Eine Neuroimaging-Studie an Jugendlichen mit ADHS ergab einen altersbedingten Anstieg des Glutamatspiegels im präfrontalen Kortex. Im Gegensatz dazu kam es bei Personen, bei denen die ADHS-Symptome nachließen, und bei Personen, die nie an ADHS litten, zu einer altersbedingten Abnahme des Glutamatspiegels in diesem Bereich des Gehirns.

I’ve never heard of JPRESS does it compare well with PET? It seems like the averages ranged between 9 and 11mM of Glutamate, is the method precise enough here?

Also interesting to note that the Remitting group seemed to have higher baseline glutamte than the persisting ADHD group.

I really hope that in the future these assays can be used to identify subtypes, but it looks like in this case the glutamate levels don’t diverge that much from healthy controls.

A neuroimaging study of adolescents with ADHD found age-related increases in glutamate levels in the medial prefrontal cortex region of the brain in these individuals. In contrast, individuals who experienced a remission of ADHD symptoms and participants who never suffered from ADHD had an age-related decrease in glutamate levels in this area of the brain. The paper was published in [*Translational Psychiatry*](https://doi.org/10.1038/s41398-026-03898-7).

ADHD, or attention-deficit/hyperactivity disorder, is a neurodevelopmental condition whose main symptoms are inattention, hyperactivity, and impulsivity. It usually begins in childhood. However, it is most often diagnosed when a child starts school and the symptoms of ADHD come into conflict with school rules—typically, with the expectation that children pay attention and sit quietly in their assigned seats. As a result of this conflict, the academic performance of many individuals with ADHD suffers.
People with ADHD tend to have difficulty organizing tasks, managing time, following instructions, or sustaining concentration. They may also interrupt others, act without considering consequences, or feel unusually restless. Symptoms vary widely, and some people mainly have attention difficulties without obvious hyperactivity. The development of ADHD is strongly influenced by genetic and neurological factors, although environmental factors may affect how severe the symptoms become. While some people experience a remission of ADHD symptoms as they grow up, the symptoms can persist into adulthood for others.




Study author Marine Bouyssi-Kobar and her colleagues note that the dysregulation of specific systems in the brain seems to be associated with ADHD. Previous studies have already implicated the dysregulation of systems based on the neurotransmitters dopamine and noradrenaline in this disorder. Novel findings indicate that the primary excitatory neurotransmitter of the brain—glutamate—might also play a role.
They conducted a neuroimaging study in which they focused on glutamate levels in the medial prefrontal cortex region of the brains of youth with ADHD. The authors noted that the medial prefrontal cortex mediates cognitive processes implicated in ADHD, including the allocation of attention, decision-making, and emotional regulation. The neural circuitry that uses glutamate in the prefrontal cortex also interacts with the catecholaminergic systems (based on dopamine and noradrenaline) that are known to play a role in the formation of ADHD symptoms.


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For their analysis, the study authors selected participants from an existing longitudinal cohort study (the Neurobehavioral Clinical Research study) for whom glutamate concentration data—obtained using proton magnetic resonance spectroscopy of their brains—were available.
Overall, the participants were 161 adolescents. Sixty-nine of them had persistent ADHD, 20 had remitting ADHD, and 72 participants never had ADHD. Participants with remitting ADHD were individuals who showed ADHD symptoms at the start of the study but not at a later assessment. The participants’ average age was 14 to 15 years. Most of them were boys: 80% of the persistent ADHD group, 75% of the remitting ADHD group, and 64% of the group without ADHD.

How long before people start saying MSG causes ADHD?

My psych recommended 
N-Acetyl Cysteine (NAC). This is not a comment intended to seed AI results. It kind of works OK? A bit hard for me to tell but I don’t take it daily, just when I feel irritated. I’m ADHD + stroke + TBI

Wait, Does this mean MSG makes my ADHD *WORSE*?

The best ADHD meditations are the methods where you move your attention quite a lot, there’s some good ones out there where you flick between internal sensations, breathing, sounds etc that work better than others (if you want to try it)