Neurotoxicology最新文献

{"title":"World Trade Center response activities and cognitive health: A moderated mediation study of the role of surgical/nuisance dust mask usage","authors":"Yuan Yang ,&nbsp;Jaymie Meliker ,&nbsp;Lauren L. Richmond ,&nbsp;Frank D. Mann ,&nbsp;Minos Kritikos ,&nbsp;Dylan M. Smith ,&nbsp;Tesleem Babalola ,&nbsp;Melissa A. Carr ,&nbsp;Benjamin J. Luft ,&nbsp;Sean A.P. Clouston","doi":"10.1016/j.neuro.2025.02.002","DOIUrl":"10.1016/j.neuro.2025.02.002","url":null,"abstract":"<div><h3>Objective</h3><div>This study explores the relationship between World Trade Center (WTC) response activities (WRAs) and cognitive impairment (CI) and uses a moderated-mediation model to examine the role of wearing a surgical/nuisance dust mask.</div></div><div><h3>Methods</h3><div>This study includes 3285 WTC responders. Responders were placed into eight WRA groups based on self-report structured responses and free-text descriptions of activities at the WTC. The presence/absence of surgical/nuisance dust mask usage was self-reported. The outcome was CI as determined using a Montreal Cognitive Assessment score &lt; 23. Robust Poisson regression was used to examine the main effect, and counterfactual moderated-mediation analysis was used to determine the role of mask usage.</div></div><div><h3>Results</h3><div>The risk of CI was higher across most WRAs when compared to supervision. Mask usage was reported by 63 % of responders and varied across WRAs and was associated with a reduced risk of CI (adjusted risk ratio [aRR]=0.77, p = 0.008) after controlling for WRAs. Moderation effects indicated that responders are more likely to wear masks when encountering more dangerous exposures, even within the same WRA group. Responders in the WRA-enclosed group had a lower risk of CI through a moderated intermediary effect of mask usage (aRR=0.92, p = 0.05).</div></div><div><h3>Conclusion</h3><div>Surgical/nuisance dust mask usage provided mild protection against air pollution exposures during WTC response activities when compared to not wearing a mask. Results suggest that response workers at disaster sites might benefit from wearing surgical/nuisance dust masks when respirators are unavailable even when the air seems safe.</div></div>","PeriodicalId":19189,"journal":{"name":"Neurotoxicology","volume":"108 ","pages":"Pages 1-10"},"PeriodicalIF":3.4,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143441550","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":"Polysaccharide alleviates neurodegeneration and behavioral deficit by enhancing mitochondrial autophagy in chronic methamphetamine mice","authors":"Han Yang ,&nbsp;Yuanhe Wang ,&nbsp;Shan Liu ,&nbsp;Shan Zhang ,&nbsp;Yuemeng Chen ,&nbsp;Jiuyang Ding ,&nbsp;Shunqin Chen ,&nbsp;Faze Zhu ,&nbsp;Bing Xia ,&nbsp;Peng Luo ,&nbsp;Yubo Liu","doi":"10.1016/j.neuro.2025.02.004","DOIUrl":"10.1016/j.neuro.2025.02.004","url":null,"abstract":"<div><div>Methamphetamine (METH) is a psychostimulant drug widely abused because of its addictive properties.Its impact on the central nervous system is a major area of interest due to its unique ability to cross the blood-brain barrier, facilitated by its dual water and lipid solubility. Studies have indicated that oxidative stress, neuroinflammation, neuronal apoptosis, and mitochondrial dysfunction are primary mechanisms of METH-induced neurotoxicity. Mitophagy, a process regulated by the phosphatase and tensin homolog deleted on chromosome 10 (PTEN) induced kinase 1 (PINK1)/Parkin signaling pathway, has emerged as a critical mechanism for preserving mitochondrial function. Polysaccharides derived from bamboo fungus have shown potential in mitigating neurotoxicity. However, the role of these polysaccharides in ameliorating methamphetamine-induced neurotoxicity remains unclear. This study aimed to investigate whether polysaccharides could alleviate neurodegeneration in a chronic METH mice model and elucidate the underlying mechanisms and elucidate the mechanisms underlying METH-induced neuronal damage.