Evidence map›Paper›PMID 39363047›Full record

ArticleMolecular psychiatry2025

Blood biomarkers of neuronal injury and astrocytic reactivity in electroconvulsive therapy.

Robert Sigström, Andreas Göteson, Erik Joas, Erik Pålsson, Benny Liberg, Axel Nordenskjöld, Kaj Blennow, Henrik Zetterberg, Mikael Landén

Abstract read
In one paragraph

Article in Molecular psychiatry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

5 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Robert SigströmDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden. robert.sigstrom@gu.se.ORCID 0000-0003-1505-1532
Andreas GötesonDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden.ORCID 0000-0001-6118-6054
Erik JoasDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden.
Erik PålssonDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden.
Benny LibergDepartment of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
Axel NordenskjöldUniversity Health Care Research Centre, Faculty of Medicine and Health, Örebro University, Örebro, Sweden.ORCID 0000-0001-7454-3065
Kaj BlennowDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden.ORCID 0000-0002-1890-4193
Henrik ZetterbergDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden.ORCID 0000-0003-3930-4354
Mikael LandénDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden.ORCID 0000-0002-4496-6451

Funding

Alzheimerfonden AF-930351, AF-939721, AF-968270Alzheimer's Association ADSF-21-831376-CAlzheimer's Association ADSF-21-831377-CAlzheimer's Association ADSF-21-831381-CAlzheimer's Association SG-23-1038904 QCAlzheimer's Association ZEN-21-848495Alzheimer's Drug Discovery Foundation (ADDF) 201809-2016862EC | Horizon 2020 Framework Programme (EU Framework Programme for Research and Innovation H2020) 101053962EC | Horizon 2020 Framework Programme (EU Framework Programme for Research and Innovation H2020) 860197EU Joint Programme - Neurodegenerative Disease Research (Programi i Përbashkët i BE-së për Kërkimet mbi Sëmundjet Neuro-degjeneruese) JPND2019-466-236EU Joint Programme - Neurodegenerative Disease Research (Programi i Përbashkët i BE-së për Kërkimet mbi Sëmundjet Neuro-degjeneruese) JPND2021-00694Fredrik och Ingrid Thurings Stiftelse (Fredrik and Ingrid Thurings Foundation) 2019-00478Hjärnfonden (Swedish Brain Foundation) FO2022-0270Sahlgrenska Universitetssjukhuset (Sahlgrenska University Hospital) ALFGBG-71320Sahlgrenska Universitetssjukhuset (Sahlgrenska University Hospital) ALFGBG-715986, ALFGBG-965240Sahlgrenska Universitetssjukhuset (Sahlgrenska University Hospital) ALFGBG-942684Sahlgrenska Universitetssjukhuset (Sahlgrenska University Hospital) ALFGBG-965444Stiftelsen för Strategisk Forskning (Swedish Foundation for Strategic Research) KF10-0039Vetenskapsrådet (Swedish Research Council) 2017-00915Vetenskapsrådet (Swedish Research Council) 2019-02397Vetenskapsrådet (Swedish Research Council) 2022-00732Vetenskapsrådet (Swedish Research Council) 2022-01643Wenner-Gren Foundation (Wenner-Gren Foundation for Anthropological Research, Inc.) SSv2019-0008
6 · The paper itself

Abstract

Despite electroconvulsive therapy (ECT) being recognized as an effective treatment for major depressive episodes (MDE), its application is subject to controversy due to concerns over cognitive side effects. The pathophysiology of these side effects is not well understood. Here, we examined the effects of ECT on blood-based biomarkers of neuronal injury and astrocytic reactivity. Participants with a major depressive episode (N = 99) underwent acute ECT. Blood was sampled just before (T0) and 30 min after (T1) the first ECT session, as well as just before the sixth session (T2; 48-72 h after the fifth session). Age- and sex-matched controls (N = 99) were recruited from the general population. Serum concentrations of neurofilament light chain (NfL), total tau protein, and glial fibrillary acidic protein (GFAP) were measured with ultrasensitive single-molecule array assays. Utilizing generalized least squares regression, we compared baseline (T0) biomarker concentrations against those of our control group, and calculated the shifts in serum biomarker concentrations from baseline to immediately post-first ECT session (T1), and prior to the sixth session (T2). Baseline analysis revealed that serum levels of NfL (p < 0.001) and tau (p = 0.036) were significantly elevated in ECT recipients compared with controls, whereas GFAP levels showed no significant difference. Relative to T0, serum NfL concentration neither changed at T1 (mean change 3.1%, 95%CI -0.5% to 6.7%, p = 0.088) nor at T2 (mean change -3.2%, 95%CI -7.6% to 1.5%, p = 0.18). Similarly, no change in total tau was observed (mean change 3.7%, 95%CI -11.6% to 21.7%, p = 0.65). GFAP increased from T0 to T1 (mean change 20.3%, 95%CI 14.6 to 26.3%, p < 0.001), but not from T0 to T2 (mean change -0.7%, 95%CI -5.8% to 4.8%, p = 0.82). In conclusion, our findings suggest that ECT induces a temporary increase in serum GFAP, possibly reflecting transient astrocytic activation. Importantly, we observed no indicators of neuronal damage or long-term elevation in any assessed biomarker.

Indexed as

AstrocytesElectroconvulsive TherapyAdultAgedBiomarkersFemaleGlial Fibrillary Acidic ProteinHumansMajor Depressive DisorderMaleMiddle AgedNeurofilament ProteinsNeuronstau ProteinsBiomarkersGFAP protein, humanGlial Fibrillary Acidic Proteinneurofilament protein LNeurofilament Proteinstau Proteins

Identifiers

PMID39363047
PMCPMC11919754

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.