Evidence map›Paper›PMID 39587294›Full record

ArticleMolecular psychiatry2025

Multimodal beneficial effects of BNN27, a nerve growth factor synthetic mimetic, in the 5xFAD mouse model of Alzheimer's disease.

Maria Kokkali, Kanelina Karali, Evangelia Thanou, Maria Anna Papadopoulou, Ioanna Zota, Alexandros Tsimpolis, Paschalis Efstathopoulos, Theodora Calogeropoulou, Ka Wan Li, Kyriaki Sidiropoulou and 2 more

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 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Boosting Neurogenesis as a Strategy in Treating Alzheimer's Disease.International journal of molecular sciences · 2025
    Review
  9. Article
  10. Vertebrate and Invertebrate Animal Models for the Study of Down Syndrome.International journal of molecular sciences · 2025
    Review
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

12 authors.

Maria Kokkali *Department of Pharmacology, School of Medicine, University of Crete, Heraklion, 71003, Greece.
Kanelina Karali *Department of Pharmacology, School of Medicine, University of Crete, Heraklion, 71003, Greece.
Evangelia ThanouDepartment of Molecular and Cellular Neurobiology, Center for Neurogenomics & Cognitive Research, Neuroscience Campus Amsterdam, VU University, Amsterdam, The Netherlands.ORCID 0000-0001-6843-4591
Maria Anna PapadopoulouDepartment of Pharmacology, School of Medicine, University of Crete, Heraklion, 71003, Greece.
Ioanna ZotaDepartment of Pharmacology, School of Medicine, University of Crete, Heraklion, 71003, Greece.
Alexandros TsimpolisDepartment of Pharmacology, School of Medicine, University of Crete, Heraklion, 71003, Greece.ORCID 0000-0001-6346-7714
Paschalis EfstathopoulosDepartment of Pharmacology, School of Medicine, University of Crete, Heraklion, 71003, Greece.
Theodora CalogeropoulouInstitute of Chemical Biology, National Hellenic Research Foundation, 11635, Athens, Greece.
Ka Wan LiDepartment of Molecular and Cellular Neurobiology, Center for Neurogenomics & Cognitive Research, Neuroscience Campus Amsterdam, VU University, Amsterdam, The Netherlands.
Kyriaki SidiropoulouInstitute of Molecular Biology and Biotechnology, Foundation for Research and Technology-Hellas, Heraklion, 71003, Greece.
Achille GravanisDepartment of Pharmacology, School of Medicine, University of Crete, Heraklion, 71003, Greece.
Ioannis CharalampopoulosDepartment of Pharmacology, School of Medicine, University of Crete, Heraklion, 71003, Greece. charalampn@uoc.gr.ORCID 0000-0003-3415-7332

Funding

EC | EU Framework Programme for Research and Innovation H2020 | H2020 Priority Excellent Science | H2020 Marie Skłodowska-Curie Actions (H2020 Excellent Science - Marie Skłodowska-Curie Actions) 765704EC | Horizon 2020 Framework Programme (EU Framework Programme for Research and Innovation H2020) 101099145
6 · The paper itself

Abstract

Alzheimer's Disease (AD) is an incurable and debilitating progressive, neurodegenerative disorder which is the leading cause of dementia worldwide. Neuropathologically, AD is characterized by the accumulation of Aβ amyloid plaques in the microenvironment of brain cells and neurovascular walls, chronic neuroinflammation, resulting in neuronal and synaptic loss, myelin and axonal failure, as well as significant reduction in adult hippocampal neurogenesis. The hippocampal formation is particularly vulnerable to this degenerative process, due to early dysfunction of the cholinergic circuit. Neurotrophic factors consist major regulatory molecules and their decline in AD is considered as an important cause of disease onset and progression. Novel pharmacological approaches are targeting the downstream pathways controlled by neurotrophins, such as nerve growth factor (NGF) receptors, TrkA and p75

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsBlood-Brain BarrierBrainDisease Models, AnimalHippocampusHumansMaleMiceMice, TransgenicNerve Growth FactorNerve Growth FactorsNeurogenesisNeuronsNeuroprotective AgentsAmyloid beta-PeptidesNerve Growth FactorNerve Growth FactorsNeuroprotective AgentsReceptors, Nerve Growth FactorReceptor, trkA

Identifiers

PMID39587294
PMCPMC12092300

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.