Evidence map›Paper›PMID 39225429›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2024

Nanotherapeutic Approaches of Interleukin-3 to Clear the α-Synuclein Pathology in Mouse Models of Parkinson's Disease.

Wenlong Zhang, Jian Ren, Liuyan Ding, Shaohui Zheng, Runfang Ma, Mengran Zhang, Yan Liu, Ruijing Liang, Yunlong Zhang

Abstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed.

  1. Article
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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

9 authors.

Wenlong ZhangDepartment of Neurology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, 510120, China.
Jian RenGuangdong Key Laboratory of Nanomedicine, CAS-HK Joint Lab for Biomaterials, Institute of Biomedicine and Biotechnology, Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences, Shenzhen, 518055, China.
Liuyan DingDepartment of Neurology, The First Affiliated Hospital of Guangzhou Medical University, Guangzhou, 510120, China.
Shaohui ZhengWestlake Laboratory of Life Sciences and Biomedicine, Hangzhou, 310024, China.
Runfang MaWestlake Laboratory of Life Sciences and Biomedicine, Hangzhou, 310024, China.
Mengran ZhangWestlake Laboratory of Life Sciences and Biomedicine, Hangzhou, 310024, China.
Yan LiuWestlake Laboratory of Life Sciences and Biomedicine, Hangzhou, 310024, China.
Ruijing LiangGuangdong Key Laboratory of Nanomedicine, CAS-HK Joint Lab for Biomaterials, Institute of Biomedicine and Biotechnology, Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences, Shenzhen, 518055, China.
Yunlong ZhangWestlake Laboratory of Life Sciences and Biomedicine, Hangzhou, 310024, China.ORCID 0000-0002-2447-9138

Funding

Basic and Applied Basic Research Foundation of Guangdong Province 2024A1515011735National Key R&D Programs of China 2021YFA0910900National Key R&D Programs of China 2023YFA0915400National Natural Science Foundation of China 82101325National Natural Science Foundation of China 82104416National Natural Science Foundation of China 82174468Natural Science Foundation of Guangdong Province 2022A1515011493Natural Science Foundation of Zhejiang Province LZ24H250001Shenzhen Science and Technology Program JCYJ20220531095814033
6 · The paper itself

Abstract

Astrocyte-microglia crosstalk is vital for neuronal survival and clearing aggregate accumulation in neurodegenerative diseases. While interleukin-3 (IL-3) has been reported to exert both protective and detrimental effects in neurodegenerative diseases, however, its role in α-synuclein pathology remains unclear. In this study, it is found that astrocytic IL-3 and microglial IL-3R are positively responsive to α-synuclein pathology in the brains of transgenic A53T Parkinson's disease (PD) mice and in an adeno-associated virus (AAV)-human α-synuclein (AAV-hα-Syn)-injected PD mouse model. Exogenous IL-3 infusion reduces behavioral abnormities and nigrostriatal α-synuclein pathology. Mechanistically, IL-3 induces microglial phagocytosis of pathological α-synuclein while simultaneously stimulating dopaminergic (DA) neurons to clear pathological α-synuclein via induction of autophagy through the IFN-β/Irgm1 pathway. Due to its limited efficiency in crossing the blood-brain barrier, a precise IL-3 delivery strategy is developed by cross-linking IL-3 and RVG29 with PEG-Linker (RVG-modified IL-3 nanogels-RVG-IL3 NGs). Intravenous administration of RVG-IL3 NGs shows efficient uptake by microglia and DA neurons within the brain. RVG-IL3 NGs ameliorate motor deficits and pathological α-synuclein by improving microglial and neuronal function in the AAV-hα-Syn mouse model of PD. Collectively, IL-3 may represent a feasible therapeutic strategy for PD.

Indexed as

alpha-SynucleinDisease Models, AnimalInterleukin-3Mice, TransgenicParkinson DiseaseAnimalsMiceMicrogliaalpha-SynucleinInterleukin-3DA neuronIL‐3microgliaParkinson's diseaseα‐synuclein

Identifiers

PMID39225429
PMCPMC11558132

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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.