</div></div>","PeriodicalId":19189,"journal":{"name":"Neurotoxicology","volume":"107 ","pages":"Pages 53-61"},"PeriodicalIF":3.4,"publicationDate":"2025-02-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143425799","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":"Silver nanoparticle (AgNP), neurotoxicity, and putative adverse outcome pathway (AOP): A review","authors":"Julie Juyoung Park ,&nbsp;Elaine M. Faustman","doi":"10.1016/j.neuro.2025.02.001","DOIUrl":"10.1016/j.neuro.2025.02.001","url":null,"abstract":"<div><div>Various silver nanoparticles (AgNPs) exist with different sizes, coatings, and shapes. AgNPs have unique physical and chemical properties, such as high surface-to-volume ratio and antimicrobial properties, which allow them to be used in a wide array of applications in consumer products and medical applications, including clothing, cosmetics, food packaging, medical devices, and wound dressings. They are also one of the most studied engineered nanomaterials (ENMs). Though the liver and lung have been identified as the primary targets of AgNP exposures, an increasing number of studies have reported accumulations of AgNPs in the brains of AgNP-exposed animals. These findings have raised concerns because the brain plays a critical function in our body and may have difficulty clearing AgNPs, unlike the liver and lung. Studies have been conducted to investigate potential neurotoxicity effects of AgNP exposures, but they use various types of AgNPs and routes of administration, which makes it difficult to compare across studies. Therefore, the goal of this review was to (1) assess factors that may affect AgNP-induced neurotoxicity, (2) identify potential mechanisms of neurotoxicity exerted by AgNPs, (3) review existing <em>in vitro</em> dose-response and <em>in vivo</em> exposure-response AgNP-induced neurotoxicity studies, and (4) provide an example application of benchmark doses (BMDs) in comparing across different studies. A combination of aggregate exposure pathway (AEP) and adverse outcome pathway (AOP) framework was utilized to link AgNP exposure sources and routes to molecular initiating events (MIEs) and then to adverse neurotoxicity outcomes at the cellular, organ, organism, and population levels. This review is the first to propose an AEP/AOP specific to AgNP-induced neurotoxicity, which may contribute toward identifying plausible key event relationships between MIEs and adverse neurotoxicity outcomes and improving the current risk assessment of AgNPs.</div></div>","PeriodicalId":19189,"journal":{"name":"Neurotoxicology","volume":"108 ","pages":"Pages 11-27"},"PeriodicalIF":3.4,"publicationDate":"2025-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143389966","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 pranlukast against cuprizone-induced inflammatory demyelination and sensory impairment in mice: Comparison with fingolimod","authors":"Greice Nascimento Pires ,&nbsp;Renata Pereira Laurindo ,&nbsp;Luiza Dos Santos Heringer ,&nbsp;Stefanny Calixto da Silva ,&nbsp;Débora Magalhães Portela ,&nbsp;Ricardo Cardoso ,&nbsp;Ana Carolina de Pádua ,&nbsp;Ana Beatriz Miranda De Sá ,&nbsp;Saulo Augusto Alves Da Cruz ,&nbsp;Sheila Espírito Santo Araújo ,&nbsp;Ana Maria Blanco Martinez ,&nbsp;Milena Batista Carneiro ,&nbsp;Henrique Rocha Mendonça","doi":"10.1016/j.neuro.2025.01.004","DOIUrl":"10.1016/j.neuro.2025.01.004","url":null,"abstract":"<div><div>Inflammatory demyelination is present in debilitating diseases such as Multiple Sclerosis (MS). Several drugs are available for MS treatment, with fingolimod as a first-line oral option in the United States. However, a cure has yet to be established, and therapeutic failures are common, highlighting the need for continued research into new pharmacological targets. Pranlukast has shown positive effects on myelination in cell cultures and after LPC-induced demyelination in mice, but it is not yet part of the therapeutic arsenal for this disease. This study investigates pranlukast’s effect on demyelination protection in an MS animal model, compared to fingolimod. For this purpose, young adult Swiss mice were treated for five weeks with a 0.2 % cuprizone diet and received daily intraperitoneal injections of pranlukast (0.1 mg/kg), fingolimod (1 mg/kg), or vehicle. Pranlukast treatment, like fingolimod, partially preserved sensory function in the tactile sensitivity test. Both treatments partially preserved myelin basic protein (MBP) levels, but only fingolimod preserved lipids and myelinated fibers in the corpus callosum (CC) at all g-ratio ranges. Cuprizone and Pranlukast groups presented more microglia/macrophages in the CC, but fewer presenting reactive microglia/macrophages and less NOS2 staining in pranlukast-treated when compared to the cuprizone group, while fingolimod treatment prevented the increase in Iba1 in the CC. In summary, this study demonstrated that pranlukast is a good candidate as a novel drug for use in conditions of inflammatory demyelination, such as MS, by restoring function through modulation of the inflammatory environment.