Neurochemistry international最新文献

{"title":"Knockdown of repulsive guidance molecule a promotes polarization of microglia into an anti-inflammatory phenotype after oxygen-glucose deprivation-reoxygenation in vitro","authors":"Guanru Shen ,&nbsp;Hongmei Xiao ,&nbsp;Siyuan Huang,&nbsp;Xiaofan Yuan,&nbsp;Zhang Rongrong,&nbsp;Yue Ma,&nbsp;Xinyue Qin","doi":"10.1016/j.neuint.2023.105546","DOIUrl":"10.1016/j.neuint.2023.105546","url":null,"abstract":"<div><p><span><span>Repulsive guidance molecule<span> a (RGMa) is a glycosylphosphatidylinositol-anchored glycoprotein<span><span> that has been demonstrated to influence neuroinflammatory-related diseases in addition to regulating neuronal differentiation and survival during brain development. However, any function or mechanism of RGMa in the polarization of </span>microglia after </span></span></span>ischemic stroke remains unclear. In the current study, RGMa was found to be expressed at reduced levels in microglia after oxygen-glucose deprivation-reoxygenation (OGD/R) </span><em>in vitro</em><span><span>. RGMa overexpression induced HAPI microglia to predominantly polarize to the M1 phenotype, promoting the release of proinflammatory cytokines<span> and knockdown induced the M2 phenotype, promoting the release of anti-inflammatory cytokines. RGMa overexpression also regulated the polarization of HAPI microglia by inhibiting the transportation of peroxisome proliferator-activated receptor γ (PPARγ) from the nucleus to cytoplasm. The opposite effect resulted from RGMa-knockdown and was reversed by the PPARγ antagonist, GW9662. In addition, RGMa-knockdown HAPI microglial conditioned medium improved the survival of </span></span>oligodendrocytes after OGD/R </span><em>in vitro</em><span>. Thus, inhibition of RGMa may constitute a therapeutic strategy for reducing neuroinflammation after ischemic stroke.</span></p></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"170 ","pages":"Article 105546"},"PeriodicalIF":4.2,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10132010","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":"Mitigating neuroinflammation in Parkinson's disease: Exploring the role of proinflammatory cytokines and the potential of phytochemicals as natural therapeutics","authors":"Prashant Sharma,&nbsp;Abhinoy Kishore,&nbsp;Indranil De,&nbsp;Swarnima Negi,&nbsp;Gulshan Kumar,&nbsp;Sahil Bhardwaj,&nbsp;Manish Singh","doi":"10.1016/j.neuint.2023.105604","DOIUrl":"10.1016/j.neuint.2023.105604","url":null,"abstract":"<div><p><span>Parkinson's disease<span><span> (PD) is one of the most prevalent neuroinflammatory illnesses, characterized by the progressive loss of neurons in the brain. Proinflammatory cytokines play a key role in initiating and perpetuating </span>neuroinflammation, which can lead to the activation of </span></span>glial cells<span> and the deregulation of inflammatory pathways, ultimately leading to permanent brain damage<span><span>. Currently, available drugs for PD mostly alleviate symptoms but do not target underlying inflammatory processes. There is a growing interest in exploring the potential of phytochemicals<span><span> to mitigate neuroinflammation. Phytochemicals such as resveratrol, </span>apigenin<span><span><span>, catechin, </span>anthocyanins<span>, amentoflavone, </span></span>quercetin<span>, berberine<span>, and genistein<span> have been studied for their ability to scavenge free radicals and reduce proinflammatory cytokine levels in the brain. These plant-derived compounds offer a natural and potentially safe alternative to conventional drugs for managing neuroinflammation in PD and other neurodegenerative diseases. However, further research is necessary to elucidate their underlying mechanisms of action and clinical effectiveness. So, this review delves into the </span></span></span></span></span></span>pathophysiology<span> of PD and its intricate relationship with proinflammatory cytokines, and explores how their insidious contributions fuel the disease's initiation and progression via cytokine-dependent signaling pathways. Additionally, we tried to give an account of PD management using existing drugs along with their limitations. Furthermore, our aim is to provide a thorough overview of the diverse groups of phytochemicals, their plentiful sources, and the current understanding of their anti-neuroinflammatory properties. Through this exploration, we posit the innovative idea that consuming nutrient-rich phytochemicals could be an effective approach to preventing and treating PD.