Amidst rising Parkinson\'s disease (PD) incidence in an aging global population, the need for non-invasive and reliable diagnostic methods is increasingly critical. This review evaluates the strategic role of transcranial sonography (TCS) in the early detection and monitoring of PD. TCS\'s ability to detect substantia nigra hyperechogenicity offers profound insights into its correlation with essential neuropathological alterations-namely, iron accumulation, neuromelanin depletion, and glial proliferation-fundamental to PD\'s pathophysiology. Our analysis highlights TCS\'s advantages, including its non-invasiveness, cost-effectiveness, and ease of use, positioning it as an invaluable tool for early diagnosis and continual disease progression monitoring. Moreover, TCS assists in identifying potential risk and protective factors, facilitating tailored therapeutic strategies to enhance clinical outcomes. This review advocates expanding TCS utilization and further research to maximize its diagnostic and prognostic potential in PD management, contributing to a more nuanced understanding of the disease.

BACKGROUND: Parkinson\'s disease (PD) is a progressive neurodegenerative disease with increasing prevalence. Effective diagnostic markers and therapeutic methods are still lacking. Exploring key molecular markers and mechanisms for PD can help with early diagnosis and treatment improvement.
METHODS: Three datasets GSE174052, GSE77668, and GSE168496 were obtained from the GEO database to search differentially expressed circRNA (DECs), miRNAs (DEMis), and mRNAs (DEMs). GO and KEGG enrichment analyses, and protein-protein interaction (PPI) network construction were implemented to explore possible actions of DEMs. Hub genes were selected to establish circRNA-related competing endogenous RNA (ceRNA) networks.
RESULTS: There were 1005 downregulated DECs, 21 upregulated and 21 downregulated DEMis, and 266 upregulated and 234 downregulated DEMs identified. The DEMs were significantly enriched in various PD-associated functions and pathways such as extracellular matrix organization, dopamine synthesis, PI3K-Akt, and calcium signaling pathways. Twenty-one hub genes were screened out, and a PD-related ceRNA regulatory network was constructed containing 31 circRNAs, one miRNA (miR-371a-3p), and one hub gene (KCNJ6).
CONCLUSIONS: We identified PD-related molecular markers and ceRNA regulatory networks, providing new directions for PD diagnosis and treatment.

It has been proposed that pyrethroid exposure contributes to the increasing prevalence of neurodegenerative diseases. However, the potential mechanisms remain unclear. The current study aimed to investigate the effects of the widely used pyrethroid bifenthrin on Parkinson\'s disease (PD) risk. Bifenthrin (1S-cis-bifenthrin, 1R-cis-bifenthrin, raceme) was administered to male Parkin-/- mice and C57BL/6 mice by oral gavage at a dose of 10 mg/kg bw/day for 28 days. Bifenthrin exposure significantly increased the time of pole climbing and decreased the period of rotarod running, indicating that bifenthrin decreased motor coordination in Parkin-/- mice, which was more evident by 1S-cis-bifenthrin. Furthermore, administration of bifenthrin induced obvious decreases in tyrosine hydroxylase (TH)+ cell count and the protein expression of TH. Increased protein of mitochondrial autophagy LC3B and p62 was observed after exposure to bifenthrin. Increased iron deposition and protein expression of iron transport transferrin (Tf) and transferrin receptor 2 (TfR2) was detected. 1S-cis-bifenthrin bound with Tf, TfR2, and GPX4 with lower binding energies than 1R-cis-bifenthrin, resulting in stronger interactions with these proteins. These results show structure-dependent PD-like effects of bifenthrin on motor activity and coordination associated with the disturbed mitochondrial autophagy and ferroptosis-related pathway. These data demonstrate that pyrethroid exposure increases the potential of Parkinson\'s-like symptoms via the ferroptosis pathway in Parkin-/- mice that is more pronounced than in C57BL/6 mice, providing a prospective enantioselective toxic effect of environmental neurotoxins on PD risk.

