Poly (ADP-ribose) polymerase-1 (PARP-1) is the most extensively studied member of the PARP superfamily, with its primary function being the facilitation of DNA damage repair processes. Parthanatos is a type of regulated cell death cascade initiated by PARP-1 hyperactivation, which involves multiple subroutines, including the accumulation of ADP-ribose polymers (PAR), binding of PAR and apoptosis-inducing factor (AIF), release of AIF from the mitochondria, the translocation of the AIF/macrophage migration inhibitory factor (MIF) complex, and massive MIF-mediated DNA fragmentation. Over the past few decades, the role of PARP-1 in central nervous system health and disease has received increasing attention. In this review, we discuss the biological functions of PARP-1 in neural cell proliferation and differentiation, memory formation, brain ageing, and epigenetic regulation. We then elaborate on the involvement of PARP-1 and PARP-1-dependant parthanatos in various neuropathological processes, such as oxidative stress, neuroinflammation, mitochondrial dysfunction, excitotoxicity, autophagy damage, and endoplasmic reticulum (ER) stress. Additional highlight contains PARP-1's implications in the initiation, progression, and therapeutic opportunities for different neurological illnesses, including neurodegenerative diseases, stroke, autism spectrum disorder (ASD), multiple sclerosis (MS), epilepsy, and neuropathic pain (NP). Finally, emerging insights into the repurposing of PARP inhibitors for the management of neurological diseases are provided. This review aims to summarize the exciting advancements in the critical role of PARP-1 in neurological disorders, which may open new avenues for therapeutic options targeting PARP-1 or parthanatos.

Non-steroidal anti-inflammatory drugs (NSAIDs) are widely used in human and animal health care to reduce persistent inflammation, pain and fever because of their anti-inflammatory, analgesic and antipyretic effects. However, the improper discharge and disposal make it becomes a major contaminant in the environment, which poses a big threat to the ecosystem. For this reason, accurate, sensitive, effective, green, and economic techniques are urgently required and have been rapidly developed in recent years. This review summarizes the advancement of sample preparation technologies for NSAIDs involving solid-phase extraction, solid-phase microextraction, liquid-phase microextraction, QuEChERS, and matrix solid-phase dispersion. Meanwhile, we overview and compare analytical technologies for NSAIDs, including liquid chromatography-based methods, gas chromatography-based methods, capillary electrophoresis, and sensors, particularly the development of liquid chromatography-based methods. Furthermore, we focus on their progress and conduct a comparison between their advantages and disadvantages.

Parkinson’s disease (PD) is a progressive age-related neurodegenerative disease whose annual incidence is increasing as populations continue to age. Although its pathogenesis has not been fully elucidated, oxidative stress has been shown to play an important role in promoting the occurrence and development of the disease. Long noncoding RNAs (lncRNAs), which are more than 200 nucleotides in length, are also involved in the pathogenesis of PD at the transcriptional level via epigenetic regulation, or at the post-transcriptional level by participating in physiological processes, including aggregation of the α-synuclein, mitochondrial dysfunction, oxidative stress, calcium stabilization, and neuroinflammation. LncRNAs and oxidative stress are correlated during neurodegenerative processes: oxidative stress affects the expression of multiple lncRNAs, while lncRNAs regulate many genes involved in oxidative stress responses. Oxidative stress and lncRNAs also affect other processes associated with neurodegeneration, including mitochondrial dysfunction and increased neuroinflammation that lead to neuronal death. Therefore, modulating the levels of specific lncRNAs may alleviate pathological oxidative damage and have neuroprotective effects. This review discusses the general mechanisms of oxidative stress, pathological mechanism underlying the role of oxidative stress in the pathogenesis of PD, and teases out the mechanisms through which lncRNAs regulate oxidative stress during PD pathogenesis, as well as identifies the possible neuroprotective mechanisms of lncRNAs. Reviewing published studies will help us further understand the mechanisms underlying the role of lncRNAs in the oxidative stress process in PD and to identify potential therapeutic strategies for PD.

It is widely accepted that trace elements have been implicated in various metabolic processes. Valproic acid (VPA) is a remarkably safe and effective antiepileptic drug. There is no consensus optio...

Traumatic brain injury (TBI) is a serious condition that poses a significant threat to human health globally. It is typically caused by direct trauma to the brain due to external forces such as impact or compression. The progression of TBI occurs in two stages based on physiological and pathological changes: primary and secondary brain injury. During the secondary stage, a large number of damage-associated molecular patterns (DAMPs) are released from injured cells into the extracellular space. These DAMPs trigger or exacerbate pathological conditions, including neuroinflammation, brain edema, diffuse axonal injury (DAI), and programmed cell death. The three main types of neural cells—neurons, microglia, and astrocytes—facilitate intercellular communication and functional crosstalk through the release and transmission of DAMPs. This forms the cellular foundation of secondary brain injury pathology. In the later stages of TBI, DAMPs are transported to various organs throughout the body via extracellular vesicles (EVs), leading to systemic changes and secondary injuries. Recent research has increasingly recognized the correlation between TBI and specific DAMPs. However, there remains a lack of comprehensive reviews exploring this relationship from a broader perspective. This review summarizes the primary pathological changes that occur after TBI, the types of DAMPs and their related signaling pathways, the role of DAMPs in mediating intercellular communication and neuronal crosstalk, the relationship between DAMPs and systemic changes following TBI. This study also highlights that DAMPs represent promising targets for the clinical diagnosis and treatment, which emphasizes the critical role of DAMPs in TBI.

PANX2 forms large-pore channels mediating ATP release in response to physiological and pathological stimuli. Although PANX2 shows involvements in glioma genesis, the underlying mechanism remains unclear. PANX2 mRNA expression was analyzed via Oncomine and was confirmed via Gene Expression Profiling Interactive Analysis (GEPIA). The influence of PANX2 on overall survival (OS) of glioma was evaluated using LinkedOmics and further assessed through Cox regression analysis. The correlated genes with PANX2 acquired from LinkedOmics were validated through GEPIA and cBioPortal. Protein-protein interaction (PPI) of these genes was then obtained using Search Tool for the Retrieval of Interacting Genes (STRING) and Cytoscape with MCODE plug-in. All the PANX2-related genes underwent Gene Ontology (GO) enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses. The correlation between PANX2 and cancer immune infiltrates was evaluated via Tumor Immune Estimation Resource (TIMER). A higher expression of PANX2 only revealed a better OS in brain low grade glioma (LGG). PANX2-related genes in LGG functionally enriched in neuroactive ligand-receptor interaction, synaptic vesicle cycle, and calcium signaling. The hub genes from highest module of PPI were mainly linked to chemical synaptic transmission, plasma membrane, neuropeptide, and the pathway of neuroactive ligand-receptor interaction. Besides, PANX2 expression was negatively associated with infiltrating levels of macrophage, dendritic cells, and CD4+ T cells. This study demonstrated that PANX2 likely participated in LGG pathogenesis by affecting multiple molecular pathways and immune-related processes. PANX2 was associated with LGG prognosis and might become a promising therapeutic target of LGG.