Neurochemical and neurobiological mosaic of autism

Introduction

This classification provides an overview of how autism was categorized and described in the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV)⁽¹⁾. Autism was categorized as part of pervasive developmental disorders (PDD) in DSM-IV. Autism is considered the prototype of this category.

The term autism spectrum disorders encompasses three main conditions under PDD:

• Autistic disorder (classic autism).
• Asperger disorder (commonly referred to as Asperger syndrome).
• Pervasive developmental disorder not otherwise specified (PDD-NOS) – a catch-all diagnosis for those who didn’t fully meet the criteria for the other two but still had significant symptoms.

These are collectively referred to as autism spectrum disorders, affecting up to 1% of children⁽²⁾. These disorders are marked by impairments in three main areas.

Social skills

Communicative use of verbal and nonverbal language

Restricted and repetitive behaviors (which are often detail-focused and associated with difficulties grasping broader concepts). This reflects how autism and related disorders were classified before changes were introduced in the DSM-5, where the term autism spectrum disorder (ASD) became an umbrella diagnosis, merging the distinctions between autistic disorder, Asperger disorder, and PDD-NOS⁽³⁾. The genetic perspective provides a more integrated view of how autism may involve a network of dysfunctions across multiple biological systems. Autism is considered a polygenic disorder, meaning multiple genes contribute to its development, with a hereditability index of 0.90, indicating a strong genetic component⁽⁴⁾. A significant genetic association has been found between autism and the C allele in the promoter region of the MET receptor tyrosine kinase gene. This gene plays a crucial role in cell signaling pathways that influence various cellular behaviors, such as proliferation, differentiation and survival. In families with more than one child affected by autism⁽⁵⁾, inheriting two copies of this allele (the CC genotype) confers a 2.27-fold increased risk of an autism diagnosis. This genotype also leads to a two-fold reduction in MET promoter activity and a decrease in the transcription factor binding, potentially impairing important signaling processes. Other important neurobiological aspects can be enumerated, which are presented below.

Systems affected by MET signaling

Neocortical and cerebellar development: these areas of the brain, which are critical for higher cognitive functions and motor control, are influenced by MET signaling.

Immune system function: MET signaling is also involved in regulating immune responses, which have been implicated in autism-related dysfunctions.

Gastrointestinal repair: MET signaling contributes to gut health, and many individuals with autism experience gastrointestinal issues.

Multiorgan dysfunction in autism

This genetic finding suggests a possible mechanistic link for the simultaneous dysfunction seen across the brain, immune system, and gastrointestinal system in individuals with autism⁽⁶⁾. This contrasts with earlier theories that posited dysfunction in one system (e.g., the immune system or gut), leading to brain dysfunction and subsequently to autism.

Related genetic research

Chromosome 7q31: previous research had identified this chromosome region as a candidate gene area for autism.

Cortical interneuron inhibitory hypothesis: research has also focused on abnormalities in cortical minicolumns, a small groups of neurons in the brain, which may reflect a deficiency in interneurons⁽⁷⁾ (neurons that play an inhibitory role), potentially contributing to the neural characteristics of autism.

This genetic perspective provides a more integrated view of how autism may involve a network of dysfunctions across multiple biological systems. There are findings from structural magnetic resonance imaging (MRI) studies related to brain development in individuals with autism.

Increased brain volume in autism: MRI studies confirmed an increase in total brain volume, a phenomenon initially inferred from the increased head circumference observed in young children with autism. This increase is noticeable starting between 2 to 4 years of age^(8,9), around the time of early clinical recognition of autism.

Persistence and age factor: the increased brain volume persists through childhood, but it does not extend into adolescence⁽¹⁰⁾.

Specific brain tissues: the increase in brain volume is mainly due to the enlargement of both total cerebral white matter and total cortical gray matter. However, the extent of the gray matter increase can vary depending on the brain parcellation method used to study it.

White matter parcellation: a study focusing on children aged 6 to 11 categorized cerebral white matter into two areas: 1) the outer zone of radiate white matter – this area is composed of interhemispheric cortico-cortical connections, and it showed an increase in volume across all cerebral lobes, with a predominance in the frontal lobe; 2) the inner zone of white matter – this includes regions like corpus callosum and internal capsule, which connect different parts of the brain. These areas did not show any volume increase⁽¹¹⁾. The increased volume of outer radiate white matter, particularly in the frontal lobes, suggests an overgrowth of short- and medium-range interhemispheric cortico-cortical connections (connections within the same hemisphere). In contrast, there was no detected overgrowth in interhemispheric connections (between hemispheres) or connections bet­ween the cortex and subcortical structures.