UNASSIGNED: Cell transplants as a treatment for Parkinson\'s disease have been studied for decades, and stem cells may be the most promising cell sources for this treatment. We aimed to investigate whether stem cell transplantation contributes to the cure for Parkinson\'s disease and the factors that may influence the efficacy for this therapy.
UNASSIGNED: PubMed, Embase, Cochrane Library, Web of Science, SinoMed, China National Knowledge Infrastructure (CNKI), China Science and Technology Journal Database (VIP), and ChinaInfo were thoroughly searched to find controlled trials or randomized controlled trials performing stem cell transplantation in patients with Parkinson\'s disease. The pooled effects were analyzed to evaluate the weighted mean difference (WMD) with 95% confidence intervals.
UNASSIGNED: Nine articles were identified including 129 individuals. Stem cell transplantation was an effective treatment for Parkinson\'s disease (WMD = -14.86; 95% CI: -16.62 to -13.10; p < 0.00001), with neural stem cells, umbilical cord mesenchymal stem cells (UCMSCs), and bone marrow mesenchymal stem cells (BMMSCs) being effective cell sources for transplantation. Stem cell transplantation can be effective for at least 12 months, but its long-term effectiveness remains unknown due to the limited studies monitoring patients for more than 1 year, not to mention decades.
UNASSIGNED: Data from controlled trials suggest that stem cell transplantation as a therapy for Parkinson\'s disease can be effective for at least 12 months. The factors that may influence its curative effect are time after transplantation and stem cell types.
UNASSIGNED: (Registration ID: CRD42022353145).

Parkinson\'s disease (PD) is a complex syndrome for which there is no disease-modifying treatment on the market. However, a group of drugs from the Glucagon-like peptide-1 (GLP-1) class have shown impressive improvements in clinical phase II trials. Exendin-4 (Bydureon), Liraglutide (Victoza, Saxenda) and Lixisenatide (Adlyxin), drugs that are on the market as treatments for diabetes, have shown clear effects in improving motor activity in patients with PD in phase II clinical trials. In addition, Liraglutide has shown improvement in cognition and brain shrinkage in a phase II trial in patients with Alzheimer disease (AD). Two phase III trials testing the GLP-1 drug semaglutide (Wegovy, Ozempic, Rybelsus) are ongoing. This perspective article will summarize the clinical results obtained so far in this novel research area. We are at a crossroads where GLP-1 class drugs are emerging as a new treatment strategy for PD and for AD. Newer drugs that have been designed to enter the brain easier are being developed already show improved effects in preclinical studies compared with the older GLP-1 class drugs that had been developed to treat diabetes. The future looks bright for new treatments for AD and PD.

Long noncoding RNA nuclear-enriched abundant transcript 1 (NEAT1) is involved in the progression of Parkinson\'s disease (PD), but the specific regulatory role needs further exploration. This study showed that the expression of NEAT1 was upregulated in the cerebrospinal fluid (CSF) and peripheral blood of patients with different stages of PD. 1-Methyl-4-phenylpyridine (MPP)-treated PC 12 cells were transfected with si-NEAT1, and MPP treatment promoted cell apoptosis, oxidative stress and inflammatory factor secretion. Si-NEAT1 reversed the effects of MPP. NEAT1 silencing eliminated the effect of MPP on the protein expression levels of LC3-II and p62/SQSTM1. By using an online bioinformatics database, Fused in Sarcoma (FUS) was confirmed to be an RNA binding protein of NEAT1, and it was highly expressed in the CSF and peripheral blood of patients with PD. Si-FUS was transfected into MPP-treated PC 12 cells to detect cell apoptosis, oxidative stress, inflammatory factor secretion and autophagy, and the results were the same as those of transfection of si-NEAT1. Furthermore, MPP treatment reduced the phosphorylation levels of PI3K, Akt and mTOR, whereas si-FUS reversed the effects of MPP. In vivo, compared with the model group, the PD mice showed reduced NEAT1 and FUS expression levels and activated PI3K pathway after being injected with si-NEAT1. The brain tissue of NEAT1-silenced PD mice had decreased inflammatory infiltration and apoptosis and increased neurological scores. In conclusion, NEAT1 is involved in PD progression through FUS-mediated inhibition of the PI3K/AKT/mTOR signalling pathway.

BACKGROUND: This study aimed to verify whether the combined use of Da Dingfengzhu and Western medicine in treating Parkinson\'s disease (PD) can lead to therapeutic efficacy and symptom alleviation, thereby achieving a complementary and synergistic effect.
METHODS: In this study, 158 patients were initially enrolled, with 116 eligible patients randomly divided into a control and an observation group. The control group received levodopa/benserazide and pramipexole, while the observation group received Da Dingfengzhu combined with levodopa/benserazide and pramipexole for 12 weeks. Baseline patient characteristics, adverse reactions, and blood samples were collected at baseline and 12 weeks post-treatment. The Unified Parkinson\'s Disease Rating Scale (UPDRS) was used to assess symptom severity at baseline, four weeks into treatment, and 12 weeks post-treatment.
RESULTS: Adverse reactions during treatment were similar in both groups, suggesting that the combined therapy in the observation group did not increase adverse effects. Both groups showed improvements in UPDRS scores, with the observation group displaying more significant symptom alleviation at 4 and 12 weeks. Moreover, the observation group exhibited more pronounced increases in serum neurotrophic factor-3 and dopamine levels and greater reductions in oxidative stress and inflammatory response markers.
CONCLUSIONS: In conclusion, the combination of Da Dingfengzhu with levodopa/benserazide and pramipexole for treating PD shows significant clinical potential and is worthy of broader application.

