Evidence map›Paper›PMID 38454085›Full record

ArticleMolecular psychiatry2024

Glial-restricted precursors stimulate endogenous cytogenesis and effectively recover emotional deficits in a model of cytogenesis ablation.

Joana Martins-Macedo, Bruna Araújo, Sandra I Anjo, Tiago Silveira-Rosa, Patrícia Patrício, Nuno Dinis Alves, Joana M Silva, Fábio G Teixeira, Bruno Manadas, Ana J Rodrigues and 4 more

Open access · greenAbstract read
In one paragraph

Article in Molecular psychiatry, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.2field-weighted citation impact, top 23% of its field
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

4 citing papers in PubMed, 3 citations in OpenAlex.

  1. Review
  2. Glial Cells in Behavioral and Psychological Symptoms of Alzheimer's Disease.International journal of molecular sciences · 2026
    Review
  3. Review
  4. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

14 authors at 4 institutions in 2 countries.

Joana Martins-MacedoLife and Health Sciences Research Institute (ICVS), School of Medicine, University of Minho, Braga, Portugal.ORCID 0000-0003-0442-927X
Bruna AraújoLife and Health Sciences Research Institute (ICVS), School of Medicine, University of Minho, Braga, Portugal.
Sandra I AnjoCNC-Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal.ORCID 0000-0003-2180-3518
Tiago Silveira-RosaLife and Health Sciences Research Institute (ICVS), School of Medicine, University of Minho, Braga, Portugal.ORCID 0000-0001-6159-1623
Patrícia PatrícioLife and Health Sciences Research Institute (ICVS), School of Medicine, University of Minho, Braga, Portugal.
Nuno Dinis AlvesLife and Health Sciences Research Institute (ICVS), School of Medicine, University of Minho, Braga, Portugal.
Joana M SilvaLife and Health Sciences Research Institute (ICVS), School of Medicine, University of Minho, Braga, Portugal.ORCID 0000-0002-8257-3413
Fábio G TeixeiraCenter for Translational Health and Medical Biotechnology Research (TBIO), School of Health (ESS), Polytechnic of Porto, Porto, Portugal.
Bruno ManadasCNC-Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal.ORCID 0000-0002-2087-4042
Ana J RodriguesLife and Health Sciences Research Institute (ICVS), School of Medicine, University of Minho, Braga, Portugal.ORCID 0000-0003-1968-7968
Angelo C LeporeDepartment of Neuroscience, Vickie and Jack Farber Institute for Neuroscience, Sidney Kimmel Medical College, Thomas Jefferson University, Philadelphia, PA, USA.
António J SalgadoLife and Health Sciences Research Institute (ICVS), School of Medicine, University of Minho, Braga, Portugal.
Eduardo D GomesLife and Health Sciences Research Institute (ICVS), School of Medicine, University of Minho, Braga, Portugal.
Luísa PintoLife and Health Sciences Research Institute (ICVS), School of Medicine, University of Minho, Braga, Portugal. luisapinto@med.uminho.pt.ORCID 0000-0002-7724-0446
University of Minho · PTi3S - Instituto de Investigação e Inovação em Saúde, Universidade do Porto · PTUniversity of Coimbra · PTThomas Jefferson University · US

Funding

Respiratory Motor Neuron Protection Following Cervical Spinal Cord InjuryR01NS079702 · NINDS · THOMAS JEFFERSON UNIVERSITY · PI Angelo C. Lepore · 2013 to 2026
$6.0M
Exploring the EphB2-NMDA receptor interaction in spinal cord injury-induced neuropathic painR01NS110385 · NINDS · THOMAS JEFFERSON UNIVERSITY · PI MANUEL L COVARRUBIAS, Matthew B Dalva · 2018 to 2026
$4.4M
"la Caixa" Foundation (Caixa Foundation) ID 100010434NINDS NIH HHS R01 NS079702NINDS NIH HHS R01 NS110385U.S. Department of Health & Human Services | NIH | National Institute of Neurological Disorders and Stroke (NINDS) R01NS079702, R01NS110385
6 · The paper itself

Abstract

Adult cytogenesis, the continuous generation of newly-born neurons (neurogenesis) and glial cells (gliogenesis) throughout life, is highly impaired in several neuropsychiatric disorders, such as Major Depressive Disorder (MDD), impacting negatively on cognitive and emotional domains. Despite playing a critical role in brain homeostasis, the importance of gliogenesis has been overlooked, both in healthy and diseased states. To examine the role of newly formed glia, we transplanted Glial Restricted Precursors (GRPs) into the adult hippocampal dentate gyrus (DG), or injected their secreted factors (secretome), into a previously validated transgenic GFAP-tk rat line, in which cytogenesis is transiently compromised. We explored the long-term effects of both treatments on physiological and behavioral outcomes. Grafted GRPs reversed anxiety-like deficits and demonstrated an antidepressant-like effect, while the secretome promoted recovery of only anxiety-like behavior. Furthermore, GRPs elicited a recovery of neurogenic and gliogenic levels in the ventral DG, highlighting the unique involvement of these cells in the regulation of brain cytogenesis. Both GRPs and their secretome induced significant alterations in the DG proteome, directly influencing proteins and pathways related to cytogenesis, regulation of neural plasticity and neuronal development. With this work, we demonstrate a valuable and specific contribution of glial progenitors to normalizing gliogenic levels, rescuing neurogenesis and, importantly, promoting recovery of emotional deficits characteristic of disorders such as MDD.

Indexed as

Disease Models, AnimalNeurogenesisNeurogliaNeuronsAnimalsAnxietyCell DifferentiationDentate GyrusEmotionsHippocampusMajor Depressive DisorderMaleNeuronal PlasticityRatsRats, Transgenic

Identifiers

PMID38454085
PMCPMC11632613
OpenAlexW4392562118

What OpenQuestion holds

Textmetadata
LicenceTDM
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.