness may also reflect delayed cortical maturation and reduced synaptic pruning during early development, processes that are thought to contribute to atypical neural organisation and connectivity in ASD (Zielinski et al., 2014). This increased cortical thickness measures in ASD could arise from various microstructural grey matter (GM) changes, such as a greater number or larger neurons/glia, increased dendritic arborisation (branching out of neurons) potentially with a greater number of synapses, larger or more axons, or potentially greater capillary support (Huttenlocher 1991; Chklovskii 2004; Muotri & Gage 2006).

Furthermore, dysfunction in the cortical gyrification of these regions may affect the self-regulation of emotion and the appearance of ASD behavioural characteristics, such as those of reduced cognitive flexibility (difficulty adapting to change) and behavioural rigidity (preference for routine and the appearance of repetitive behaviour) (Pitskel et al., 2014; Rolls, 2019). Alongside this, genetic and environmental influences contribute to the distinctive patterns of cortical folding development in children with ASD (Hegarty et al., 2020). Therefore, self-regulation ability may be developed through cortical gyrification in the right middle frontal gyrus and right lateral orbitofrontal cortex and also nurtured through daily interactions and encounters (Ni et al., 2020). Supporting these findings, Khundrakpam et al. (2017) analysed MRI data from over 500 individuals and found widespread increases in cortical thickness during childhood in ASD, with differences becoming less pronounced in adulthood. Greater cortical thickness was also associated with increased social and communication difficulties, suggesting that atypical cortical maturation may contribute to the behavioural characteristics of ASD (Khundrakpam et al., 2017).

4. Discussion

Both pharmacological and therapeutic approaches have been developed as interventional techniques to reduce ASD symptomatology. It is important to note that although pharmacological treatments may alleviate associated symptoms such as irritability, hyperactivity, anxiety or aggression, they generally do not address the core deficits in social communication and restricted or repetitive behaviours that characterise ASD. That being said, pharmacological interventions include psychostimulants, atypical antipsychotics, antidepressants and alpha-2 adrenergic receptor agonists (Sharma et al., 2018). These medications provide direct partial symptomatic relief of the core symptoms of ASD and manage comorbid conditions (Sharma et al., 2018). Therapeutic approaches indicating significant improvement within social and verbal communication include music therapy, cognitive behavioural therapy and social behavioural therapy (Sharma et al., 2018). Other studies have shown significant behavioural improvement and enhanced social communication with joint-attention-based interventions, especially child-centred approaches (Özkan et al., 2023). Further explored therapeutic approaches to ASD include digital therapies, non-invasive brain stimulation, antioxidants, oxytocin, AVP1a antagonists, PPAR agonists and mTOR inhibitors (Wang et al., 2025). Since ASD is heterogeneous, there is no single intervention that works for everyone. Thus, treatment plans are tailored according to the severity of symptoms, cognitive profile, communication ability, age and co-occurring conditions.

Of the various interventional techniques investigated, the most effective have been established based on the principles of ABA (applied behaviour analysis), which antecedent research has shown to reduce behavioural deficits through language development and communication-based approaches (Kodak & Bergmann, 2020). Although ABA continues to be one of the most researched behavioural interventions, it has also been a topic of discussion within the autistic community regarding treatment goals, intensity and the focus on changing autistic behaviour (Mathur et al., 2024). As a result, many of the current ABA programmes are becoming more child-centred and individualised, with an emphasis on communication, independence and quality of life (Rodgers et al., 2020; Evers et al., 2022). Behavioural interventions for ASD target the increase of functional independence of autistic individuals (Eckes et al., 2023). ABA analyses how an individual’s nurture influences behavioural outcomes and provides explanations for interventions that apply the findings to change behaviour (Eckes et al., 2023). The basis of ABA therapy is operant conditioning, and it assesses and changes challenging behaviour while promoting and generalising more adaptive behaviour through systematic reinforcement (Eckes et al., 2023). Early intensive applied behaviour analysis is typically delivered to young children with ASD for several years on a one-to-one basis, for approximately 20-50 hours per week (Hodgson et al., 2022). Well-known examples of ABA interventions include early intensive behavioural interventions (EIBI) (Eckes et al., 2023). EIBI is a behavioural intervention approach based on the principles of ABA and emphasises teaching skills through structured task completion and rewards (Hodgson et al., 2022). EIBI has been adapted to incorporate many of the primary principles of ABA through naturalistic developmental behavioural interventions (NDBIs), which combine behaviour-based techniques with child-led teaching (Hodgson et al., 2022). The advantage of ABA desensitisation procedures is the ability to influence a child’s particular skill and the continuous collection of behavioural data (Portnova et al., 2020). Through ABA-based interventions, children with ASD find significant symptom relief in improved intellectual abilities, communication skills, expressive language skills, receptive language skills, adaptive behaviour and socialisation (Makrygianni et al., 2018).

5. Conclusion

In all, autism spectrum disorder is a neurodevelopmental disorder classified by deficits and repetitive patterns of interests, activities and behaviour, with prevalence affecting one in 36 children annually, with significant risk for failure of adaptation in social, educational and psychological regions (Brentani et al., 2013). While the hallmark of heterogeneity of ASDs may be an underlying factor, it does not impede the understanding of ASD subgroups, markers of pathological states and cross-cultural factors that are imperative to advancing treatments (Masi et al., 2017). Currently, the diagnosis of ASD continues to be entirely based on the observation of behaviours (Masi et al., 2017). However, there is greater recognition of complex symptomatology, including medical and mental health comorbidities (Masi et al., 2017). Identifying objective rather than subjective biomarkers and biological signatures that contribute to ASD subgroups will aid in advancing personalised medicine and treatment models (Masi et al., 2017).

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