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<p>Parkinson’s disease (PD) is a chronic and progressive neurodegenerative disorder, characterized by dopaminergic neuronal loss within the substantia nigra pars compacta (SNpc). The gradual progression of neuronal loss results in a significant decline in dopamine levels in the striatum, leading to several hallmarks of motor complications, including resting tremors, rigidity, postural instability, bradykinesia, and a variety of non-motor symptoms, like cognitive decline, mood disturbances, and autonomic dysfunction, reflecting the widespread neurochemical and structural involvement beyond the nigrostriatal pathway. Galectin-3 (Gal-3), a lectin that can bind beta-galactosidase, regulates a diverse spectrum of biological processes, including cell adhesion, tissue development, wound healing, and immune response via different signalling cascades. Recent research has identified its role as a neuroinflammatory mediator in PD pathology, as it induces microglial activation and the secretion of proinflammatory cytokines. In this context, it also influences several biological mechanisms such as phagocytosis, autophagy, and lysosomal degradation, which are all essential for preserving protein homeostasis and clearing misfolded α-syn. Elevated levels of Gal-3 in the blood, cerebrospinal fluid (CSF), and brain tissue of PD patients demonstrate disease severity and progression. Recent preclinical and clinical findings suggested that inhibiting Gal-3 may reduce neuroinflammation and protect dopaminergic neurons, making it an encouraging therapeutic target in PD management. This review highlights the multifaceted role of Gal-3 in the pathophysiology and progression of PD, focusing on its involvement in neuroinflammation and neurodegeneration. Additionally, this review also explores its underdeveloped potential as a diagnostic biomarker and a therapeutic target to retard the disease progression.</p>

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Galectin-3 as a Key Driver of Neuroinflammation and α-Synuclein Aggregation in Parkinson’s Disease: Unlocking New Paths for Biomarkers and Therapies

  • 期刊论文

  • 发表日期：

    2025年9月27日

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  • Pratyush Porel,
  • Gulam Varish,
  • Khadga Raj Aran

摘要

Parkinson’s disease (PD) is a chronic and progressive neurodegenerative disorder, characterized by dopaminergic neuronal loss within the substantia nigra pars compacta (SNpc). The gradual progression of neuronal loss results in a significant decline in dopamine levels in the striatum, leading to several hallmarks of motor complications, including resting tremors, rigidity, postural instability, bradykinesia, and a variety of non-motor symptoms, like cognitive decline, mood disturbances, and autonomic dysfunction, reflecting the widespread neurochemical and structural involvement beyond the nigrostriatal pathway. Galectin-3 (Gal-3), a lectin that can bind beta-galactosidase, regulates a diverse spectrum of biological processes, including cell adhesion, tissue development, wound healing, and immune response via different signalling cascades. Recent research has identified its role as a neuroinflammatory mediator in PD pathology, as it induces microglial activation and the secretion of proinflammatory cytokines. In this context, it also influences several biological mechanisms such as phagocytosis, autophagy, and lysosomal degradation, which are all essential for preserving protein homeostasis and clearing misfolded α-syn. Elevated levels of Gal-3 in the blood, cerebrospinal fluid (CSF), and brain tissue of PD patients demonstrate disease severity and progression. Recent preclinical and clinical findings suggested that inhibiting Gal-3 may reduce neuroinflammation and protect dopaminergic neurons, making it an encouraging therapeutic target in PD management. This review highlights the multifaceted role of Gal-3 in the pathophysiology and progression of PD, focusing on its involvement in neuroinflammation and neurodegeneration. Additionally, this review also explores its underdeveloped potential as a diagnostic biomarker and a therapeutic target to retard the disease progression.