Taraxasterol is one of the bioactive triterpenoids found in dandelion, a member of the family Asteraceae. In the animal or cellular models of several ailments, including liver damage, gastritis, colitis, arthritis, pneumonia, tumors, and immune system diseases, taraxasterol has been shown to have significant preventive and therapeutic effects. This review aims to evaluate the current state of research and provide an overview of the possible applications of taraxasterol in various diseases. The reported phytochemical properties and pharmacological actions of taraxasterol, including anti-inflammatory, anti-oxidative, and anti-carcinogenic properties, and its potential molecular mechanisms in developing these diseases are highlighted. Finally, we further explored whether taraxasterol has protective effects on neuronal death in neurodegenerative diseases. In addition, more animal and clinical studies are also required on the metabolism, bioavailability, and safety of taraxasterol to support its applications in pharmaceuticals and medicine.

Parkinson’s disease is a common neurodegenerative disease with movement disorders associated with the intracytoplasmic deposition of aggregate proteins such as α-synuclein in neurons. As one of the major intracellular degradation pathways, the autophagy-lysosome pathway plays an important role in eliminating these proteins. Accumulating evidence has shown that upregulation of the autophagy-lysosome pathway may contribute to the clearance of α-synuclein aggregates and protect against degeneration of dopaminergic neurons in Parkinson’s disease. Moreover, multiple genes associated with the pathogenesis of Parkinson’s disease are intimately linked to alterations in the autophagy-lysosome pathway. Thus, this pathway appears to be a promising therapeutic target for treatment of Parkinson’s disease. In this review, we briefly introduce the machinery of autophagy. Then, we provide a description of the effects of Parkinson’s disease–related genes on the autophagy-lysosome pathway. Finally, we highlight the potential chemical and genetic therapeutic strategies targeting the autophagy–lysosome pathway and their applications in Parkinson’s disease.

The autophagy‐lysosomal pathway (ALP) is involved in the degradation of protein aggregates and damaged organelles. Transcription factor EB (TFEB), a major regulator of ALP, has emerged as a leading factor in addressing neurodegenerative disease pathology, including Alzheimer's disease (AD), Parkinson's disease (PD), PolyQ diseases, and Amyotrophic lateral sclerosis (ALS). In this review, we delineate the regulation of TFEB expression and its functions in ALP. Dysfunctions of TFEB and its role in the pathogenesis of several neurodegenerative diseases are reviewed. We summarize the protective effects and molecular mechanisms of some TFEB‐targeted agonists in neurodegenerative diseases. We also offer our perspective on analyzing the pros and cons of these agonists in the treatment of neurodegenerative diseases from the perspective of drug development. More studies on the regulatory mechanisms of TFEB in other biological processes will aid our understanding of the application of TFEB‐targeted therapy in neurodegeneration.

Backgrounds: Parkinson’s disease (PD) is a common neurodegenerative disorder characterized by motor symptoms and non-motor symptoms. It has been found that intestinal issues usually precede motor symptoms. Microorganisms in the gastrointestinal tract can affect central nervous system through the microbiota-gut-brain axis. Accumulating evidence has shown that disturbances in the microbiota-gut-brain axis are linked with PD. Thus, this pathway appears to be a promising therapeutic target for treatment of PD. Objectives: In this review, we mainly described gut dysbiosis in PD and their underlying mechanisms for mediating neuroinflammation and peripheral immune response in PD pathology and futher discussed the potential small-molecule compounds and genic therapeutic strategies targeting the microbiota-gut-brain axis and their applications in PD. Conclusions: Studies have found that some small molecule compounds and alterations of inflammation-related genes can improve the motor and non-motor symptoms of PD by improving the microbiota-gut-brain axis, which may provide potentially beneficial drugs and molecular targets for the therapies of PD.

Parkinson’s disease (PD) is the second most common neurodegenerative disease, which is characterized by a progressive loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc) of the middle brain. Excessive reactive oxygen species (ROS) accumulation due to mitochondrial dysfunction or inflammation is the main factor contributing to the degeneration of dopaminergic neurons. In the preclinical and clinical studies, carotenoids and their major components including vitamin and astaxanthin were found to have antioxidant, anti-inflammatory, autophagy-promoting, and mitochondrial dysfunction improving functions. This chapter focuses on the current status of research on carotenoids and their major components in PD, which can provide help for the prevention and treatment of PD.

Isolated congenital coronary artery fistula (ICCAF) is an exceedingly rare anomaly in which there is a direct abnormal connection between a coronary artery and other cardiac chambers or any of great vessels. The left circumflex artery (LCX) is the least common source of ICCAF. Here we reported a rare case of large ICCAF originated from the LCX in a 9-year-old boy. He presented fatigability, murmurs and NYHA class II. Echocardiography and cardiac CT revealed that an aneurysmal dilatation of the LCX along with the dilated coronary sinus entered into the right atrium (RA) through the great cardiac vein. However, it showed that the dilated LCX directly drained into the RA by coronary angiography, which was confirmed by the surgery. During the surgical procedure, the LCX fistula was identified in a 3^*3 cm bulbous structure, the aneurysmal dilation of RA tissue. The end of fistula was located in the lower-middle interatrial septum, which was near the coronary sinus and above the opening of inferior vena cava (IVC). Transcardiac chamber closure with cardiopulmonary bypass (CPB) was successfully performed for the correction of the fistula. It indicated that preoperative angiography is essential to define the details of large ICCAF with aneurysmal dilation. Moreover, transcardiac chamber closure with CPB is the optimal procedure for the treatment of large ICCAF, while interventional catheterization is not feasible due to the presence of aneurysmal dilation of the LCX. The description of this rare case might have great value for the diagnosis and treatment of large ICCAF originated from the LCX.