Neurochemistry international最新文献

{"title":"Astaxanthin inhibits the aggregation and cytotoxicity of tau4RDΔK280 via possible interaction with the aggregation-prone segments","authors":"Huahua Shi ,&nbsp;Yan Zhao","doi":"10.1016/j.neuint.2025.106103","DOIUrl":"10.1016/j.neuint.2025.106103","url":null,"abstract":"<div><div>Tauopathies are a group of neurodegenerative disorders characterized by the presence of abnormal aggregates of microtubule associated protein tau in the brain. In the most common tauopathy, Alzheimer's disease (AD), the aggregation of tau is closely linked with synaptic dysfunction and neuronal death, while targeting the aggregation of tau has been demonstrated to have therapeutic potential. Astaxanthin is a carotenoid with neuroprotective function, which has been shown to inhibit Aβ-induced pathology in AD animal and cell models. However, the effects of astaxanthin on tau aggregation and toxicity are much less explored. In this study, we generated a cell model of tauopathy overexpressing the amyloidogenic pro-aggregant tau repeat domains carrying the FTDP-17 mutation ΔK280 in N2a cells (N2a-tau_4RDΔK280). It was found that astaxanthin treatment alleviated the cytotoxicity of N2a-tau_4RDΔK280 cells while reducing the amount of tau_4RDΔK280 aggregates in the cells. Results from the thioflavin T aggregation assay demonstrated that astaxanthin inhibited the aggregation of tau_4RDΔK280 <em>in vitro</em>. Further analyses with transmission electron microscopy confirmed that astaxanthin reduced the formation of amyloid fibril structures of tau_4RDΔK280 <em>in vitro</em>. Thus, astaxanthin might inhibit the cytotoxicity of N2a-tau_4RDΔK280 cells by preventing the formation of tau_4RDΔK280 aggregates. Molecular docking simulation analyses revealed that astaxanthin was able to directly interact with tau_4RDΔK280 as well as several key aggregation-prone segments of tau protein. In conclusion, our results demonstrated that astaxanthin might exert neuroprotection by inhibiting the formation of tau aggregates via direct interaction with the key aggregation-prone segments.</div></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"192 ","pages":"Article 106103"},"PeriodicalIF":4.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145751434","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Alcohol disrupts neural differentiation through endoplasmic reticulum stress and PERK pathway activation","authors":"Zuohui Zhang,&nbsp;Wen Wen,&nbsp;Hong Lin,&nbsp;Di Hu,&nbsp;Hui Li,&nbsp;Jia Luo","doi":"10.1016/j.neuint.2025.106108","DOIUrl":"10.1016/j.neuint.2025.106108","url":null,"abstract":"<div><div>Prenatal alcohol exposure (PAE) can lead to fetal alcohol spectrum disorder (FASD), a condition marked by developmental brain defects that result in neurobehavioral and cognitive impairments. However, the underlying molecular mechanisms remain poorly understood. Brain development is a highly regulated process, with neurogenesis playing a crucial role. A key stage in this process is neural differentiation, which is essential for proper brain function. This study aims to investigate how alcohol disrupts neural differentiation. NE-4C cells, a neural stem cell line derived from the mouse embryonic brain, were utilized as an <em>in vitro</em> model. As an <em>in vivo</em> model, pregnant mice were exposed to alcohol between gestation days 14 and 16, after which newly formed neurons in the ventricular zone (VZ) were analyzed. To examine the role of endoplasmic reticulum (ER) stress, tunicamycin (TM), and MANF-deficient NE-4C cells were employed. Neural differentiation was assessed using immunofluorescence, immunoblotting and flow cytometry. Alcohol impaired the differentiation of NE-4C cells into neurons and astrocytes without impacting cell migration. It also induced ER stress, preferably activating the PERK pathway. Similarly, ER stress caused by TM and MANF deficiency disrupted neural differentiation and activated PERK. Inhibiting PERK mitigated alcohol-induced impairment of neuronal differentiation. PAE decreased the number of newly formed neurons in the VZ of fetal brain while having little effects on cell survival and proliferation. Inhibiting PERK partially reversed the reduction of new neurons caused by PAE. Thus, alcohol-induced ER stress, particularly PERK activation, may contribute to impaired neurogenesis linked to FASD.