Evidence map›Paper›PMID 35934920›Full record

ArticleCNS neuroscience & therapeutics2022

Connectivity of corticostriatal circuits in nonmanifesting LRRK2 G2385R and R1628P carriers.

Dongling Zhang, Junye Yao, Jinghong Ma, Linlin Gao, Junyan Sun, Jiliang Fang, Hongjian He, Tao Wu

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in CNS neuroscience & therapeutics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.2field-weighted citation impact, top 44% 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

2 citing papers in PubMed, 2 citations in OpenAlex.

  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

8 authors at 3 institutions in 1 country.

Dongling ZhangDepartment of Neurology, Center for Movement Disorders, Beijing Tiantan Hospital, Capital Medical University, Beijing, China.ORCID 0000-0002-0399-6179
Junye YaoCenter for Brain Imaging Science and Technology, College of Biomedical Engineering and Instrument Science, Zhejiang University, Hangzhou, China.
Jinghong MaDepartment of Neurobiology, Beijing Institute of Geriatrics, Xuanwu Hospital of Capital Medical University, Beijing, China.
Linlin GaoDepartment of Neurobiology, Beijing Institute of Geriatrics, Xuanwu Hospital of Capital Medical University, Beijing, China.
Junyan SunDepartment of Neurology, Center for Movement Disorders, Beijing Tiantan Hospital, Capital Medical University, Beijing, China.
Jiliang FangDepartment of Radiology, Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, China.
Hongjian HeCenter for Brain Imaging Science and Technology, College of Biomedical Engineering and Instrument Science, Zhejiang University, Hangzhou, China.
Tao WuDepartment of Neurology, Center for Movement Disorders, Beijing Tiantan Hospital, Capital Medical University, Beijing, China.
Capital Medical University · CNZhejiang University of Science and Technology · CNChinese Academy of Medical Sciences & Peking Union Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNeuroimaging studies have shown that the functional connectivity (FC) of corticostriatal circuits in nonmanifesting leucine-rich repeat kinase 2 (LRRK2) G2019S mutation carriers mirrors neural changes in idiopathic Parkinson's disease (PD). In contrast, neural network changes in LRRK2 G2385R and R1628P mutations are unclear. We aimed to investigate the FC of corticostriatal circuits in nonmanifesting LRRK2 G2385R and R1628P mutation carriers (NMCs).

methodsTwenty-three NMCs, 28 PD patients, and 29 nonmanifesting noncarriers (NMNCs) were recruited. LRRK2 mutation analysis was performed on all participants. Clinical evaluation included MDS-UPDRS.

resultsWhen compared to NMNCs, NMCs showed significantly reduced FC between the caudate nucleus and superior frontal gyrus and cerebellum, and between the nucleus accumbens and parahippocampal gyrus, amygdala, and insula. We also found increased striatum-cortical FC in NMCs.

conclusionsAlthough the corticostriatal circuits have characteristic changes similar to PD, the relatively intact function of the sensorimotor striatum-cortical loop may result in less possibility of developing parkinsonian motor symptoms for the NMCs. This study helps explain why LRRK2 G2385R and R1628P mutations are risk factors rather than pathogenic mutations for PD and suggests that various LRRK2 mutations have distinct effects on neural networks.

Indexed as

Parkinson DiseaseCorpus StriatumHumansLeucine-Rich Repeat Serine-Threonine Protein Kinase-2MutationLeucine-Rich Repeat Serine-Threonine Protein Kinase-2LRRK2 protein, humancorticostriatal circuitsfunctional connectivityLRRK2Parkinson's diseaseresting-state fMRI

Identifiers

PMID35934920
PMCPMC9627388
OpenAlexW4292200253

What OpenQuestion holds

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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.