</span></span></span></p></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"170 ","pages":"Article 105604"},"PeriodicalIF":4.2,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10229355","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":"A review of studies on the implication of NLRP3 inflammasome for Parkinson’s disease and related candidate treatment targets","authors":"Nannan Zeng ,&nbsp;Qi Wang ,&nbsp;Chong Zhang ,&nbsp;Yali Zhou ,&nbsp;Jianguo Yan","doi":"10.1016/j.neuint.2023.105610","DOIUrl":"10.1016/j.neuint.2023.105610","url":null,"abstract":"<div><p><span>Parkinson's disease<span><span> (PD) is a neurodegenerative disease for which the prevalence is second only to </span>Alzheimer's disease (AD). This disease primarily affects people of middle and old age, significantly impacting their health and quality of life. The main pathological features include the degenerative nigrostriatal </span></span>dopaminergic<span><span><span> (DA) neuron loss and Lewy body (LB) formation. Currently, available PD medications primarily aim to alleviate clinical symptoms, however, there is no universally recognized therapy worldwide that effectively prevents, clinically treats, stops, or reverses the disease. Consequently, the evaluation and exploration of potential therapeutic targets for PD are of utmost importance. Nevertheless, the </span>pathophysiology<span> of PD remains unknown, and neuroinflammation mediated by </span></span>inflammatory cytokines<span><span> that prompts neuron death is fundamental for the progression of PD. The nucleotide-binding oligomerization domain-like receptor </span>pyrin<span><span> domain-containing 3 (NLRP3) inflammasome is a key complex of proteins linking the neuroinflammatory cascade in PD. Moreover, mounting evidence suggests that </span>traditional Chinese medicine<span> (TCM) alleviates PD by suppressing the NLRP3 inflammasome. This article aims to comprehensively review the available studies on the composition and activating mechanism of the NLRP3 inflammasome, along with its significance in PD pathogenesis and potential treatment targets. We also review natural products or synthetic compounds which reduce neuroinflammation via modulating NLRP3 inflammasome activity, aiming to identify new targets for future PD diagnosis and treatment through the exploration of NLRP3 inhibitors. Additionally, this review offers valuable references for developing new PD treatment methods.</span></span></span></span></p></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"170 ","pages":"Article 105610"},"PeriodicalIF":4.2,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10271931","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":"6-hydroxydopamine affects multiple pathways to induce cytotoxicity in differentiated LUHMES dopaminergic neurons","authors":"Nilufar Ali ,&nbsp;Mukta S. Sane ,&nbsp;Huiyuan Tang ,&nbsp;Jadon Compher ,&nbsp;Quinlan McLaughlin ,&nbsp;Christopher D. Jones ,&nbsp;Shivani Kaushal Maffi","doi":"10.1016/j.neuint.2023.105608","DOIUrl":"10.1016/j.neuint.2023.105608","url":null,"abstract":"<div><p>The debilitating effects of Parkinson's disease<span><span> (PD) progress over time and are pathophysiologically characterized by the formation of Lewy bodies<span> due to the accumulation of α-synuclein aggregates resulting in the death of dopaminergic<span> neurons. In the present study, we determined cell death pathways activated by acute exposure to 6-hydroxydopamine (6-OHDA) in differentiated LUHMES cells empirically followed by a 24 h toxin free interval, henceforth termed as washout/recovery period. Acute 6-OHDA exposure led to morphological changes in LUHMES cells and resulted in significant loss of neurite<span> length and neurite thickness. Generation of reactive oxygen species<span><span> and loss of mitochondrial membrane potential in the neuronal processes were persistent even after the recovery period. Our results show that 6-OHDA exposure leads to significant reduction in expression of mitochondrial </span>OXPHOS complexes I, II, and IV and activation of </span></span></span></span></span>caspase<span><span><span> mediated apoptotic cell death cascade as observed by enhanced protein expression of cleaved-PARP-1 and cleaved-Caspase-3. Immunofluorescence microscopy approach confirmed that cell death occurs independent of the </span>AIF<span> translocation to the nucleus. Our experimental model, led to a ∼5-fold lower α-synuclein monomer expression and, interestingly, resulted in loss of </span></span>protein ubiquitination<span> in whole cell lysates. Altogether, this work provides evidence of multiple pathways targeted by 6-OHDA in differentiated LUHMES cells and expands research avenues for addressing the knowledge gap regarding the effect of 6-OHDA in the ubiquitin proteasome system for PD therapies.