</div></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"192 ","pages":"Article 106108"},"PeriodicalIF":4.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145877444","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Interplay and intervention of epigenetic dysregulation in traumatic brain injury pathology","authors":"Samuel G. Faasen,&nbsp;Vijay Arruri,&nbsp;Reid S. Alisch","doi":"10.1016/j.neuint.2025.106094","DOIUrl":"10.1016/j.neuint.2025.106094","url":null,"abstract":"<div><div>Traumatic brain injury (TBI) occurs when an external mechanical force damages brain tissue, leading to temporary or lasting disturbances in brain structure and function. The heterogeneous molecular and phenotypic nature of TBI poses a major challenge to translating basic research discoveries into clinically effective interventions. Emerging evidence indicates that epigenetic and epitranscriptomic mechanisms, including histone modifications, DNA methylation, and RNA modifications, play pivotal roles in the molecular response to TBI. In this review, we discuss post-TBI epigenomic alterations with a focus on histone modifications, DNA methylation, and RNA modifications, and we highlight preclinical interventions that modulate these alterations and improve related post-TBI behavioral outcomes.</div></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"192 ","pages":"Article 106094"},"PeriodicalIF":4.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145627306","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Therapeutic potential of KATP channels in the attenuation of Parkinson's disease pathogenesis and progression – A review","authors":"Barbara Gundi ,&nbsp;Hio Lam Ho ,&nbsp;Xinyang Zhang ,&nbsp;Amanda He ,&nbsp;Danielle Xin ,&nbsp;Ana Flávia F. Ferreira ,&nbsp;Luiz Roberto Britto ,&nbsp;Zhong-Ping Feng ,&nbsp;Hong-Shuo Sun","doi":"10.1016/j.neuint.2025.106091","DOIUrl":"10.1016/j.neuint.2025.106091","url":null,"abstract":"<div><div>Parkinson's disease (PD) is one of the most prevalent progressive neurodegenerative diseases today. However, existing treatments primarily focus on symptom management rather than attenuating disease progression and pathogenesis. ATP-sensitive potassium (K_ATP) ion channels play a significant role in motor control and coordination within the basal ganglia and have been implicated in the dopaminergic depletion mechanisms underlying PD. Recent studies have explored the potential of K_ATP channel inhibitors to slow PD pathogenesis and progression. Both pharmacological inhibition and genetic inactivation of these channels have been shown to reduce oxidative stress, dopamine (DA) depletion, and subsequent motor deficits. Contrastingly, alternative evidence suggests that K_ATP channel openers (KCOs) may elicit similar effects, highlighting the need for further exploration of K_ATP-mediated DA depletion mechanisms in PD. Future studies expanding our understanding of the mechanistic action of K_ATP in PD are essential to effectively leverage the channel's potential as a therapeutic target for combating PD pathology.</div></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"192 ","pages":"Article 106091"},"PeriodicalIF":4.