UNASSIGNED: Parkinson\'s disease (PD) is the second most common neurodegenerative disease. Patients often present with balance dysfunction. Several studies have applied visual feedback training to stroke patients and demonstrated significant improvement. However, the application of visual feedback balance training in PD patients has not been reported.
UNASSIGNED: To observe the effects of visual feedback balance training combined with conventional rehabilitation training on the balance function of patients with early PD.
UNASSIGNED: Fifty patients with early PD were randomly divided into control group and observation group. The control group received conventional rehabilitation training, including body position transfer, weight shifting, movement in all directions and gait training. The observation group were added with visual feedback balance training on the basis of the training above. All patients were trained 5 times per week for 4 weeks. Berg Balance Scale (BBS), Time Up-and-Go test (TUG) and Pro-Kin balance training instrument were used to evaluate the balance function of patients before and after treatment, and the balance function were compared between the two groups.
UNASSIGNED: The BBS and TUG scores of the observation group and the control group were improved significantly (P<0.01), and the BBS and TUG scores of the observation group were improved more obviously than control group (P<0.01). The length and area of eye open and closed condition in the observation group and the control group were significantly reduced compared with those before training (P<0.01), and the degree of reduction in the observation group was more obvious (P<0.01). The length and area of the observation group and the control group before and after training when eye open were smaller than those when eye closed (P<0.01).
UNASSIGNED: The conventional rehabilitation therapy can improve the balance function of PD patients, but the combination of visual feedback balance training and conventional rehabilitation therapy can improve the balance function more significantly.

The treatment of Parkinson\'s disease is a global medical challenge. α-Synuclein (α-Syn) is the causative protein in Parkinson\'s disease and is closely linked to its progression. Therefore, inhibiting the pathological aggregation of α-Syn and its neurotoxicity is essential for the treatment of Parkinson\'s disease. In this study, α-Syn and recombinant human HspB5-ACD structural domain protein (AHspB5) were produced using the BL21(DE3) E. coli prokaryotic expression system, and then the role and mechanism of AHspB5 in inhibiting the pathological aggregation of α-Syn and its neurotoxicity were investigated. As a result, we expressed α-Syn and AHspB5 proteins and characterised the proteins. In vitro experiments showed that AHspB5 could inhibit the formation of α-Syn oligomers and fibrils; in cellular experiments, AHspB5 could prevent α-Syn-induced neuronal cell dysfunction, oxidative stress damage and apoptosis, and its mechanism of action was related to the TH-DA pathway and mitochondria-dependent apoptotic pathway; in animal experiments, AHspB5 could inhibit behavioural abnormalities, oxidative stress damage and loss of dopaminergic neurons. In conclusion, this work is expected to elucidate the mechanism and biological effects of AHspB5 on the pathological aggregation of α-Syn, providing a new pathway for the treatment of Parkinson\'s disease and laying the foundation for recombinant AHspB5.

UNASSIGNED: This study aims to utilize Weighted Gene Co-expression Network Analysis (WGCNA) and Support Vector Machine (SVM) algorithm for screening biomarkers and constructing a diagnostic model for Parkinson\'s disease.
UNASSIGNED: Firstly, we conducted WGCNA analysis on gene expression data from Parkinson\'s disease patients and control group using three GEO datasets (GSE8397, GSE20163, and GSE20164) to identify gene modules associated with Parkinson\'s disease. Then, key genes with significantly differential expression from these gene modules were selected as candidate biomarkers and validated using the GSE7621 dataset. Further functional analysis revealed the important roles of these genes in processes such as immune regulation, inflammatory response, and cell apoptosis. Based on these findings, we constructed a diagnostic model by using the expression data of FLT1, ATP6V0E1, ATP6V0E2, and H2BC12 as inputs and training and validating the model using SVM algorithm.
UNASSIGNED: The prediction model demonstrated an AUC greater than 0.8 in the training, test, and validation sets, thereby validating its performance through SMOTE analysis. These findings provide strong support for early diagnosis of Parkinson\'s disease and offer new opportunities for personalized treatment and disease management.
UNASSIGNED: In conclusion, the combination of WGCNA and SVM holds potential in biomarker screening and diagnostic model construction for Parkinson\'s disease.