Publications by authors named "Hengxu Mao"

Background And Purpose: This study investigated the neural mechanisms underlying Parkinson's disease (PD) subtypes-tremor dominant (TD) and postural instability gait difficulty (PIGD)-by analyzing regional homogeneity (ReHo) values from resting-state functional MRI.

Methods: Fifty-nine PD patients (29 TD patients, 30 PIGD patients) and 30 healthy controls (HCs) were enrolled. ReHo values were analyzed via analysis of variance and a two-sample t-test, with age and sex as covariates.

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The spectrum of synucleinopathies, including Parkinson's disease (PD), multiple system atrophy (MSA), and dementia with Lewy bodies (DLB), is characterized by α-synuclein (αSyn) pathology, which serves as the definitive diagnostic marker. However, current diagnostic methods primarily rely on motor symptoms that manifest years after the initial neuropathological changes, thereby delaying potential treatment. The symptomatic overlap between PD and MSA further complicates the diagnosis, highlighting the need for precise and differential diagnostic methods for these overlapping neurodegenerative diseases.

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Injecting α-synuclein pre-formed fibrils (αSyn PFFs) into various tissues and organs involves converting monomeric αSyn into a fibrillar form, inducing extensive αSyn pathology that effectively models Parkinson's disease (PD). However, the distinct physicochemical properties of αSyn amyloid fibrils can potentially reduce their seeding activity, especially during storage. In this study, it is demonstrated that αSyn PFFs exhibit significant sensitivity to low temperatures, with notable denaturation occurring between -20 and 4 °C, and gradual disassembly persisted even under storage conditions at -80 °C.

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Background: Seed amplification assays (SAA) enable the amplification of pathological misfolded proteins, including α-synuclein (αSyn), in both tissue homogenates and body fluids of Parkinson's disease (PD) patients. SAA involves repeated cycles of shaking or sonication coupled with incubation periods. However, this amplification scheme has limitations in tracking protein propagation due to repeated fragmentation.

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The seeding amplification assay (SAA) has recently emerged as a valuable tool for detecting α-synuclein (αSyn) aggregates in various clinically accessible biospecimens. Despite its efficiency and specificity, optimal tissue-specific conditions for distinguishing Parkinson's disease (PD) from non-PD outside the brain remain underexplored. This study systematically evaluated 150 reaction conditions to identify the one with the highest discriminatory potential between PD and non-synucleinopathy controls using skin samples, resulting in a modified SAA.

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Ubiquitin-proteasome system dysfunction triggers α-synuclein aggregation, a hallmark of neurodegenerative diseases, such as Parkinson's disease (PD). However, the crosstalk between deubiquitinating enzyme (DUBs) and α-synuclein pathology remains unclear. In this study, we observed a decrease in the level of ubiquitin-specific protease 14 (USP14), a DUB, in the cerebrospinal fluid (CSF) of PD patients, particularly females.

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Background: The overexpression, accumulation, and cell-to-cell transmission of α-synuclein leads to the deterioration of Parkinson's disease (PD). Previous studies suggest that Baicalein (BAI) can bind to α-synuclein and inhibit α-synuclein aggregation and secretion. However, it is still unclear whether BAI can intervene with the pathogenic molecules in α-synuclein-mediated PD pathways beyond directly targeting α-synuclein per se.

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Parkinson's disease (PD) is a progressive movement disorder characterized by dopaminergic (DA) neuron degeneration and the existence of Lewy bodies formed by misfolded α-synuclein. Emerging evidence supports the benefits of dietary interventions in PD due to their safety and practicality. Previously, dietary intake of α-ketoglutarate (AKG) was proved to extend the lifespan of various species and protect mice from frailty.

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Background: Parkinson's disease (PD) is the second most common neurodegenerative disease after Alzheimer's dementia. Mitochondrial dysfunction is involved in the pathology of PD. Coiled-coil-helix-coiled-coil-helix domain-containing 2 (CHCHD2) was identified as associated with autosomal dominant PD.

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The intracellular aggregation of α-synuclein in neurons/glia is considered to be a key step in the pathogenesis of synucleinopathy [including Parkinson's disease (PD), dementia with Lewy body (DLB), multiple system atrophy (MSA), etc.]. Increasing evidence indicates that the initial pathological α-synuclein aggregates can replicate themselves and propagate in a "seeding" manner to multiple areas of the brain and even to peripheral tissue, which makes it the most important biomarker for the diagnosis of synucleinopathies in recent years.