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145585674","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"GDNF-AS1 mediated LHX2/METTL3/NCOA4 axis inhibits glioma progression via induction of ferroptosis","authors":"Yangbo zhou,&nbsp;Zhongyue Liu,&nbsp;Wenjia Ma","doi":"10.1016/j.neuint.2025.106085","DOIUrl":"10.1016/j.neuint.2025.106085","url":null,"abstract":"<div><div>Glioma, particularly glioblastoma (GBM), represents the most aggressive primary brain tumor with limited treatment options and poor prognosis. Emerging evidence highlights ferroptosis induction as a promising therapeutic strategy, while long non-coding RNAs (lncRNAs) have gained attention as potential biomarkers and regulators in glioma pathogenesis. This study aimed to investigate the molecular mechanism of lncRNA Glial Cell Line-Derived Neurotrophic Factor Antisense RNA 1 (GDNF-AS1) in glioma cell ferroptosis through the LIM Homeobox 2 (LHX2)/Methyltransferase-Like 3 (METTL3)/Nuclear Receptor Coactivator 4 (NCOA4) pathway using Normal Human Astrocytes (NHA) and glioma cell lines (U87MG, T98G, U251, and A172), along with intracranial and subcutaneous xenotransplantation models established in BALB/c nude mice. Functional experiments demonstrated that GDNF-AS1, LHX2, and NCOA4 were downregulated while METTL3 was upregulated in glioma cells. GDNF-AS1 overexpression promoted mitochondrial damage and oxidative stress by enhancing ferroptosis, ultimately impairing glioma cell biological functions. METTL3 silencing augmented GDNF-AS1's effects, further exacerbating ferroptosis and oxidative stress while inhibiting glioma progression. Mechanistically, GDNF-AS1 recruited transcription factor LHX2 to upregulate its enrichment at the METTL3 promoter, thereby suppressing METTL3 transcription, reducing N6-Methyladenosine (m6A) levels, promoting NCOA4 expression, and inducing ferroautophagy and ferroptosis in glioma cells. These findings demonstrate that GDNF-AS1 inhibits glioma development by activating ferroptosis through the LHX2/METTL3/NCOA4 axis.</div></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"192 ","pages":"Article 106085"},"PeriodicalIF":4.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145585640","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tricyclic antidepressant amitriptyline potentiates brain-derived neurotrophic factor expression mediated by PKC delta–NF–kappa B signaling in primary cultured astrocytes with connexin43-knockdown","authors":"Nozomi Tokunaga,&nbsp;Rikako Fujimoto,&nbsp;Yoki Nakamura,&nbsp;Kazue Hisaoka-Nakashima,&nbsp;Norimitsu Morioka","doi":"10.1016/j.neuint.2025.106102","DOIUrl":"10.1016/j.neuint.2025.106102","url":null,"abstract":"<div><div>Depression is a major mental illness, and its underlying mechanisms remain unclear. Emerging evidence suggests that astrocytes, which play a crucial role in brain function, may be involved in the pathophysiology of depression. We previously showed that downregulation of astrocytic connexin43 (Cx43) enhances the antidepressant effect of amitriptyline. However, the precise molecular mechanisms underlying this phenomenon remain unknown. In the present study, we investigated the signaling pathways involved in the antidepressant action of amitriptyline using an <em>in vitro</em> model involving Cx43-knockdown astrocytes. We found that amitriptyline potentiated the expression of brain-derived neurotrophic factor (BDNF), a key neurotrophic factor, in Cx43-knockdown astrocytes. This potentiation was mediated by the activation of Gq protein-coupled lysophosphatidic acid (LPA) receptors, a pathway that was sensitized by Cx43 downregulation. We further demonstrated that this signaling cascade involved the activation of Protein Kinase C (PKC) δ and transcription factor NF-κB, but not the conventional BDNF transcription factor CREB. We propose that Cx43 downregulation enhances the antidepressant effect of amitriptyline by specifically engaging the Gq-PKCδ–NF–κB pathway. These findings suggest that Cx43 downregulation in astrocytes, which has been considered a pathological feature of depression, may paradoxically contribute to the therapeutic efficacy of antidepressants by sensitizing a specific signaling pathway. Our study provides new insights into the molecular mechanism of antidepressant action and highlights the potential role of astrocytic Cx43 in modulating therapeutic responses.</div></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"192 ","pages":"Article 106102"},"PeriodicalIF":4.