</span></span></span></p></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"170 ","pages":"Article 105608"},"PeriodicalIF":4.2,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10595853","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":"BTD: A TRPC5 activator ameliorates mechanical allodynia in diabetic peripheral neuropathic rats by modulating TRPC5-CAMKII-ERK pathway","authors":"Pratik Adhya,&nbsp;Bhupesh Vaidya,&nbsp;Shyam Sunder Sharma","doi":"10.1016/j.neuint.2023.105609","DOIUrl":"10.1016/j.neuint.2023.105609","url":null,"abstract":"<div><p><span>Mechanical allodynia<span><span> is a serious complication of painful diabetic neuropathy (PDN) with limited treatment options. The transient </span>receptor potential canonical 5 (TRPC5) channel is a promising target in pain; however, its role in painful diabetic neuropathy has not yet been elucidated. In this study, we have investigated the role of TRPC5 channels using BTD [N-{3-(adamantan-2-yloxy)-propyl}-3-(6-methyl-1,1-dioxo-2H-1λ</span></span>⁶<span><span>,2,4-benzothiadiazin-3-yl)-propanamide)],a potent TRPC5 activator and HC070, as TRPC5 channel inhibitor in rat model of PDN. In this study, streptozotocin<span><span> was used to induce diabetes in male Sprague-Dawley rats. The alterations in mechanical and thermal pain thresholds, nerve functional deficits in diabetic animals were assessed by various behavioral and functional parameters.TRPC5 involvement was investigated by treating neuropathic rats with BTD, TRPC5 channel activator (1 and 3 mg/kg, i.p. for 14 days) and HC070, a TRPC5 channel inhibitor (1 and 3 mg/kg). BTD and HC070 effects in pain reduction were assessed by western blotting, estimating </span>oxidative stress<span> and inflammatory markers in the lumbar spinal cord. BTD treatment (3 mg/kg, i.p.) once daily for 14 days ameliorated mechanical allodynia but not thermal hyposensation or nerve functional deficit in diabetic neuropathic rats. BTD treatment down-regulated TRPC5 expression by increasing the activity of protein kinase C. It also subsequently down-regulated the downstream pain markers (CAMKII, ERK) in the spinal cord. Additionally, a decrease in </span></span></span>inflammatory cytokines (TNF-α, IL-6) also demonstrated BTD's potent anti-inflammatory properties in reducing mechanical allodynia. On the other hand, HC070 did not exert any beneficial effects on behavioural and nerve functional parameters. The study concludes that BTD ameliorated mechanical allodynia in a rat model of painful diabetic neuropathy not only through modulation of the TRPC5-CAMKII-ERK pathway but also through its anti-inflammatory and anti-apoptotic properties. Overall, BTD is a promising therapeutic molecule in the treatment of mechanical allodynia in painful diabetic neuropathy.</span></p></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"170 ","pages":"Article 105609"},"PeriodicalIF":4.2,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10170751","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":"HIF-1, an important regulator in potential new therapeutic approaches to ischemic stroke","authors":"Sneha Vatte,&nbsp;Rajesh Ugale","doi":"10.1016/j.neuint.2023.105605","DOIUrl":"10.1016/j.neuint.2023.105605","url":null,"abstract":"<div><p>Ischemic stroke<span><span><span> is a leading cause of disability and mortality worldwide due to the narrow therapeutic window<span><span> of the only approved therapies like intravenous thrombolysis and thrombectomy. Hypoxia inducible factor-1α (HIF-1α) is a sensitive regulator of oxygen </span>homeostasis, and its expression is rapidly induced after hypoxia/ischemia. It plays an extensive role in the </span></span>pathophysiology<span> of stroke by regulating multiple pathways including glucose metabolism<span><span>, angiogenesis, neuronal survival, </span>neuroinflammation<span> and blood brain barrier<span> regulation. Here, we give a brief overview of the HIF-1α-targeting strategies currently under investigation and summarise recent research on how HIF-1α is regulated in various brain cells, including neurons and microglia, at various stages in ischemic stroke. The roles of HIF-1 in stroke varies with </span></span></span></span></span>ischemic time<span> and degree of ischemia<span>, are still up for debate. More focus has been placed on prospective HIF-1α targeting drugs, such as HIF-1α activator, HIF-1α stabilizers, and natural compounds. In this review, we have highlighted the regulation of HIF-1α in the novel therapeutic approaches for treatment of stroke.</span></span></span></p></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"170 ","pages":"Article 105605"},"PeriodicalIF":4.2,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10188807","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 protective effects of EGCG was associated with HO-1 active and microglia pyroptosis inhibition in experimental intracerebral hemorrhage","authors":"Bing Bao ,&nbsp;Xiao-Ping Yin ,&nbsp;Xiao-Qing Wen ,&nbsp;Yi-Jun Suo ,&nbsp;Zhi-Ying Chen ,&nbsp;Dong -Ling Li ,&nbsp;Qin Lai ,&nbsp;Xian-Ming Cao ,&nbsp;Qiu-Min Qu","doi":"10.1016/j.neuint.2023.105603","DOIUrl":"10.1016/j.neuint.2023.105603","url":null,"abstract":"<div><p><span><span><span>Intracerebral hemorrhage (ICH), which has high mortality and disability rate is associated with microglial </span>pyroptosis and </span>neuroinflammation, and the effective treatment methods are