</div></div>","PeriodicalId":19189,"journal":{"name":"Neurotoxicology","volume":"107 ","pages":"Pages 37-52"},"PeriodicalIF":3.4,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143080649","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":"In silico and In vivo protective effect of biochanin-A mitigating doxorubicin- induced cognitive deficits and neuroinflammation: Insights to the role of p-Tau and miR-132","authors":"Sarah A. Hussein ,&nbsp;Mai F. Tolba ,&nbsp;Haidy E. Michel ,&nbsp;Amgad Albohy ,&nbsp;Samar S. Azab","doi":"10.1016/j.neuro.2025.01.003","DOIUrl":"10.1016/j.neuro.2025.01.003","url":null,"abstract":"<div><div>Doxorubicin (DOX)-induced chemobrain has been reported in several studies. Its main culprit is the induction of massive amounts of reactive oxygen species (ROS), hence triggering damage to brain tissues and thus leading to neuroinflammation. Biochanin A (BIO-A) is known to be an antioxidant, anti-inflammatory, and neuroprotective agent. An <em>in silico</em> study was designed to examine the potential neuroprotective effect of BIO-A. An <em>in vivo</em> study was used to evaluate the modulatory effect of BIO-A on cognitive impairment engendered by DOX. The <em>insilico</em> investigation proved the putative neuroprotective effect of BIO-A. In the <em>in vivo</em> study, BIO-A treatment counteracted DOX-induced memory deficits, as evidenced by improved spatial memory in rats compared to the DOX-only group. BIO-A also reversed DOX-triggered hippocampal neurodegeneration and neuroinflammation, supported by a significant decrease in tissue contents of NF-κB (p65) by 32 % and NLRP3 by 36 % versus the DOX-only group. BIO-A also abrogated DOX-induced neurodegneration, as evidenced by increasing SIRT1 content by 2-fold and BDNF content by 2-fold versus the DOX-only group in hippocampal tissues. In addition, BIO-A ameliorated DOX-augmented apoptosis in the hippocampus, as evidenced by lowering caspase-3 content in the hippocampus by 26 % versus the DOX-only group. Regarding tauopathy, BIO-A reversed DOX-increased tauopathy by 35 % versus the DOX-only group. The neuroprotectant miR-132 was increased by BIO-A in hippocampal tissues by 4-fold, contrary to the DOX-only group. Thus, BIO-A treatment modulated DOX-induced behavioral, histological, and molecular changes in the hippocampi of rats. Further studies are recommended to evaluate BIO-A in early clinical trials for the purpose of protection against chemobrain in cancer patients.</div></div>","PeriodicalId":19189,"journal":{"name":"Neurotoxicology","volume":"107 ","pages":"Pages 22-36"},"PeriodicalIF":3.4,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143029208","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":"BPDE induces ferroptosis in hippocampal neurons through ACSL3 suppression","authors":"Hui He ,&nbsp;Tingyu Ji ,&nbsp;Yi Lyu ,&nbsp;Fengjie Tian ,&nbsp;Emily Mu ,&nbsp;Sophia Mu ,&nbsp;Jinping Zheng","doi":"10.1016/j.neuro.2025.01.002","DOIUrl":"10.1016/j.neuro.2025.01.002","url":null,"abstract":"<div><div>Benzo(a)pyrene (B[<em>a</em>]P) and its ultimate active metabolite, benzo(a)pyrene-7,8-dihydrodiol-9,10-epoxide (BPDE), are known to have neurotoxic effects that can damage hippocampal neurons and cause cognitive impairments. Ferroptosis, a form of programmed cell death distinct from apoptosis, is associated with multiple neurodegenerative conditions. Recently, we have found that BPDE triggers ferroptosis in hippocampal neurons, though the underlying molecular mechanism remains unclear. Here, we firstly identified ACSL3 as the target of BPDE-induced ferroptosis through transcriptomics, and then investigated its role in ferroptosis using gene transfection technology in HT22 cells and primary hippocampal neurons. Our results showed that BPDE treatment caused significant transcriptional changes in HT22 cells, notably decreasing ACSL3 expression, which was further validated in both HT22 cells and primary hippocampal neurons. Furthermore, overexpression of ACSL3 effectively rescued the ferroptosis induced by BPDE in HT22 cells and primary mouse hippocampal neurons, characterized by increased cell viability, enhanced glutathione and glutathione peroxidase activities, and reduced levels of intracellular free Fe²⁺, reactive oxygen species, and malondialdehyde. In summary, our findings demonstrated that BPDE induces ferroptosis in hippocampal neurons by inhibiting ACSL3 expression, providing new insights into the toxicological mechanisms underlying BPDE-induced neurotoxicity.