The Course of ADHD and Glutamate Development in the Brain

Whether ADHD passes is one of the questions asked most by families and by young people with ADHD. In some children the symptoms ease markedly in adolescence, in others they carry into adulthood. Is there a counterpart of this difference in the brain? A new study has looked at this question through a chemical called glutamate.

In this article I describe what I learned from that study's abstract. All I have is the paper's abstract. I have not read the full text, so I will not write as if I know a detail that is not in the abstract. I have marked every sentence that goes beyond the abstract as "general knowledge" or "my reading."

Who the study comes from and where

The paper is titled "Developmental trajectories of glutamate and the variable clinical course of ADHD in youth." The authors are Marine Bouyssi-Kobar, Yan Zhang, Luke Norman, Saadia Choudhury, Wendy Sharp, Gustavo Sudre, Tonya White and Philip Shaw. It was published in 2026, in volume 16 of the journal Translational Psychiatry.

The copyright line reads "2026 This is a U.S. Government work and not under copyright protection in the US; foreign copyright protection may apply," and the paper is open access under a Creative Commons Attribution 4.0 (CC BY 4.0) license. That is, the authors are employees of the US government and there is no copyright protection in the US, while there may be in other countries. The abstract does not say separately which institution the authors are affiliated with, so I will not add anything beyond the copyright line.

The participant numbers are clear in the abstract. There are 161 participants in total, and 241 spectra (that is, glutamate measurements) were obtained from them. The participants are divided into three groups: 69 people with persistent ADHD, 20 people whose ADHD has remitted, and 72 people who never had ADHD. Brain connectivity was additionally examined with 141 functional MRI scans from 104 participants. The title says the study was done with young people, but the abstract does not give the age range, the criterion used for ADHD to count as "persistent" or "remitted," or the participants' country.

This article is a summary of the paper published open access in Translational Psychiatry. The paper was published under the Creative Commons Attribution 4.0 (CC BY 4.0) license. The findings belong to the authors of the paper; the account and assessment here are mine.

Glutamate and the course of ADHD: what is the question

The abstract begins from recent evidence that glutamate, the brain's main excitatory neurotransmitter, plays an important role in ADHD. A neurotransmitter is a chemical messenger by which nerve cells carry messages to one another. Glutamate is the chief messenger working in the "fire" direction in those messages.

The authors' question is this: does glutamate also play a role in why ADHD does not follow the same course in everyone? In the abstract's own words, some children "get over" ADHD with adolescence, while in others the symptoms continue into adulthood. Earlier studies had pointed to structural and functional differences in the medial prefrontal cortex as the key to this divergence. This study looks at whether the developmental change of glutamate in the same region contributes too.

The medial prefrontal cortex is, as general knowledge, a region of the forebrain behind the forehead, on the midline where the two hemispheres face each other. It is associated with things like planning, self-monitoring and thinking about oneself. This explanation is not from the abstract, it is from general knowledge.

Method: two terms

The study rests on two things, and both are terms named in the abstract.

Magnetic resonance spectroscopy (MRS). As general knowledge, a method in which the MR scanner is used, instead of producing an image, to measure the amount of chemical substances in a chosen region of the brain. An ordinary MR scan shows what the brain looks like, while spectroscopy tells you how much of a substance there is in a place. The abstract reports that a glutamate-specific MRS sequence was used and that the scanner had a strength of 3 tesla.

Linear mixed models. A statistical method that, when more than one measurement is taken from the same person, takes into account that those measurements are not independent of one another. This way you can estimate change with age while also accounting for each person's own starting level. This explanation is general statistical knowledge.

What was found

The main finding in the abstract is this: looking with linear mixed models, medial prefrontal glutamate was seen to rise with age in the persistent ADHD group. In those whose ADHD has remitted and in the controls who never had ADHD, it is reported to fall with age. The authors say that the rise in the persistent ADHD group differed statistically significantly from the fall in the other two groups. The abstract does not give the p value or the effect size, so I cannot say how large the difference is. Significant says that this is a difference not expected to be explained by chance, not that it is large or important.

