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Matti Gärtner

7 papers in the library · 52 citations · publishing 2019-2025

Papers

Predicting Antidepressant Effects of Ketamine: the Role of the Pregenual Anterior Cingulate Cortex as a Multimodal Neuroimaging Biomarker

The International Journal of Neuropsychopharmacology August 10, 2022 Anne Weigand, Matti Gärtner, Milan Scheidegger et al. 22 citations

Activity in the pregenual anterior cingulate cortex (pgACC) during emotional stimulation can predict how well a single intravenous infusion of ketamine will relieve depression symptoms in people with major depressive disorder. In 24 patients, pgACC activity was linked to an increase in glutamate in the same brain region 24 hours after the infusion, and this glutamate increase was associated with greater symptom improvement. The findings suggest pgACC activity may serve as a neuroimaging biomarker for early treatment response to ketamine.

Acute effects of ketamine on the pregenual anterior cingulate: linking spontaneous activation, functional connectivity, and glutamate metabolism

European Archives of Psychiatry and Clinical Neuroscience January 12, 2022 Matti Gärtner, Anne Weigand, Milan Scheidegger et al. 13 citations

Ketamine's rapid antidepressant effects involve the glutamatergic system. A multimodal imaging study of 23 healthy volunteers used resting state fMRI and proton magnetic resonance spectroscopy to examine links between metabolic and functional brain changes during intravenous ketamine infusion. The pregenual anterior cingulate cortex (pgACC) was the focus. Functional connectivity changed from the pgACC to the right frontal pole and anterior mid cingulate cortex (aMCC). Absolute glutamate and glutamine concentrations in the pgACC did not differ significantly from baseline. Stronger pgACC activation during ketamine was linked to lower glutamine concentration, and reduced connectivity between pgACC and aMCC was related to increased pgACC activation and reduced glutamine.

Increase in thalamic cerebral blood flow is associated with antidepressant effects of ketamine in major depressive disorder

The World Journal of Biological Psychiatry January 5, 2022 Matti Gärtner, Mischa de Rover, Lena Václavů et al. 11 citations

In patients with Major Depressive Disorder, increased blood flow in the thalamus one day after a single low-dose ketamine infusion is linked to greater improvement in depressive symptoms. Lower thalamus blood flow before treatment predicts both a larger increase in flow after ketamine and stronger symptom reduction. The study used arterial spin labelling, a brain imaging technique that directly measures cerebral blood flow, avoiding the ambiguity of standard BOLD imaging. These findings suggest that measuring regional blood flow could help guide ketamine treatment decisions.

Functional activity and connectivity signatures of ketamine and lamotrigine during negative emotional processing: a double-blind randomized controlled fMRI study.

Translational psychiatry October 14, 2024 Marvin S Meiering, David Weigner, Matti Gärtner et al. 4 citations

In healthy adults, a single dose of ketamine reduced activity in the hippocampus and the default mode network (DMN) and increased connections between frontal and limbic brain regions while participants viewed emotional faces. These effects occurred both during the infusion and 24 hours later. Pretreatment with lamotrigine, which blocks glutamate release, prevented the increase in brain connectivity and the delayed reduction in DMN activity, but did not affect the acute drop in hippocampal and DMN activity. The findings suggest that ketamine's acute changes in brain connectivity and its sustained effects on DMN activity depend on glutamate transmission, whereas its immediate suppression of limbic and DMN activity does not.

Negative emotionality shapes the modulatory effects of ketamine and lamotrigine in subregions of the anterior cingulate cortex.

Translational psychiatry June 18, 2024 Matti Gärtner, Anne Weigand, Marvin Sören Meiering et al. 1 citation

Ketamine reduces spontaneous brain activity in three subregions of the anterior cingulate cortex (ACC) during administration in healthy people. Lamotrigine, which inhibits glutamate release, attenuates this effect only in the ventral ACC subregions, suggesting glutamate involvement there. ACC activity returns to baseline 24 hours later, though group differences persist between the lamotrigine and ketamine groups. Trait negative emotionality is closely linked to activity changes in the subgenual ACC after ketamine. These findings clarify how ketamine affects different ACC subregions and may relate to its antidepressant mechanisms.

Mindfulness-based therapy regulates brain connectivity in major depression

May 29, 2019 Michael Lifshitz, Matthew D. Sacchet, Julia M. Huntenburg et al. 1 citation

Major depressive disorder involves abnormal communication between large-scale brain networks. A randomized, active-controlled trial tested whether mindfulness-based therapy could alter resting-state functional connectivity in clinically depressed patients. A brief, clinically effective mindfulness intervention functionally decoupled top-down control regions from brain areas involved in sensory, affective, and attentional processing. These findings identify specific neural targets of mindfulness training, offering new insight into how this therapeutic approach works.

Functional connectivity alterations of the pregenual anterior cingulate cortex by ketamine and the modulation by lamotrigine.

Journal of psychopharmacology (Oxford, England) June 19, 2025 David Weigner, Marvin Sören Meiering, Anne Weigand et al.

Ketamine infusion significantly increased functional connectivity between the pregenual anterior cingulate cortex and the dorsomedial prefrontal cortex during a working memory task, and between the pregenual anterior cingulate cortex and the left insula during rest. These effects were absent when participants were pretreated with lamotrigine, a glutamate-release inhibitor. The findings suggest that ketamine's beneficial effects on brain communication, observed in psychiatric conditions linked to chronic stress, may depend on glutamate release.