</div></div>","PeriodicalId":19189,"journal":{"name":"Neurotoxicology","volume":"107 ","pages":"Pages 11-21"},"PeriodicalIF":3.4,"publicationDate":"2025-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143008458","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":"The stoichiometry of the α4β2 neuronal nicotinic acetylcholine receptors determines the pharmacological properties of the neonicotinoids, and recently introduced butenolide and sulfoximine","authors":"Sara Kaaki ,&nbsp;Alison Cartereau ,&nbsp;Khalid Boussaine ,&nbsp;Emiliane Taillebois ,&nbsp;Steeve H. Thany","doi":"10.1016/j.neuro.2025.01.001","DOIUrl":"10.1016/j.neuro.2025.01.001","url":null,"abstract":"<div><div>Although neonicotinoids were considered safe for mammals for many decades, recent research has proven that these insecticides can alter cholinergic functions by interacting with neuronal nicotinic acetylcholine (ACh) receptors (nAChRs). One such receptor is the heteromeric α4β2 nAChR, which exists under two different stoichiometries: high sensitivity and low sensitivity α4β2 nAChRs. To replace these insecticides, new classes of insecticides have been developed, such as, sulfoximine, sulfoxaflor, and the butenolide, flupyradifurone. In this study, we injected <em>Xenopus laevis</em> oocytes with 1:10 and 10:1 α4:β2 subunit RNA ratios, in order to express the high (α4)₂(β2)₃ and low sensitivity (α4)₃(β2)₂ nAChRs. Using the two-electrode voltage-clamp technique, we found that the low sensitivity (α4)₃(β2)₂ nAChRs were activated by all tested insecticides, whereas the high sensitivity (α4)₂(β2)₃ nAChR was only activated by ACh. Imidacloprid, sulfoxaflor and flupyradifurone confirmed their agonist effects by reducing the responses to the ACh EC₈₀ concentrations, for both low (α4)₃(β2)₂ and high sensitivity (α4)₂(β2)₃ stoichiometries. Clothianidin only inhibited ACh responses of the low sensitivity (α4)₃(β2)₂ stoichiometry. Mutation E226P in the α4 subunit of the low sensitivity (α4)₃(β2)₂ receptors inhibits the agonist potency of imidacloprid and flupyradifurone, whereas mutation L273T (in the β2 subunit) in the high sensitivity (α4)₂(β2)₃ nAChR leads to activation by all insecticides. Major agonist effects were found with the double mutation of the E226P in the α4 subunit, and the L273T in the β2 subunit of the high sensitivity (α4)₂(β2)₃ stoichiometry.</div></div>","PeriodicalId":19189,"journal":{"name":"Neurotoxicology","volume":"107 ","pages":"Pages 1-10"},"PeriodicalIF":3.4,"publicationDate":"2025-01-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142971710","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Acyclovir provides protection against 6-OHDA-induced neurotoxicity in SH-SY5Y cells through the kynurenine pathway","authors":"Selma Sezen ,&nbsp;Mehmet Karadayi ,&nbsp;Fatma Yesilyurt ,&nbsp;Feyza Burul ,&nbsp;Yusuf Gulsahin ,&nbsp;Mustafa Ozkaraca ,&nbsp;Ufuk Okkay ,&nbsp;Medine Gulluce","doi":"10.1016/j.neuro.2024.11.005","DOIUrl":"10.1016/j.neuro.2024.11.005","url":null,"abstract":"<div><div>Parkinson's disease is one of the most prevalent neurodegenerative disorders worldwide. The kynurenine pathway associated with oxidative stress and neuroinflammation is recognized to contribute to its pathophysiology, although the exact mechanism is not fully elucidated. In neuroinflammation, IDO-1 catalyzes the conversion of tryptophan to neurotoxic QUIN through the kynurenine pathway. Consequently, QUIN increases oxidative stress via nNOS and NMDA, which causes neurodegeneration. Few studies have reported on the effect of different antiviral drugs in Parkinson's disease; the exact mechanism is still unknown. The antiviral acyclovir has been shown to have