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145751458","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"","authors":"","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"196 ","pages":""},"PeriodicalIF":4.0,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147614550","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Characterizing stroke-related cellular changes in the surviving neurons of mouse ischemic stroke","authors":"Takeshi Ikegami ,&nbsp;Tsutomu Sasaki ,&nbsp;Takashi Shimbo ,&nbsp;Tomomi Kitayama ,&nbsp;Yukari Yamamoto ,&nbsp;Yuya Ouchi ,&nbsp;Sho Yamazaki ,&nbsp;Shintaro Sugiyama ,&nbsp;Kumiko Nishiyama ,&nbsp;Yasufumi Gon ,&nbsp;Shuhei Okazaki ,&nbsp;Kenichi Todo ,&nbsp;Shigenobu Matsumura ,&nbsp;Katsuto Tamai ,&nbsp;Hideki Mochizuki","doi":"10.1016/j.neuint.2025.106086","DOIUrl":"10.1016/j.neuint.2025.106086","url":null,"abstract":"<div><div>Rapid restoration of cerebral blood flow through endovascular therapy is crucial for minimizing neuronal injury in ischemic stroke. This study characterized cellular and molecular alterations during the acute and subacute phases of distal middle cerebral artery occlusion (dMCAO) in mice using single-nucleus (snRNA-seq) and single-cell (scRNA-seq) RNA sequencing. C57BL/6 mice were assigned to control, sham, dMCAO 3-day, and dMCAO 14-day groups. snRNA-seq identified diverse cell populations, including neurons (glutamatergic and GABAergic), fibroblast-like cells, astrocytes, oligodendrocytes, microglia, endothelial cells, and pericytes. Microglia shifted from homeostatic (<em>Siglech</em>, <em>P2ry12</em>) to acute-phase (<em>Lgals1</em>, <em>Top2a</em>, <em>Mki67</em>) and disease-associated states, consistent with previous evidence confirming that our dataset captured stroke-related dynamics. snRNA-seq enabled efficient recovery and analysis of neurons, revealing stroke-induced cell state changes.; notably, glutamatergic neurons declined on day 3, while endothelial cells increased. Gene ontology analysis indicated neuronal death, autophagy, and cAMP biosynthesis pathways. Elevated <em>Syngap1</em>, <em>Ikbkb</em>, and <em>Rock1</em> expression across glutamatergic subclusters suggested roles in cell death–related mechanisms and vulnerability to ischemic injury. Dissociation of SynGAP1 from PSD-95 after ischemia may enhance ERK1/2 phosphorylation, whereas ischemic preconditioning suppresses this dissociation and prevents ERK1/2 overactivation. Immunohistochemistry confirmed <em>Syngap1</em> and cAMP response element-binding (CREB) pathway activation at 3 and 14 days post-ischemia, aligning with sequencing results. Suppressing CREB with pAAV-A-CREB reduced neuronal survival, underscoring its role in autophagy and neuroprotection. These findings provide mechanistic insight into stroke-induced molecular alterations and identify autophagy and cAMP pathways within the penumbra as promising therapeutic targets.</div></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"191 ","pages":"Article 106086"},"PeriodicalIF":4.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145501324","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Astrocytic HIF-1α/VEGF induces endothelial PI3K/Akt activation to accelerate post-ischemic angiogenesis upon LCN2 inhibition","authors":"Ning Tian ,&nbsp;Xiaoxia Li ,&nbsp;Yanlin Jiang ,&nbsp;Jungang Deng ,&nbsp;Hao Wang ,&nbsp;Bing Guo ,&nbsp;Meiling Chen ,&nbsp;Rujia Liao","doi":"10.1016/j.neuint.2025.106078","DOIUrl":"10.1016/j.neuint.2025.106078","url":null,"abstract":"<div><div>Therapeutic angiogenesis represents a pivotal yet underexplored avenue for functional recovery following cerebral ischemia. Although lipocalin-2 (LCN2) participates in neuropathological processes, its cell-type-specific regulation of post-ischemic vascular remodeling remains unknown. Here, we demonstrate that CRISPR/Cas9-mediated C8D1A astrocyte-like cells-specific LCN2 knockout significantly enhances vascular network formation in endothelial co-cultures under oxygen-glucose deprivation/reperfusion (OGD/R). Clinically, elevated LCN2 (GDS4521 dataset) correlates