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.
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.
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Authors and funding
7 authors.
Funding
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.
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42400678What Socratic holds
Registered trials
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.