Clinical implications: the onset of brain overgrowth coincided with the emergence of autism symptoms, suggesting that this abnormal brain growth may be linked to the pathology of autism.

Neurochemistry of autistic brain

Autism spectrum disorder has been a major focus in neurochemical research due to its distinct and consistent impact on social interaction, communication and cognitive development. Over the past few decades, various neurochemical systems have been studied to understand their roles in autism, with neurotransmitters, neural pathways and genetic components contributing to the complex neurochemistry underlying the condition.

The critical role of neurotransmitters and neuropeptides in brain development and their contribution to various cognitive and behavioral functions is implicated in autistic pathology⁽¹²⁾. Neurotransmitters and neuropeptides are involved in several fundamental processes of brain maturation, including:

Neuronal cell migration – the movement of neurons to their proper positions in the brain.

Differentiation – the specialization of neurons for specific functions.

Synaptogenesis – the formation of synapses (connections) between neurons.

Synaptic pruning – the elimination of excess synap­ses, which is crucial for optimizing brain function and efficiency.

Apoptosis – the programmed cell death that helps refine and shape the brain.

A dysfunction in neurotransmitter systems can disrupt these critical developmental processes. Such impairments in brain development can potentially lead to neurodevelopmental disorders like autism⁽¹³⁾. The proper functioning of neurotransmitter systems is vital for normal brain development, and any disruption in these systems could contribute to the onset of autism by affecting key developmental processes. Here are some of the main neurochemical systems implicated in autism research:

1. Gamma-aminobutyric acid (GABA) is a crucial neurotransmitter with a unique developmental role in the brain. It originates from glutamate, which undergoes conversion by the enzyme glutamate decarboxylase (GAD), a process essential for maintaining the balance between excitation and inhibition in neural circuits. This balance is vital for healthy brain function, as it prevents over-excitation, which can lead to neurotoxicity and disorders involving excessive neuronal firing, like epilepsy⁽¹⁴⁾. In children with autism spectrum disorder, the neurochemical profiles involving GABA, glutamate and glutamine show marked differences compared to typically developing controls, pointing to an altered excitatory-inhibitory balance and amino acid metabolism⁽¹⁵⁾. The pharmacological approach using GABA modulators in autism aims to address the disrupted balance between excitatory (glutamatergic) and inhibitory (GABAergic) pathways, by enhancing GABAergic signaling or modifying glutamatergic activity. Arbaclofen, acamprosate, bumetanide and valproate are the most studied substances.

2. Glutamate, the main excitatory neurotransmitter, is involved in synaptic plasticity, learning and memory. Elevated glutamate levels can lead to neurotoxicity and disrupt neural connectivity. Abnormal glutamatergic signaling may contribute to cognitive deficits and stereotyped behaviors. Valproic acid (VPA)-induced rodent models of autism have provided valuable insights into how neurochemical and synaptic modifications might contribute to autism-like behaviors. In these models, the selective overexpression of NR2A and NR2B subunits of NMDA (N-methyl-D-aspartate) receptors leads to enhanced NMDA receptor-mediated synaptic currents. This amplification in NMDA signaling results in heightened postsynaptic plasticity, particularly in neocortical pyramidal neurons, which are crucial for higher-order processing such as cognition, perception and sensory integration. Overexpression of NR2A and NR2B in NMDA can impact synaptic plasticity – the NR2A and NR2B subunits are essential for modulating synaptic strength and plasticity. Overexpression of these subunits intensifies NMDA receptor activity, which in turn enhances synaptic currents and potentially leads to excessive synaptic potentiation in affected neural circuits. This excessive activity can lead to neural network hyperexcitability, disrupting the balance between excitatory and inhibitory signaling, a common feature in autism. In autism-like behavior, heightened postsynaptic plasticity in these models is linked to behavioral phenotypes resembling those seen in autism, such as impaired social interactions, repetitive behaviors, and sensory processing abnormalities. In the developing brain, such modifications could lead to atypical neural circuit formation, which might underlie some core symptoms of autism⁽¹⁶⁾.