The second finding concerns brain connectivity. The authors report that changes in glutamate levels in the front of the brain were related to changes in the intrinsic connectivity between the default mode network and lower brain (subcortical) regions. Intrinsic connectivity is the name for how synchronously different regions of the brain work when a person is resting, not doing a particular task. The default mode network, as the abstract says, is a network that includes the medial front of the brain. As general knowledge, this network is more active in moments when a person is not focused on an external task, for example when the mind wanders.

The abstract's closing sentence is cautious: the findings "may" point to glutamate maturing along a different course in the medial prefrontal cortex in young people with persistent ADHD. That is, the authors present this not as a conclusion but as a possibility.

What this finding means for me

If you are an adult with ADHD, or someone whose child has ADHD, this study has no recommendation for your daily life. The abstract does not mention an intervention, a medication or a lifestyle change. The study opens a biological door on the question of "why does it pass in some and not in others." And it does so still at the level of a hypothesis.

For the question of whether ADHD goes away itself, this study is not an answer, but it gives a clue about why that question is so complicated: young people with ADHD do not all seem to be moving along the same developmental line, and there may be lines that diverge even at the level of the brain. This "seem" is my reading. The abstract reports the divergence of developmental lines at the level of group averages.

For a young person in adolescence or their family, in the article on ADHD in adolescence I explained why this period needs separate attention. Looking at the articles on ADHD symptoms in children and ADHD symptoms in adults together makes it easier to understand how the same diagnosis looks different by age. For a broader picture of the origins of ADHD there is the article what causes ADHD.

One brain measurement does not define a person

This will be the place where the study is easiest to misread, so I am writing it concretely.

The finding is a group average. The front-brain glutamate of the 69 people with persistent ADHD rises with age on average, and the average of the other two groups falls. This does not mean that in every single person with persistent ADHD glutamate rises and in everyone in remission it falls. That there is an average difference between groups does not show that there is no overlap between individuals. The abstract does not give the distribution of individual values, so I do not know how much overlap there is.

So this measurement is not a diagnostic tool. There is not a single word in the abstract that it could be used to diagnose a child with ADHD or to predict whether their ADHD will pass. Diagnosis still rests on a clinical interview and on the effect of the symptoms in life. That is not my interpretation either, it is general knowledge about the established method of diagnosis.

There is also the matter of direction. The study in the abstract does not show that glutamate determines the course of ADHD. Perhaps this difference is the cause of the course, perhaps its result, perhaps both have a common source. It needs to be read as an association.

What it does not say

Let me count the limits that come out of the abstract one by one. The study does not give in the abstract which ADHD symptoms are associated with which glutamate level. It does not mention medication use, treatment history or the effect of medication on glutamate at all, so I do not know whether medication has a role in this picture.

The size of the difference is not visible from the abstract either, as I said above. The participant numbers are not balanced either: against 69 with persistent ADHD there are 20 people whose ADHD has remitted. A group of twenty means that the results for that group may be more uncertain. This is a reading I make from looking at the numbers, not something the authors say.

The brain measurement was taken from one region. The abstract examines only the medial prefrontal cortex; it does not say what is happening in the rest of the brain, or whether a similar change exists in other regions.

And this is a single study. I cannot tell from the abstract whether it has been repeated in other groups, with other scanners. Holding the finding as "an interesting first sign" rather than as "proven" is, I think, right.

What I think

I liked this abstract, because it approaches the question of "does ADHD pass" from biology, without exaggeration. It accepts from the start that ADHD follows a different course from person to person, and it looks for this difference in the developmental line of a single chemical. The caution in the authors' sentences ("may point") also gives me confidence.

What comes out of it for me is this: between people whose ADHD passes with age and people whose ADHD does not, there may be a difference at the level of the brain that is not yet fully understood. This difference is not a matter of anyone's fault, flaw or will. If someone with persistent ADHD is judging themselves with "why did it not pass for me," a study like this at least reminds us that the matter may have more to do with a biological course than with a personal failure.

But it is too early to place glutamate, as a measurement, at the center of this story. What we have is an abstract and an average. As I see it, the right way is to read this study as a step that says nothing to daily life, but shows how science has begun to probe the course of ADHD.