with poor stroke prognosis. Functional analyses revealed that AAV-shRNA-mediated LCN2 knockdown in photothrombotic stroke mice reduced infarct volume, attenuated peri-infarct neuronal loss, increased peri-infarct vascular density, and improved neurobehavioral outcomes at 7 days post-ischemia. Mechanistically, transcriptomic profiling identified hypoxia-inducible factor 1α (HIF-1α) as the master regulator of ischemia-induced angiogenesis. Molecular docking confirmed LCN2-HIF1α interaction. Furthermore, LCN2 ablation unleashes a HIF-1α/VEGF signaling cascade in C8D1A astrocyte-like cells, which activates endothelial phosphatidylinositol-3-kinase/protein kinase B (PI3K/Akt) via paracrine mechanisms to drive functional revascularization. These findings not only redefine ischemic pathophysiology but also pioneers LCN2 inhibition as a translational strategy to overcome the limitations of current pro-angiogenic therapies in cerebrovascular disease.</div></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"191 ","pages":"Article 106078"},"PeriodicalIF":4.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145306622","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Striatal injection of aminochrome in Wistar rats induces early-stage behavioral changes of Parkinson's disease and dopaminergic degeneration in the caudal and medial regions of the nigra pars compacta","authors":"Jéssica Teles-Souza ,&nbsp;Juciele Valeria Ribeiro de Oliveira ,&nbsp;Fillipe Mendes de Araújo ,&nbsp;Flávia Santos Sanches ,&nbsp;Lívia Bacelar de Jesus ,&nbsp;Suzane Lopes de Souza ,&nbsp;Amanda Dias Pinheiro Santos Brito ,&nbsp;Camilla Melo Oliveira Leite ,&nbsp;Gabriel de Jesus Ferrolho ,&nbsp;Emiliano Fernandez-Villalba ,&nbsp;Deise Souza Vilas Bôas ,&nbsp;Rejane Conceição Santana ,&nbsp;Silvia Lima Costa ,&nbsp;Maria Trinidad Herrero ,&nbsp;Victor Diogenes Amaral Silva","doi":"10.1016/j.neuint.2025.106083","DOIUrl":"10.1016/j.neuint.2025.106083","url":null,"abstract":"<div><div>Most preclinical Parkinson's disease (PD) models use neurotoxic agents to cause rapid dopaminergic neuron degeneration, mimicking the late stage of PD. That creates a gap in understanding early-stage pathophysiology, critical for neuroprotective therapies and early diagnosis. To replicate the prodromal stage of PD, it is pivotal that preclinical study models promote a slow and selective death of dopaminergic neurons, triggering degenerative processes and early symptoms. In this context, we investigated behavioral and neuronal changes using a model of unilateral aminochrome injection (6 nmol/6 μL) in the striatum of adult male Wistar rats (CEUA-ICS, Protocol 3006070223), focusing on subtle changes representative of the early stages of PD. On the fourteenth day after the stereotaxic injection, we observed behavioral impairments marked by a reduction of frequency of entries, time spent and distance traveled in the central quadrants in the open field test, reduction of frequency of rearing and grooming in the open field, as well as an increase in the rate of motor asymmetry in the cylinder test. In addition, we observed a decrease in the transition of animals through the elevated plus maze, with a reduction in the number of entries into the open arm. Immunohistochemical analyses indicated that aminochrome induces cytotoxicity for tyrosine hydroxylase-positive (TH⁺) cells and induces astrogliosis and microgliosis. Our findings show that striatal injection of aminochrome induces a reduction in the density of TH⁺ fibers in the striatum, a slight reduction in the number of dopaminergic neurons in the caudal and medial regions of the nigra pars compacta (SNpc), and subtle motor deficits typical of an early stage of PD. Here, we provided evidence that aminochrome can induce a rodent model of the prodromal stages of PD.</div></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"191 ","pages":"Article 106083"},"PeriodicalIF":4.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145476577","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}