3. Serotonin

The serotonin (5-HT) system has been implicated in the etiology of autism, particularly during early brain development, influencing key processes like cell division, cortical proliferation, migration, differentiation, cortical plasticity and synaptogenesis. As a monoamine neurotransmitter, serotonin plays a crucial role in brain development and various cognitive and behavioral functions, including memory, learning, mood regulation and sleep. Polymorphisms in the SLC6A4 gene, which encodes the serotonin transporter (SERT or 5-HTT), have been linked to autism, suggesting a gene­tic basis for serotonin dysregulation observed in ASD. The serotonin transporter plays a key role in serotonin reuptake from the synaptic cleft back into presynaptic neurons, which regulates serotonin availability and modulates signaling duration. Abnormalities in this process can disrupt serotonin balance, potentially impacting neurodevelopment and behaviors associated with autism^(17,18).

4. Dopamine

Dopamine, beyond its well-known role in motor control, is crucial in regulating social cognition and behaviors, largely through the mesocorticolimbic pathway. This dopaminergic pathway – which includes connections between the ventral tegmental area (VTA), nucleus accumbens and the prefrontal cortex – is central to reward processing, motivation and social interactions. In autism and related neuropsychiatric disorders, dopamine dysfunction in this pathway is thought to contribute to social and cognitive challenges⁽¹⁹⁾.

Research has suggested that distinct dopaminergic circuits may underlie specific behavioral characteristics of autism. According to some studies, social deficits in autism may be linked to dysfunctions in the mesocorticolimbic circuit, while stereotyped behaviors (repetitive, rigid patterns of behavior) are more closely associated with abnormalities in the nigrostriatal circuit⁽²⁰⁾.

5. Acetylcholine

Acetylcholine (ACh) serves multiple functions across both the peripheral and central nervous systems, supporting motor control, autonomic regulation and neuromodulation. In the central nervous system (CNS), acetylcholine is essential for cognitive functions like attention, learning and memory, where it acts as both a neurotransmitter and a neuromodulator.

Acetylcholine and the cholinergic system in ASD

Emerging research highlights abnormalities in the cholinergic system in autism, with a primary finding being a significant reduction in the nicotinic á4â2 subtype of acetylcholine receptors (nAChRs) within regions of the brain associated with cognition and behavior, namely the parietal and frontal cortices⁽²¹⁾.

Key aspects of acetylcholine’s role in ASD

Reduced nicotinic receptors and cognitive impact: nico­tinic acetylcholine receptors (nAChRs), especially the á4â2 subtype, are crucial for attention, working me­mory and other executive functions. These receptors, located in high densities in the frontal and parietal cortices, modulate neurotransmitter release and influence cortical excitability and plasticity. A reduction in á4â2 nAChRs could impair cognitive functions such as attention and executive control, which are often affected in ASD. Lower receptor density may contribute to difficulties in processing and integrating sensory information, maintaining attention and regulating behavioral responses⁽²²⁾.

Frontal and parietal cortices and ASD symptoms

The frontal cortex plays a central role in social behavior, decision-making and inhibition control, all of which can be atypical in autism. Abnormal cholinergic signaling in this region may contribute to challenges in these areas. The parietal cortex is involved in sensory processing and in integrating information from various sensory modalities. Dysfunction here could be linked to sensory processing issues in ASD, where individuals may show hypersensitivity or hyposensitivity to sensory stimuli.

Cholinergic influence on neurodevelopment: acetylcholine is critical for neurodevelopmental processes, such as neuronal differentiation, synapse formation and plasticity. Abnormalities in the cholinergic system may impact these developmental pathways, leading to atypical brain connectivity and function, which are observed in autism. Reduced receptor density during critical periods of brain development could lead to lasting impacts on neural circuitry involved in cognition, social behavior and sensory integration.

Interaction with other neurotransmitter systems: the cholinergic system interacts with other neurotransmitter systems, including dopamine, GABA and glutamate⁽²³⁾. Imbalances in acetylcholine may, therefore, exacerbate broader neurotransmitter dysregulation in autism, influencing both excitatory and inhibitory signaling.

6. Oxytocin and arginine-vasopressin

 Oxytocin (OXT) and arginine-vasopressin (AVP) are two neuropeptides with significant implications in social behavior, emotional regulation and stress response, areas often affected in autism spectrum disorder. Due to their close genetic and structural relationship – being separated by only 12 kilobases of DNA on chromosome 20p13 and having opposite transcriptional orientations – they can influence each other’s functions, and have effects on similar neural structures in the central and autonomic nervous systems⁽²⁴⁾.

