Evidence map›Paper›PMID 39228080›Full record

ArticleCNS neuroscience & therapeutics2024

Luteolin as potential treatment for Huntington's disease: Insights from a transgenic mouse model.

Abuelnor Mohammed, Azza Ramadan, Asim Ahmed Elnour, Ali Awadallah Ali Mohamed Saeed, Nadia Al Mazrouei, Fahad T Alsulami, Yousef Saeed Alqarni, Vineetha Menon, Abdulla Al Amoodi, Sami Fatehi Abdalla

Abstract read
In one paragraph

Article in CNS neuroscience & therapeutics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed.

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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

10 authors.

Abuelnor MohammedDepartment of Basic Medical Sciences, College of Medicine-Dar Al Uloom University, Riyadh, Saudi Arabia.ORCID 0000-0003-4435-3791
Azza RamadanCollege of Pharmacy, Al Ain University, Abu Dhbai, United Arab Emirates.ORCID 0000-0001-5988-7783
Asim Ahmed ElnourAAU Health and Biomedical Research Center, Al Ain University, Abu Dhabi, United Arab Emirates.ORCID 0000-0002-4143-7810
Ali Awadallah Ali Mohamed SaeedDepartment of Pharmacology, Faculty of Clinical and Industrial Pharmacy, National University, Mycetoma Research Center, Khartoum, Sudan.ORCID 0000-0003-3524-4825
Nadia Al MazroueiDepartment of Pharmacy Practice and Pharmacotherapeutics, Faculty of Pharmacy, University of Sharjah, Sharjah, United Arab Emirates.ORCID 0000-0002-1339-9730
Fahad T AlsulamiClinical Pharmacy Department, College of Pharmacy, Taif university, Taif, Saudi Arabia.ORCID 0000-0001-8989-7958
Yousef Saeed AlqarniDepartment of pharmacy practice, college of pharmacy, Imam abdulrahman bin faisal university, Dammam, Saudi Arabia.ORCID 0000-0002-4195-3110
Vineetha MenonDepartment of Pharmacy Practice, College of Pharmacy, Gulf Medical University, Ajman, United Arab Emirates.ORCID 0000-0002-2030-0962
Abdulla Al AmoodiAmbulatory Healthcare Services, Academic Affairs, Abu Dhabi Health Services (SEHA), Abu Dhabi, United Arab Emirates.ORCID 0000-0001-5248-9598
Sami Fatehi AbdallaClinical Department, College of Medicine, Almaarefa University (Diriyah), Riyadh, Saudi Arabia.ORCID 0000-0002-7396-8376

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsThe study aimed to evaluate the potential benefits of luteolin treatment in Huntington's disease (HD), an inherited progressive neurodegenerative disorder.

methodsHD N171-82Q transgenic and WT mice received luteolin or vehicle for treatment at 6 weeks of age. The mice's body weight changes and survival rates were monitored throughout the study, and a series of motor functional tests were conducted. Serum level of the marker NfL was also determined. Immunohistochemical staining and western blotting were utilized to assess the expression of huntingtin aggregates.

resultsLuteolin treatment enhanced survival and prevented weight loss in HD mice compared to the vehicle-treated HD group. Furthermore, the luteolin-treated HD mice exhibited enhanced motor coordination and balance and significantly reduced motor dysfunction. Also, luteolin decreased serum NfL levels in HD mice. Notably, the accumulation of huntingtin aggregates was significantly reduced in the brain's cortex, hippocampus, and striatum of luteolin-treated HD mice compared to the vehicle-treated HD group.

conclusionLuteolin holds promise as a therapeutic agent for improving survival outcomes, managing motor dysfunction, and reducing huntingtin aggregates in HD. The findings are of significance as currently, there are no approved therapeutic interventions that reverse HD pathology or slow down its progression.

Indexed as

Disease Models, AnimalHuntingtin ProteinHuntington DiseaseLuteolinMice, TransgenicAnimalsBrainHumansMaleMiceMotor ActivityNeurofilament ProteinsHuntingtin ProteinLuteolinneurofilament protein LNeurofilament Proteinshuntingtin aggregationshuntington's diseaseluteolinmotor behaviorneuroprotection

Identifiers

PMID39228080
PMCPMC11371662

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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.