Evidence map›Paper›PMID 42400678›Full record

ReviewNeurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology2026

Brain-muscle axis regulation of neuroinflammation and sarcopenia in Parkinson's disease: the bridging role of lactylation.

WenXia Sun, Huiwen Huang, Xiyan Lan, An Yin, Qiong Deng, Yanbiao Zhong, MaoYuan Wang

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In one paragraph

Review in Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology, 2026. 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
–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

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

7 authors.

WenXia SunSchool of Rehabilitation Medicine, Gannan Medical University, Ganzhou City, Jiangxi Province, 341000, China.ORCID http://orcid.org/0000-0003-1952-101X
Huiwen HuangSchool of Rehabilitation Medicine, Gannan Medical University, Ganzhou City, Jiangxi Province, 341000, China.
Xiyan LanJiangxi Medical College of Nanchang University, Nanchang, Jiangxi Province, 330000, China.
An YinDepartment of Rehabilitation Medicine, The First Affiliated Hospital of Gannan Medical University, Ganzhou City, Jiangxi Province, 341000, China.
Qiong DengFirst Clinical Medical College of Gannan Medical University, Ganzhou City, Jiangxi Province, 341000, China.
Yanbiao ZhongGanzhou Intelligent Rehabilitation Technology Innovation Center, Ganzhou City, Jiangxi Province, 341000, China.
MaoYuan WangSchool of Rehabilitation Medicine, Gannan Medical University, Ganzhou City, Jiangxi Province, 341000, China. wmy.gmu.kf@gmail.com.ORCID http://orcid.org/0009-0000-3190-8458

Funding

the Key Science and Technology Project of Ganzhou Science and Technology Bureau 2023LNS37155the National Natural Science Foundation of China 82560457
6 · The paper itself

Abstract

backgroundSarcopenia is a common and often overlooked nonmotor symptom of Parkinson's disease (PD), significantly increasing the risk of falls and exacerbating the disease burden. Increasing evidence suggests that PD is not merely a neurodegenerative disease confined to the central nervous system (CNS) but also involves significant systemic metabolic disturbances and peripheral tissue dysfunction, indicating a systemic pathological character. In recent years, epigenetic modifications have gradually become an important perspective for understanding the inflammatory progression of PD. Lactate is no longer simply considered the end product of glycolysis, but can regulate gene transcription and protein function through protein lactylation.

objectiveThis paper systematically proposes that lactylation is a key molecular bridge between neuroinflammation and sarcopenia in PD.

methodsWe searched literature from the PubMed database from 2010 to 2026, screened qualified English articles, and integrated the latest research advances in neuroimmunology, skeletal muscle biology, and metabolic epigenetics.

resultsIn PD, microglia epigenetic modifications and metabolic reprogramming lead to lactate accumulation, which may drive a persistent neuroinflammatory response through lactate modification. Simultaneously, chronic inflammation and metabolic abnormalities can propagate along the brain-muscle axis, promoting skeletal muscle protein metabolic imbalance and accelerating the development of sarcopenia. Based on this, this paper systematically proposes that lactylation is a key molecular bridge between neuroinflammation and sarcopenia in PD. Combining the latest research advances in neuroimmunology, skeletal muscle biology, and metabolic epigenetics, this paper elucidates the potential mechanisms by which abnormal lactate metabolism and lactylation play a role in altered glial cell inflammatory phenotypes and skeletal muscle homeostasis imbalances. Furthermore, in conjunction with exercise intervention studies, this paper explores how lactylation, as a key regulatory molecule, can achieve bidirectional improvement in CNS inflammation and peripheral muscle function, providing a new theoretical basis for systemic intervention strategies for PD.

Indexed as

BrainLactic AcidMuscle, SkeletalNeuroinflammatory DiseasesParkinson DiseaseSarcopeniaAnimalsHumansInflammationLactic AcidLactateLactylationNeuroinflammationParkinson’s diseaseSarcopenia

Identifiers

What Socratic 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 Socratic graph.