Oxytocin (OXT) and autism. Oxytocin, often called the “social bonding hormone”, plays a key role in promoting social behaviors, trust and attachment. Studies have indicated its importance.

Social behavior and emotional processing: oxytocin affects brain areas related to social cognition, such as the amygdala, hypothalamus and ventromedial prefrontal cortex. In autism, lower levels or altered responses to oxytocin may be linked to social deficits, difficulties with emotional processing and reduced social motivation⁽²⁵⁾.

Therapeutic interest in oxytocin for ASD: researchers are exploring intranasal oxytocin as a potential therapeutic intervention for autism to enhance social engagement, reduce repetitive behaviors and improve emotional recognition. Although the results are mixed, some studies suggest that oxytocin administration may temporarily improve certain social behaviors, making it a promising, if still exploratory, challenge⁽²⁵⁾.

Arginine-vasopressin (AVP) and autism. Arginine-vasopressin, which is structurally similar to oxytocin, is primarily involved in regulating social behaviors and the stress response.

Social communication and aggression: AVP affects social behavior in areas such as dominance, aggression and social communication, often by acting on regions like the amygdala and the ventral pallidum. AVP dysregulation in autism may contribute to challenges in social communication, emotional regulation, and potentially higher levels of irritability or aggression.

Stress sensitivity: AVP influences the hypothalamic-pituitary-adrenal (HPA) axis, a key player in the body’s stress response. Dysregulation in this system can lead to heightened stress sensitivity, a common characteristic in ASD⁽²⁶⁾. Increased AVP activity has been linked to stress-related behaviors and may exacerbate social avoidance and anxiety, both of which are prevalent in autism.

7. N-acetyl aspartate

N-acetyl aspartate (NAA) is a metabolite with one of the highest concentrations in the human central nervous system (CNS). Although its exact function is still uncertain, it is predominantly found in neurons, oligodendrocytes and myelin, suggesting a role in neuronal health, myelination and, possibly, neurotransmitter regulation. NAA is synthesized in the mitochondria from aspartic acid, linking its presence and availability to mitochondrial function and cellular energy production⁽²⁷⁾. In autism spectrum disorder, decreased levels of N-acetyl aspartate (NAA) have been observed in several brain regions, notably those involved in social and cognitive processing, such as the prefrontal cortex, temporal lobes and cerebellum. NAA is a key metabolite in the brain synthesized within mitochondria and serves as an indicator of neuronal health and mitochondrial function⁽²⁸⁾. Given the links between NAA levels and mitochondrial activity, reduced NAA concentrations in autism suggest underlying mitochondrial dysfunction and neuronal health challenges, both of which may contribute to core features of autism.

8. Melatonin

The role of melatonin in addressing sleep disorders in children with autism spectrum disorder and its broader implications in neurodevelopment are outlined by some of the key points. Regarding sleep disorders, children with ASD often face challenges, including difficulty falling asleep, staying asleep and experiencing para­somnia⁽²⁹⁾. Melatonin, primarily known for regulating sleep-wake cycles, can reduce sleep latency (time to fall asleep), act as a powerful antioxidant, and support neurodevelopment and neural plasticity by contributing to placental health and immune function⁽³⁰⁾. Patients with ASD often show lower levels of melatonin and melatonin metabolites in plasma, along with reduced excretion of melatonin sulfate in urine⁽³¹⁾.

Maternal melatonin and neurodevelopment: maternal melatonin can cross the placenta, providing the fetus with crucial photoperiodic information and aiding in the establishment of the circadian rhythm essential for brain development. It also appears to offer neuroprotection against inflammation and injury before the fetal pineal gland matures⁽³¹⁾. Many children and adults with ASD experience sleep issues, such as difficulty falling asleep, staying asleep, or poor sleep quality. These issues include insomnia and parasomnias (unusual behaviors during sleep).

Sleep challenges are common in autism spectrum disorders, affecting up to 80% of individuals, and they can exacerbate behavioral problems, emotional regulation difficulties and daytime functioning. Supplementing with melatonin has been shown to help ASD individuals by reducing sleep onset latency (time to fall asleep), increasing total sleep duration, and improving overall sleep quality.

