Evidence map›Paper›PMID 39905728›Full record

ArticleMolecular therapy : the journal of the American Society of Gene Therapy2025

FKBP51 inhibition ameliorates neurodegeneration and motor dysfunction in the neuromelanin-SNCA mouse model of Parkinson's disease.

Marta Garcia-Gomara, Naroa Legarra-Marcos, Maria Serena, Elvira Rojas-de-Miguel, Maria Espelosin, Irene Marcilla, Alberto Perez-Mediavilla, Maria Rosario Luquin, Jose Luis Lanciego, Maria Angeles Burrell and 2 more

Abstract read
In one paragraph

Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed.

  1. FKBP51: A new target for Parkinson's disease.Neural regeneration research · 2026
    Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Neuromelanin-induced cellular stress and neurotoxicity in the pathogenesis of Parkinson's disease.Apoptosis : an international journal on programmed cell death · 2025
    Review
  10. Neurobiology of stress · 2025
    Review
  11. 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.

Marta Garcia-GomaraGene Therapy for CNS Disorders Program, Center for Applied Medical Research (CIMA), University of Navarra, Avenida Pio XII 55, Pamplona, 31008 Navarra, Spain; IdiSNA (Navarra Institute for Health Research), Pamplona, 31008 Navarra, Spain; Department of Pathology, Anatomy and Physiology, School of Medicine, University of Navarra, Irunlarrea 1, 31008 Pamplona, Navarra, Spain.
Naroa Legarra-MarcosComputational Biology Program, Center for Applied Medical Research (CIMA), University of Navarra, Avenida Pio XII 55, Pamplona, 31008 Navarra, Spain.
Maria SerenaGene Therapy for CNS Disorders Program, Center for Applied Medical Research (CIMA), University of Navarra, Avenida Pio XII 55, Pamplona, 31008 Navarra, Spain; Department of Pathology, Anatomy and Physiology, School of Medicine, University of Navarra, Irunlarrea 1, 31008 Pamplona, Navarra, Spain.
Elvira Rojas-de-MiguelIdiSNA (Navarra Institute for Health Research), Pamplona, 31008 Navarra, Spain; Department of Pathology, Anatomy and Physiology, School of Medicine, University of Navarra, Irunlarrea 1, 31008 Pamplona, Navarra, Spain.
Maria EspelosinGene Therapy for CNS Disorders Program, Center for Applied Medical Research (CIMA), University of Navarra, Avenida Pio XII 55, Pamplona, 31008 Navarra, Spain; IdiSNA (Navarra Institute for Health Research), Pamplona, 31008 Navarra, Spain.
Irene MarcillaGene Therapy for CNS Disorders Program, Center for Applied Medical Research (CIMA), University of Navarra, Avenida Pio XII 55, Pamplona, 31008 Navarra, Spain; IdiSNA (Navarra Institute for Health Research), Pamplona, 31008 Navarra, Spain.
Alberto Perez-MediavillaGene Therapy for CNS Disorders Program, Center for Applied Medical Research (CIMA), University of Navarra, Avenida Pio XII 55, Pamplona, 31008 Navarra, Spain; IdiSNA (Navarra Institute for Health Research), Pamplona, 31008 Navarra, Spain; Biochemistry and Genetics Department, School of Sciences, University of Navarra, Irunlarrea 1, 31008 Pamplona, Navarra, Spain.
Maria Rosario LuquinIdiSNA (Navarra Institute for Health Research), Pamplona, 31008 Navarra, Spain; Department of Neurology, Clínica Universidad de Navarra, University of Navarra, Avenida Pio XII 36, Pamplona, 31008 Navarra, Spain.
Jose Luis LanciegoGene Therapy for CNS Disorders Program, Center for Applied Medical Research (CIMA), University of Navarra, Avenida Pio XII 55, Pamplona, 31008 Navarra, Spain.
Maria Angeles BurrellIdiSNA (Navarra Institute for Health Research), Pamplona, 31008 Navarra, Spain; Department of Pathology, Anatomy and Physiology, School of Medicine, University of Navarra, Irunlarrea 1, 31008 Pamplona, Navarra, Spain.
Mar Cuadrado-TejedorGene Therapy for CNS Disorders Program, Center for Applied Medical Research (CIMA), University of Navarra, Avenida Pio XII 55, Pamplona, 31008 Navarra, Spain; IdiSNA (Navarra Institute for Health Research), Pamplona, 31008 Navarra, Spain; Department of Pathology, Anatomy and Physiology, School of Medicine, University of Navarra, Irunlarrea 1, 31008 Pamplona, Navarra, Spain. Electronic address: mcuadrado@unav.es.
Ana Garcia-OstaGene Therapy for CNS Disorders Program, Center for Applied Medical Research (CIMA), University of Navarra, Avenida Pio XII 55, Pamplona, 31008 Navarra, Spain; IdiSNA (Navarra Institute for Health Research), Pamplona, 31008 Navarra, Spain. Electronic address: agosta@unav.es.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Parkinson's disease (PD) is characterized by the loss of neuromelanin (NM)-containing dopaminergic (DA) neurons in the substantia nigra (SN) pars compacta (SNpc) and the buildup of α-synuclein (α-syn) inclusions, called Lewy bodies. To investigate the roles of NM and α-syn in DA neuron degeneration, we modeled PD by inducing NM accumulation in a humanized α-syn mouse model (Snca

Indexed as

alpha-SynucleinMelaninsParkinson DiseaseTacrolimus Binding ProteinsAnimalsDisease Models, AnimalDopaminergic NeuronsHumansMiceMice, TransgenicMicrogliaSubstantia NigraTacrolimus Binding Protein 5alpha-SynucleinMelaninsneuromelaninTacrolimus Binding Protein 5Tacrolimus Binding ProteinsagingFKBP5neuroinflammationneuromelaninneuroprotectionPAC-Tg-SNCAWTParkinson's diseaseSAFit2Snca-synuclein

Identifiers

PMID39905728
PMCPMC11897814

What Socratic holds

Textmetadata
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.