Evidence map›Paper›PMID 34165772›Full record

ArticleNeuroscience bulletin2021

Co-editing PINK1 and DJ-1 Genes Via Adeno-Associated Virus-Delivered CRISPR/Cas9 System in Adult Monkey Brain Elicits Classical Parkinsonian Phenotype.

Hao Li, Shihao Wu, Xia Ma, Xiao Li, Tianlin Cheng, Zhifang Chen, Jing Wu, Longbao Lv, Ling Li, Liqi Xu and 6 more

Open access · hybridAbstract read
In one paragraph

Article in Neuroscience bulletin, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

33 citing papers in PubMed, 44 citations in OpenAlex.

  1. Species-dependent activities of the PINK1-parkin axis.Translational neurodegeneration · 2026
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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

16 authors at 8 institutions in 1 country.

Hao Li *Key Laboratory of Animal Models and Human Disease Mechanisms of the Chinese Academy of Sciences and Yunnan Province, Kunming Institute of Zoology, Chinese Academy of Sciences, 650223, Kunming, China.
Shihao Wu *Key Laboratory of Animal Models and Human Disease Mechanisms of the Chinese Academy of Sciences and Yunnan Province, Kunming Institute of Zoology, Chinese Academy of Sciences, 650223, Kunming, China.
Xia Ma *Key Laboratory of Animal Models and Human Disease Mechanisms of the Chinese Academy of Sciences and Yunnan Province, Kunming Institute of Zoology, Chinese Academy of Sciences, 650223, Kunming, China.
Xiao Li *Institute of Neuroscience, CAS Key Laboratory of Primate Neurobiology, State Key Laboratory of Neuroscience, Chinese Academy of Sciences, Shanghai, 200031, China.
Tianlin ChengInstitute of Neuroscience, CAS Key Laboratory of Primate Neurobiology, State Key Laboratory of Neuroscience, Chinese Academy of Sciences, Shanghai, 200031, China.
Zhifang ChenInstitute of Neuroscience, CAS Key Laboratory of Primate Neurobiology, State Key Laboratory of Neuroscience, Chinese Academy of Sciences, Shanghai, 200031, China.
Jing WuKey Laboratory of Animal Models and Human Disease Mechanisms of the Chinese Academy of Sciences and Yunnan Province, Kunming Institute of Zoology, Chinese Academy of Sciences, 650223, Kunming, China.
Longbao LvNational Resource Center for Non-human Primates, Kunming Primate Research Center, and National Research Facility for Phenotypic and Genetic Analysis of Model Animals (Primate Facility), Kunming Institute of Zoology, Chinese Academy of Sciences, 650107, Kunming, China.
Ling LiDiagnostic Radiology Department, 920 Hospital of the Joint Logistics Support Force of the PLA, Kunming, 650032, China.
Liqi XuUltrasound diagnosis Department, 920 Hospital of the Joint Logistics Support Force of the PLA, Kunming, 650032, China.
Wenchao WangKey Laboratory of Animal Models and Human Disease Mechanisms of the Chinese Academy of Sciences and Yunnan Province, Kunming Institute of Zoology, Chinese Academy of Sciences, 650223, Kunming, China.
Yingzhou HuKey Laboratory of Animal Models and Human Disease Mechanisms of the Chinese Academy of Sciences and Yunnan Province, Kunming Institute of Zoology, Chinese Academy of Sciences, 650223, Kunming, China.
Haisong JiangSichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, 610072, China.
Yong YinDepartment of Rehabilitation Medicine, The Second People's Hospital of Yunnan Province, Kunming, 650021, China. yinyong@ynshhyy.com.
Zilong QiuInstitute of Neuroscience, CAS Key Laboratory of Primate Neurobiology, State Key Laboratory of Neuroscience, Chinese Academy of Sciences, Shanghai, 200031, China. zqiu@ion.ac.cn.
Xintian HuKey Laboratory of Animal Models and Human Disease Mechanisms of the Chinese Academy of Sciences and Yunnan Province, Kunming Institute of Zoology, Chinese Academy of Sciences, 650223, Kunming, China. xthu@mail.kiz.ac.cn.
Chinese Academy of Sciences · CNKunming Institute of Zoology · CN81th Hospital of PLA · CNCenter for Excellence in Brain Science and Intelligence Technology · CNPeople's Liberation Army 401 Hospital · CNSecond People's Hospital of Yunnan Province · CNState Key Laboratory of NeuroscienceUniversity of Electronic Science and Technology of China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Whether direct manipulation of Parkinson's disease (PD) risk genes in the adult monkey brain can elicit a Parkinsonian phenotype remains an unsolved issue. Here, we used an adeno-associated virus serotype 9 (AAV9)-delivered CRISPR/Cas9 system to directly co-edit PINK1 and DJ-1 genes in the substantia nigras (SNs) of two monkey groups: an old group and a middle-aged group. After the operation, the old group exhibited all the classic PD symptoms, including bradykinesia, tremor, and postural instability, accompanied by key pathological hallmarks of PD, such as severe nigral dopaminergic neuron loss (>64%) and evident α-synuclein pathology in the gene-edited SN. In contrast, the phenotype of their middle-aged counterparts, which also showed clear PD symptoms and pathological hallmarks, were less severe. In addition to the higher final total PD scores and more severe pathological changes, the old group were also more susceptible to gene editing by showing a faster process of PD progression. These results suggested that both genetic and aging factors played important roles in the development of PD in the monkeys. Taken together, this system can effectively develop a large number of genetically-edited PD monkeys in a short time (6-10 months), and thus provides a practical transgenic monkey model for future PD studies.

Indexed as

CRISPR-Cas SystemsDependovirusAnimalsBrainHaplorhiniPhenotypeProtein KinasesProtein KinasesAdeno-associated virus-delivered CRISPR/Cas9DJ-1MonkeyParkinsonian phenotypeParkinson’s diseasePINK1

Identifiers

PMID34165772
PMCPMC8423927
OpenAlexW3174830099

What Socratic 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 Socratic graph.