Evidence map›Paper›PMID 38279762›Full record

ReviewCNS & neurological disorders drug targets2024

LRRK2; Communicative Role in the Treatment of Parkinson's Disease and Ulcerative Colitis Overlapping.

Naser-Aldin Lashgari, Nazanin Momeni Roudsari, Amirhossein Niknejad, Hedieh Sadat Shamsnia, Maryam Shayan, Leila Mohaghegh Shalmani, Saeideh Momtaz, Nima Rezaei, Amir Hossein Abdolghaffari

Abstract readReview
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In one paragraph

Review in CNS & neurological disorders drug targets, 2024. 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
1.1field-weighted citation impact, top 24% 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

1 citing paper in PubMed, 3 citations in OpenAlex.

  1. Article
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 at 4 institutions in 1 country.

Naser-Aldin LashgariDepartment of Toxicology & Pharmacology, Faculty of Pharmacy, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran.
Nazanin Momeni RoudsariDepartment of Toxicology & Pharmacology, Faculty of Pharmacy, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran.
Amirhossein NiknejadDepartment of Toxicology & Pharmacology, Faculty of Pharmacy, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran.
Hedieh Sadat ShamsniaDepartment of Toxicology & Pharmacology, Faculty of Pharmacy, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran.
Maryam ShayanDepartment of Pharmacology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Leila Mohaghegh ShalmaniDepartment of Toxicology & Pharmacology, Faculty of Pharmacy, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran.
Saeideh MomtazMedicinal Plants Research Center, Institute of Medicinal Plants, ACECR, Karaj, Iran.
Nima RezaeiResearch Center for Immunodeficiencies, Children's Medical Center, Tehran University of Medical Sciences, Tehran, Iran.
Amir Hossein AbdolghaffariDepartment of Toxicology & Pharmacology, Faculty of Pharmacy, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran.
Islamic Azad University Medical Branch of Tehran · IRAcademic Center for Education, Culture and Research · IRChildren's Medical Center · IRTehran University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundInvolvement of gastrointestinal inflammation in Parkinson's disease (PD) pathogenesis and movement have progressively emerged. Inflammation is involved in the etiology of both PD and inflammatory bowel disease (IBD). Transformations in leucine-rich recurrent kinase 2 (LRRK2) are among the best hereditary supporters of IBD and PD. Elevated levels of LRRK2 have been reported in stimulated colonic tissue from IBD patients and peripheral invulnerable cells from irregular PD patients; thus, it is thought that LRRK2 directs inflammatory cycles.

objectiveSince its revelation, LRRK2 has been seriously linked in neurons, albeit various lines of proof affirmed that LRRK2 is profoundly communicated in invulnerable cells. Subsequently, LRRK2 might sit at a junction by which stomach inflammation and higher LRRK2 levels in IBD might be a biomarker of expanded risk for inconsistent PD or potentially may address a manageable helpful objective in incendiary sicknesses that increment the risk of PD. Here, we discuss how PD and IBD share covering aggregates, especially regarding LRRK2 and present inhibitors, which could be a helpful objective in ongoing treatments.

methodEnglish data were obtained from Google Scholar, PubMed, Scopus, and Cochrane library studies published between 1990-December 2022.

resultInhibitors of the LRRK2 pathway can be considered as the novel treatment approaches for IBD and PD treatment.

conclusionCommon mediators and pathways are involved in the pathophysiology of IBD and PD, which are majorly correlated with inflammatory situations. Such diseases could be used for further clinical investigations.

Indexed as

Colitis, UlcerativeLeucine-Rich Repeat Serine-Threonine Protein Kinase-2Parkinson DiseaseAnimalsHumansInflammationLeucine-Rich Repeat Serine-Threonine Protein Kinase-2LRRK2 protein, humandiseases.inflammationinflammatory bowel disease (IBD)Leucine-rich repeat kinase 2 (LRRK2)neurodegenerative diseasesParkinson’s disease (PD)

Identifiers

PMID38279762
OpenAlexW4391253021

What OpenQuestion 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 OpenQuestion graph.