Attention-deficit/hyperactivity disorder is linked to resting-state abnormalities, poor brain activity in specific neural networks, and issues with motivation and cognition.
In more recent theoretical frameworks, clinical symptoms and neuropsychological issues are combined. It is hypothesized that cognitive deficits may result from dysfunctions, particularly in frontostriatal or meso-cortical brain networks, while issues with reward processing may be related to dysfunctions in the mesolimbic dopaminergic system.
A more fundamental neuronal network approach suggests that in ADHD, in particular, Default-Mode-Network (DMN) activity, typically more pronounced during rest, may interfere with activity in neuronal networks involved in task processing, resulting in difficulties with state regulation and sporadic attentional lapses.
There is evidence that the neurotransmitters dopamine (DA) and norepinephrine (NE) play a role in the pathophysiology of ADHD. Mood, risk-taking, impulsivity, and reward are all influenced by the neurotransmitter dopamine. Attention, arousal, and mood are all modulated by norepinephrine. The dopamine receptor D4 (DRD4) receptor gene and dopamine transporter-1 overexpression may be defective, according to studies on people with ADHD (DAT1). To alter attention to and responses to one’s environment, the DRD4 receptor employs DA and NE.
There may not be enough contact between the postsynaptic receptor and the dopamine transporter protein, DAT1, which transports DA/NE into the presynaptic nerve terminal.
Neurotransmitters are involved, even though further research is needed to understand these consequences fully.