Evidence map›Paper›PMID 41673401›Full record

ArticleNPJ Parkinson's disease2026

Introducing PIGMO, a novel PIGmented MOuse model of Parkinson's disease.

Julia Chocarro, Sergio Marana, Maria Espelosin, Alberto J Rico, Goiaz Ariznabarreta, Elena Lorenzo-Ramos, Mario M Ilarduya, Ruben Hernandez-Alcoceba, Miquel Chillón, Miquel Vila and 5 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in NPJ Parkinson's disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

15 authors.

Julia Chocarro *CNS Gene Therapy Program, Center for Applied Medical Research (Cima), University of Navarra, Pamplona, Spain.
Sergio Marana *CNS Gene Therapy Program, Center for Applied Medical Research (Cima), University of Navarra, Pamplona, Spain.
Maria EspelosinCNS Gene Therapy Program, Center for Applied Medical Research (Cima), University of Navarra, Pamplona, Spain.
Alberto J RicoCNS Gene Therapy Program, Center for Applied Medical Research (Cima), University of Navarra, Pamplona, Spain.
Goiaz AriznabarretaCNS Gene Therapy Program, Center for Applied Medical Research (Cima), University of Navarra, Pamplona, Spain.
Elena Lorenzo-RamosCNS Gene Therapy Program, Center for Applied Medical Research (Cima), University of Navarra, Pamplona, Spain.
Mario M IlarduyaCNS Gene Therapy Program, Center for Applied Medical Research (Cima), University of Navarra, Pamplona, Spain.
Ruben Hernandez-AlcocebaCNS Gene Therapy Program, Center for Applied Medical Research (Cima), University of Navarra, Pamplona, Spain.
Miquel ChillónInstitut des Neurociences, Department of Biochemistry and Molecular Biology, University Autónoma de Barcelona, Barcelona, Spain.
Miquel VilaCentro de Investigación Biomédica en Red de Enfermedades Neurodegenerativas (Ciberned-ISCIII), Madrid, Spain.
Jeffrey H KordowerAligning Science Across Parkinson's (ASAP) Collaborative Research Network, Chevy Chase, MD, USA.
Anthony H V SchapiraAligning Science Across Parkinson's (ASAP) Collaborative Research Network, Chevy Chase, MD, USA.
Ana Garcia-OstaCNS Gene Therapy Program, Center for Applied Medical Research (Cima), University of Navarra, Pamplona, Spain.
Maria Del Mar Cuadrado-TejedorCNS Gene Therapy Program, Center for Applied Medical Research (Cima), University of Navarra, Pamplona, Spain.
Jose L LanciegoCNS Gene Therapy Program, Center for Applied Medical Research (Cima), University of Navarra, Pamplona, Spain. jlanciego@unav.es.

Funding

Aligning Science Across Parkinson's ASAP-020505Ministerio de Ciencia e Innovación PID2023-127802OB-I00
6 · The paper itself

Abstract

There is a pressing need for the development, characterization, and standardization of animal models of Parkinson's disease (PD) that properly mimic the cardinal features of this disorder, comprising both the motor phenotype and neuropathological signatures. In the past few years, animal modeling has moved from neurotoxin-based approaches toward viral vectors carrying a given genetic payload of interest. Here, to induce pigmentation of the mouse brain upon systemic delivery, we took advantage of a modified adeno-associated viral vector capsid engineered to bypass the blood-brain barrier and coding for the human tyrosinase gene (AAV9-P31-hTyr). Obtained results revealed an ongoing pigmentation of catecholaminergic centers related to the pathophysiology of PD, such as the substantia nigra pars compacta, ventral tegmental area, and locus coeruleus. Moreover, pigmented dopaminergic neurons exhibited Lewy body-like intracytoplasmic inclusions, a progressive nigrostriatal degeneration, and a time-dependent PD motor phenotype. The bilateral pigmented model of PD generated in this way does not require stereotactic surgery for viral vector delivery, opening up unprecedented possibilities for preclinical testing of therapeutic candidates designed to reduce disease progression rates.

Identifiers

PMID41673401
PMCPMC13005038

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Registered trials

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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.