Evidence map›Paper›PMID 40968351›Full record

Observational studyNeurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology2025

Association between metabolic syndrome, its individual components and progression of amyotrophic lateral sclerosis.

Qirui Jiang, Qianqian Wei, Tianmi Yang, Junyu Lin, Yi Xiao, Chunyu Li, Lingyu Zhang, Yanbing Hou, Ruwei Ou, Shichan Wang and 3 more

Abstract readObservational Study
PubMed Publisher
In one paragraph

Observational study in Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

13 authors.

Qirui JiangDepartment of Neurology, Laboratory of Neurodegenerative Disorders and Immunology, Rare disease center, West China Hospital, Sichuan University, Chengdu, 610041, Sichuan, China.
Qianqian WeiDepartment of Neurology, Laboratory of Neurodegenerative Disorders and Immunology, Rare disease center, West China Hospital, Sichuan University, Chengdu, 610041, Sichuan, China.
Tianmi YangDepartment of Neurology, Laboratory of Neurodegenerative Disorders and Immunology, Rare disease center, West China Hospital, Sichuan University, Chengdu, 610041, Sichuan, China.
Junyu LinDepartment of Neurology, Laboratory of Neurodegenerative Disorders and Immunology, Rare disease center, West China Hospital, Sichuan University, Chengdu, 610041, Sichuan, China.
Yi XiaoDepartment of Neurology, Laboratory of Neurodegenerative Disorders and Immunology, Rare disease center, West China Hospital, Sichuan University, Chengdu, 610041, Sichuan, China.
Chunyu LiDepartment of Neurology, Laboratory of Neurodegenerative Disorders and Immunology, Rare disease center, West China Hospital, Sichuan University, Chengdu, 610041, Sichuan, China.
Lingyu ZhangDepartment of Neurology, Laboratory of Neurodegenerative Disorders and Immunology, Rare disease center, West China Hospital, Sichuan University, Chengdu, 610041, Sichuan, China.
Yanbing HouDepartment of Neurology, Laboratory of Neurodegenerative Disorders and Immunology, Rare disease center, West China Hospital, Sichuan University, Chengdu, 610041, Sichuan, China.
Ruwei OuDepartment of Neurology, Laboratory of Neurodegenerative Disorders and Immunology, Rare disease center, West China Hospital, Sichuan University, Chengdu, 610041, Sichuan, China.
Shichan WangDepartment of Neurology, Laboratory of Neurodegenerative Disorders and Immunology, Rare disease center, West China Hospital, Sichuan University, Chengdu, 610041, Sichuan, China.
Jiyong LiuDepartment of Neurology, Laboratory of Neurodegenerative Disorders and Immunology, Rare disease center, West China Hospital, Sichuan University, Chengdu, 610041, Sichuan, China.
Yan LiangDepartment of Neurology, West China Hospital, Sichuan University, Chengdu, Sichuan, China. 179050526@qq.com.
Huifang ShangDepartment of Neurology, Laboratory of Neurodegenerative Disorders and Immunology, Rare disease center, West China Hospital, Sichuan University, Chengdu, 610041, Sichuan, China. hfshang2002@126.com.ORCID http://orcid.org/0000-0003-0947-1151

Funding

Beijing E-town Coorperation & Development Foundation YCXJ-JZ-2022-007National Natural Science Foundation of China 82101485Science and Technology Bureau Fund of Sichuan Province of China 2023YFQ0098Sichuan Science and Technology Program 2022ZDZX0023
6 · The paper itself

Abstract

backgroundMetabolic abnormalities play a pivotal role in the pathogenesis of amyotrophic lateral sclerosis (ALS). Metabolic syndrome (MetS), a cluster of metabolic disorders, is highly prevalent among the elderly. However, the association between MetS and clinical characteristics, disease progression, and survival in ALS remains unclear.

methodsWe included 529 ALS patients and collected demographic, clinical, and hematological data, including blood glucose, HbA1c, and lipid profiles. Patients were followed longitudinally. MetS was defined according to the criteria of the Chinese Diabetes Society. Multivariate logistic regression, Kaplan-Meier survival analysis, and Cox proportional hazards models were used to analyze.

resultsCompared to ALS patients without MetS, those with MetS had higher proportion of lower limb onset (44.3% vs. 24.6%, P < 0.001), and a faster disease progression rate (0.60 vs. 0.55, P = 0.022). After adjusting for confounders, MetS and hypertension were significantly associated with fast disease progression (OR = 1.808, 95% CI: 1.048-3.120, P = 0.033; OR = 2.615, 95% CI: 1.358-5.035, P = 0.004), and remained significant after multiple correction. Interaction analysis revealed significant interactions between glucose intolerance and dyslipidemia (P = 0.038), and between glucose intolerance and BMI (P = 0.040), but lost significance after multiple correction. There was no significant difference in survival between ALS patients with and without MetS. After adjusting for confounders, there was no significant association between MetS and the risk of death.

conclusionMetS, particularly in the presence of hypertension, was associated with fast disease progression in ALS, though not with survival. These suggest metabolic dysfunction may influence ALS progression and warrant further investigation.

Indexed as

Amyotrophic Lateral SclerosisDisease ProgressionMetabolic SyndromeAgedBlood GlucoseDyslipidemiasFemaleGlucose IntoleranceGlycated HemoglobinHumansHypertensionKaplan-Meier EstimateLipidsLogistic ModelsLower ExtremityMaleBlood GlucoseGlycated Hemoglobinhemoglobin A1c protein, humanLipidsAmyotrophic lateral sclerosisDisease progressionMetabolic syndromePrognosis

Identifiers

PMID40968351

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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.