neuroprotective properties and can cross the blood-brain barrier. We examined acyclovir's effects and potential mechanisms in the 6-OHDA-induced <em>in vitro</em> model of Parkinson's disease in SH-SY5Y cells using biochemical, immunocytochemical, and <em>in silico</em> methods. MTT assay demonstrated that acyclovir significantly decreased cell mortality induced by the neurotoxic 6-OHDA at dosages of 3.2 µM, 6.4 µM, 12.8 µM, 25.6 µM, and 51.2 µM. In immunocytochemical analysis, acyclovir treatment decreased α-synuclein and TNF-α expressions in cells. In biochemical analyses, while IL-17A and TOS levels decreased depending on varying doses (1.6 µM, 3.2 µM, 6.4 µM, 12.8 µM), TAC levels increased. Using <em>in silico</em> analyses to investigate the mechanism showed that acyclovir docked with TNF-α, IL-17A, IDO-1, nNOS, α-synuclein, and NMDA. The findings demonstrated that acyclovir had neuroprotective effects by modulating the kynurenine pathway and decreasing neurodegeneration via QUIN inhibition in an <em>in vitro</em> Parkinson's disease model. Although the mechanisms of acyclovir's effects in Parkinson's disease are unclear, the results obtained from the experiments are encouraging.</div></div>","PeriodicalId":19189,"journal":{"name":"Neurotoxicology","volume":"106 ","pages":"Pages 1-9"},"PeriodicalIF":3.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142770781","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":"Smoking, coffee intake, and Parkinson’s disease: Potential protective mechanisms and components","authors":"Sa Weon Hong,&nbsp;Rachel Page,&nbsp;Penelope Truman","doi":"10.1016/j.neuro.2024.12.003","DOIUrl":"10.1016/j.neuro.2024.12.003","url":null,"abstract":"<div><div>Parkinson’s disease (PD) is a common progressive neurodegenerative disease characterized by the loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc). Environmental and lifestyle factors, such as smoking and coffee drinking, have been associated with a decreased risk for PD. However, the biological mechanisms underlying protective effects on PD are still not fully understood. It has been suggested that non-nicotine components in cigarette smoke and non-caffeine components in coffee may contribute to this protective effect. The aim of this review was to explore candidate molecules and mechanisms behind the effects of smoking and coffee drinking on PD by integrating findings from previous studies. By cross-referencing an index of tobacco constituents and a list of coffee constituents with existing literature on natural compounds and their structural analogs that show inhibitory activities against monoamine oxidase B, catechol <em>O</em>-methyltransferase, and α-synuclein fibrillation, we have identified tobacco and coffee components that inhibit these targets. Furthermore, tobacco and coffee components potentially play roles in suppressing neuroinflammation, activating the Nrf2 pathway as natural activators, and altering the gut microbiome. This review suggests that the phenolic compounds from tobacco and coffee investigated may contribute to the low incidence of PD in smokers and coffee drinkers, showing moderate to strong potential as therapeutic interventions. The current review suggests that multifunctional molecules found in coffee and cigarette smoke may have potential neuroprotective effects, but none of the data indicates that multifunctionality is required for these effects. This review will deepen our understanding of how smoking and coffee drinking are linked to a reduced risk of PD and will also be important in elucidating the mechanisms underlying the protective effects of smoking and coffee drinking on PD.</div></div>","PeriodicalId":19189,"journal":{"name":"Neurotoxicology","volume":"106 ","pages":"Pages 48-63"},"PeriodicalIF":3.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142864684","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"In memoriam: Bernard Jortner, professor emeritus of biomedical sciences and pathobiology","authors":"","doi":"10.1016/j.neuro.2024.10.013","DOIUrl":"10.1016/j.neuro.2024.10.013","url":null,"abstract":"","PeriodicalId":19189,"journal":{"name":"Neurotoxicology","volume":"106 ","pages":"Pages 46-47"},"PeriodicalIF":3.4,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142854781","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}