9. Vitamin D

Vitamin D is increasingly recognized for its potential role in brain health and its possible therapeutic relevance in autism spectrum disorder. Vitamin D acts as a steroid hormone with powerful antioxidant capabilities, helping to reduce oxidative stress. Oxidative stress is common in autism spectrum disorders, and it can lead to neuronal damage if unregulated. It regulates neuronal calcium levels, which is crucial because calcium dysregulation is linked to neuronal excitability and dysfunction, potentially contributing to ASD symptoms. It also affects neurotrophic factors⁽³²⁾, proteins that support neuron growth, synaptic plasticity and overall brain function, playing a role in learning and memory. Vitamin D is crucial for neuronal growth and differentiation, being especially important during critical periods of brain development. Its influence on synaptic plasticity (the ability of synapses to strengthen or weaken over time) underpins learning and adaptation, both of which can be impaired in ASD. In autism spectrum disorders, immune dysregulation and chronic low-level neuroinflammation are common, with vitamin D playing a regulatory role in the immune system⁽³³⁾.

Animal studies suggest that vitamin D deficiency can exacerbate neuroinflammation, while supplementation appears to reduce neuroinflammation and mitigate neurotoxicity, DNA damage, and overall neuronal stress. Studies have consistently found lower vitamin D levels in individuals with ASD. Additionally, animal studies suggest that supplementation may have protective effects on brain health by reducing inflammation, enhancing neuroprotection and supporting neurotransmitter balance.

Clinical trials and observational studies are investigating vitamin D’s role in autism spectrum disorders, with some evidence suggesting that supplementation⁽³⁴⁾ could help with ASD-related symptoms, particularly those linked to mood and behavior. Vitamin D’s regulatory effects on neurotransmitters, immune responses and neuroinflammation highlight its importance for brain health and its potential significance in ASD. The link between low vitamin D levels and ASD symptoms suggests that vitamin D supplementation could offer therapeutic benefits, though more research is needed to fully understand its impact on autism spectrum disorders⁽³⁵⁾.

10. Orexin system

Orexin (or hypocretin) is a neuropeptide that plays a significant role in various brain functions, and recent research is exploring its connections to autism spectrum disorder. Orexin dysfunction appears to be related to various neurological disorders, including addiction, depression, anxiety and schizophrenia⁽³⁶⁾. Orexin, consisting of two neuropeptides (orexin-A and orexin-B), is produced by neurons in the hypothalamus. It acts through two receptors, orexin receptor-1 (OX1R) and orexin receptor-2 (OX2R).

The orexin system influences numerous physiological and psychological processes, including sleep-wake cycles, arousal, appetite, metabolism, cognitive functions and emotional regulation⁽³⁷⁾. Orexin is crucial in maintaining wakefulness and in regulating sleep cycles. Dysregulation of orexin can result in sleep disorders, such as narco­lepsy, and may contribute to the insomnia and fragmen­ted sleep commonly observed in ASD. Individuals with autism spectrum disorders frequently experience sleep disturbances, and a disrupted orexin system could be a contributing factor. This is particularly important, as poor sleep can exacerbate other ASD symptoms, such as social difficulties and behavioral challenges. The orexin system, with its role in sleep, cognition, emotion and metabolism, is an emerging area of study in ASD research. Dysregulation of orexin signaling could contribute to several core symptoms and co-occurring conditions in ASD, such as sleep disorders, attention difficulties and heightened stress. Further research into the orexin system’s role in autism may provide new insights and therapeutic targets for addressing these symptoms, potentially improving the quality of life for individuals with autism spectrum disorders.

Neurobiology of autistic brain

The neurobiology of autism spectrum disorder is complex, encompassing genetic, epigenetic and environmental factors that collectively impact brain development, structure and function. A crucial role is played by the amygdale, prefrontal lobe and nucleus accumbens which is a major component of the limbic system, and the affective loop of the cortico-striato-thalamo-cortical circuit and their associated deficit cognition is reported for impaired social behaviors in ASD individuals⁽³⁸⁾. The primary neurobiological factors and mechanisms implicated in autism spectrum disorders are presented below.

1. Genetic contributions

Gene variants and mutations: ASD has a strong genetic basis, with hundreds of genes identified as being linked to autism risk. Some well-known genes involved include SHANK3, MECP2, SCN2A and CHD8, which play different roles in synaptic function, transcription regulation and brain development.

Genetic syndromes: certain syndromes, such as Fragile X, Rett syndrome and tuberous sclerosis complex, are associated with a high risk of autism spectrum disorders, suggesting that ASD can result from disruptions in specific genetic pathways. Copy Number Variations (CNVs), or large segments of DNA that are duplicated or deleted, are more common in individuals with ASD and can affect multiple genes, contributing to the disorder’s heterogeneity.