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Article Synopsis
  • * The high-cellulose diet increases serotonin synthesis and neurotrophic factor expression, which are linked to improved gut function, along with changes in gut microbiota composition and higher acetate levels.
  • * Acetate supplementation can potentially restore gut function by modulating serotonin production and inflammation, suggesting that increasing dietary fiber or acetate intake may help combat motility issues in humans.
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Article Synopsis
  • The study investigates how MHC-I protein expression in dopaminergic neurons relates to Parkinson's disease, focusing on the role of oxidative stress and immune cell infiltration.
  • Researchers used various techniques, including PCR and immunofluorescence, to confirm MHC-I expression in both cell and mouse models treated with neurotoxins associated with Parkinson's.
  • Results showed that increased MHC-I led to more cytotoxic T cell infiltration, and reducing MHC-I expression decreased neuronal death, suggesting oxidative stress-induced MHC-I presentation contributes to neuronal degeneration in Parkinson's disease.
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The NLR family pyrin domain containing 3 (NLRP3) inflammasome was reported to be regulated by autophagy and activated during inflammatory procession of Parkinson's disease (PD). Berberine (BBR) is well-studied to play an important role in promoting anti-inflammatory response to mediate the autophagy activity. However, the effect of Berberine on NLRP3 inflammasome in PD and its potential mechanisms remain unclear.

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Tristetraprolin (TTP), an RNA-binding protein encoded by the ZFP36 gene, is vital for neural differentiation; however, its involvement in neurodegenerative diseases such as Parkinson's disease (PD) remains unclear. To explore the role of TTP in PD, an in vitro 1-methyl-4-phenylpyridinium (MPP ) cell model and an in vivo 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) of PD were used. Transfection of small interfering (si)-TTP RNA upregulated pro-oxidative NOX2 expression and ROS formation, downregulated anti-oxidative GSH and SOD activity;si-TTP upregulated pro-apoptotic cleaved-caspase-3 expression, and downregulated antiapoptotic Bcl-2 expression; while overexpression (OE)-TTP lentivirus caused opposite effects.

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Autophagy has been shown to be critically associated with the central mechanisms underlying Parkinson's disease (PD), while the mechanisms contributing to the imbalance of autophagy remain unclear. Small nucleolar RNA host gene 1 (SNHG1), a well-studied long noncoding RNA, has been reported to be significantly increased in PD. The potential biological functions of SNHG1 in the regulation of neuronal autophagy and cell death in PD, however, have not yet been completely elucidated.

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Glioma is one of the most frequent intracranial malignant tumors. Abnormal expression of microRNAs usually contributes to the development and progression of glioma. In the current study, we explored the role and underlying mechanism of miR-497 in glioma.

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The role of microglial-mediated sustained neuroinflammation in the onset and progression of Parkinson's disease (PD) is well established, but the mechanisms contributing to microglial activation remain unclear. LincRNA-p21, a well studied long intergenic noncoding RNA (lincRNA), plays pivotal roles in diverse biological processes and diseases. Its role in microglial activation and inflammation-induced neurotoxicity, however, has not yet been fully elucidated.

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Background: Parkinson's disease (PD) is the most prevalent neurodegenerative disorder that is characterised by selective loss of midbrain dopaminergic (DA) neurons. Chronic inflammation of the central nervous system is mediated by microglial cells and plays a critical role in the pathological progression of PD. Brain-specific microRNA-124 (miR-124) expression is significantly downregulated in lipopolysaccharide (LPS)-treated BV2 cells and in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) model of PD.

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Objective: To study the effect of Platycarya strobilacea Sieb. et Zucc (PSZ) extract on methuosis of human nasopharyngeal carcinoma CNE1 and CNE2 cells and explore the underlying mechanism.

Methods: CNE1 and CNE2 cells were treated with 1 mg/mL PSZ extract and the expressions of Rac1 mRNA and Rac1 protein were detected using RT-qPCR and Western blotting, respectively.

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Growing evidence indicates that microRNA (miRNA) play vital roles in glioma progression by directly regulating multiple targets. Here, we found that miR-105 expression was significantly decreased and inversely correlated with SOX9 mRNA expression in glioma tissues. SOX9 was identified as a direct target of miR-105.

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Article Synopsis
  • Increasing evidence indicates that ion channels are crucial not only for electric signaling in cells but also in the development of brain tumors, particularly gliomas.
  • A study identified a molecular signature of three ion channel genes (KCNN4, KCNB1, KCNJ10) that correlate with overall survival and assigned risk scores to Glioblastoma multiforme (pGBM) patients, revealing that those with high scores were more sensitive to chemotherapy.
  • The ion channel gene expression patterns showed particular associations with Mesenchymal subtype gliomas and indicated increased expression of proteins linked to apoptosis, immune response, and vasculature development, suggesting that these patterns could enhance molecular subtype classification of gliomas.
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