2. Brain structure and connectivity

Cortical thickness and surface area: many studies indicate that individuals with ASD may exhibit differences in cortical thickness and surface area, which may relate to atypical patterns of brain development observed during early childhood.

Macrocephaly (enlarged brain volume): some children with ASD show accelerated brain growth early in life, particularly in areas involved in social, emotional and cognitive processing. This can result in a larger overall brain volume in early childhood⁽³⁹⁾.

Atypical connectivity

Hyperconnectivity in local circuits: increased local connectivity, especially in regions related to sensory and perceptual processing, has been observed. This could explain sensory sensitivities commonly seen in ASD.

Hypoconnectivity in long-range circuits: under-connectivity between distant brain regions, such as the frontal and posterior parts of the brain, is also observed and may relate to challenges with integrative functions, like social communication and executive function.

3. Neurotransmitter imbalances

GABA and glutamate: imbalances in GABA (inhibitory) and glutamate (excitatory) signaling are common in ASD. A reduced inhibitory-to-excitatory ratio could lead to hyperexcitability in certain brain regions, contributing to sensory processing differences and repetitive behaviors.

Serotonin: higher levels of serotonin have been observed in the blood of some individuals with ASD. The role of serotonin in social behavior and mood regulation makes is  a significant area of interest, as serotonin signaling may affect social communication difficulties in ASD.

Dopamine: dopaminergic signaling is linked to reward processing and motivation, both of which are often atypical in ASD, potentially impacting social behaviors and routines.

4. Neuroinflammation and immune system dysfunction

Microglial activation: microglia, the brain’s immune cells, are often more active in ASD. This heightened state of activity, called microgliosis, is a sign of neuro­inflammation, and may affect synaptic pruning and brain connectivity.

Cytokine imbalances: cytokines, proteins that regulate inflammation, are often elevated in ASD. This imbalance may disrupt normal neural development and connectivity, particularly during early childhood, which is critical for brain maturation⁽⁴⁰⁾.

Blood-brain barrier (BBB) integrity: some research suggests the BBB may be compromised in ASD, allowing peripheral immune cells to interact with the brain and potentially contribute to neuroinflammation.

5. Synaptic and neuronal plasticity abnormalities

Synapse formation and pruning: ASD is associated with altered synaptic development, with either an excess or deficit in synapse formation and pruning during critical periods of brain development. This imbalance can lead to either hyperconnectivity or hypoconnectivity in key brain regions.

Neurotrophic factors: brain-derived neurotrophic factor (BDNF), which plays a role in synaptic plasticity and neuronal growth, is often elevated in ASD. Changes in neurotrophic factors may contribute to atypical brain development.

6. Endocrine and hormonal influences

Oxytocin and vasopressin: both oxytocin and vasopressin are linked to social bonding and stress regulation. Lower levels or altered receptor sensitivity to these hormones may play a role in the social and communication difficulties seen in ASD.

Steroid hormones: some research suggests that prenatal exposure to high levels of certain sex hormones, like testosterone, may increase the risk of ASD by affecting neural development. This could partially explain the higher prevalence of autism spectrum disorders in males.

7. Other factors

Epigenetic and environmental factors, prenatal and perinatal factors, exposure to toxins and atypical neuronal processing are important aspects discussed extensively, as well as in specialty literature papers⁽⁴¹⁾.

The neurobiology of autism involves a complex interplay between genetics, environmental factors, brain structure, neurotransmitter systems, immune respon­ses, and neural processing pathways. ASD’s heterogeneity means that multiple pathways can lead to similar behavioral and cognitive profiles, resulting in a spectrum of symptoms and abilities. Understanding these underlying mechanisms can pave the way for more personalized and effective interventions.

Conclusions

The neurochemistry and neurobiology of autism underscore the complexity of this disorder, with multiple neurotransmitter systems interacting to influence social behavior, sensory processing and cognitive functions. These findings point to a potential role for targeted therapies that address specific neurochemical imbalances, although autism’s heterogeneity means that treatments will likely need to be tailored to individual neurochemical profiles. The neuroanatomy of the autistic process plays a central role without any doubt.  

 

 

 

 

Autori pentru corespondenţă: Bogdan-Marius Istrate E-mail: istratem.bogdan@yahoo.com

CONFLICT OF INTEREST: none declared.

FINANCIAL SUPPORT: none declared.

This work is permanently accessible online free of charge and published under the CC-BY.