limited Epigallocatechin-3-gallate (EGCG) has been found to play a cytoprotective role by regulating the anti-inflammatory response to pyroptosis in other </span>systemic diseases<span><span>. However, the role of EGCG in microglial pyroptosis and neuroinflammation after ICH remains unclear. In this study, we investigated the effects of EGCG pretreatment on neuroinflammation-mediated neuronal pyroptosis and the underlying </span>neuroprotective<span><span> mechanisms in experimental ICH. EGCG pretreatment was found to remarkably improved neurobehavioral performance, and decreased the hematoma<span> volume and cerebral edema in mice. We found that EGCG pretreatment attenuated the release of hemin-induced </span></span>inflammatory cytokines<span> (IL-1β, IL-18, and TNF-α). EGCG significantly upregulated the expression of heme oxygenase-1 (HO-1), and downregulated the levels of pyroptotic molecules and inflammatory cytokines including Caspase-1, GSDMD, NLRP3<span>, mature IL-1β, and IL-18. EGCG pretreatment also decreased the number of Caspase-1-positive microglia and GSDMD along with NLRP3-positive microglia after ICH. Conversely, an HO-1-specific inhibitor (ZnPP), significantly inhibited the anti-pyroptosis and anti-neuroinflammation effects of EGCG. Therefore, EGCG pretreatment alleviated microglial pyroptosis and neuroinflammation, at least in part through the Caspase-1/GSDMD/NLRP3 pathway by upregulating HO-1 expression after ICH. In addition, EGCG pretreatment promoted the polarization of microglia from the M1 phenotype to M2 phenotype after ICH. The results suggest that EGCG is a potential agent to attenuate neuroinflammation via its anti-pyroptosis effect after ICH.</span></span></span></span></p></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"170 ","pages":"Article 105603"},"PeriodicalIF":4.2,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41187311","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":"Cell membrane-based nanomaterials for therapeutics of neurodegenerative diseases","authors":"Phuong-Trang Nguyen-Thi ,&nbsp;Thuy Trang Nguyen ,&nbsp;Hoang Long Phan ,&nbsp;Thanh-Tam Ho ,&nbsp;Toi Van Vo ,&nbsp;Giau Van Vo","doi":"10.1016/j.neuint.2023.105612","DOIUrl":"10.1016/j.neuint.2023.105612","url":null,"abstract":"<div><p><span>Central nervous system (CNS) diseases such as Alzheimer's disease<span> (AD), Parkinson's disease<span><span> (PD), glioblastoma (GBM), and </span>peripheral nerve injury have been documented as incurable diseases, which lead to serious impacts on human health especially prevalent in the aging population worldwide. Most of the treatment strategies fail due to low efficacy, toxicity, and poor brain penetration. Recently, advancements in nanotechnology have helped alleviate the challenges associated with the application of cell membrane-based </span></span></span>nanomaterials<span> against CNS diseases. In the following review, the existing types of cell membrane-based nanomaterials systems which have improved therapeutic efficacy for CNS diseases would be described. A summary of recent progress in the incorporation of nanomaterials in cell membrane-based production, separation, and analysis will be provided. Addition to, challenges relate to large-scale manufacturing of cell membrane-based nanomaterials and future clinical trial of such platforms will be discussed.</span></p></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"170 ","pages":"Article 105612"},"PeriodicalIF":4.2,"publicationDate":"2023-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10260702","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":"Stable isotope tracing reveals disturbed cellular energy and glutamate metabolism in hippocampal slices of aged male mice","authors":"Laura Mikél McNair,&nbsp;Jens Velde Andersen,&nbsp;Helle Sønderby Waagepetersen","doi":"10.1016/j.neuint.2023.105626","DOIUrl":"10.1016/j.neuint.2023.105626","url":null,"abstract":"<div><p>Neurons and astrocytes work in close metabolic collaboration, linking neurotransmission to brain energy and neurotransmitter metabolism. Dysregulated energy metabolism is a hallmark of the aging brain and may underlie the progressive age-dependent cognitive decline. However, astrocyte and neurotransmitter metabolism remains understudied in aging brain research. In particular, how aging affects metabolism of glutamate, being the primary excitatory neurotransmitter, is still poorly understood. Here we investigated critical aspects of cellular energy metabolism in the aging male mouse hippocampus using stable isotope tracing <em>in vitro</em>. Metabolism of [U–¹³C]glucose demonstrated an elevated glycolytic capacity of aged hippocampal slices, whereas oxidative [U–¹³C]glucose metabolism in the TCA cycle was significantly reduced with aging. In addition, metabolism of [1,2–¹³C]acetate, reflecting astrocyte energy metabolism, was likewise reduced in the hippocampal slices of old mice. In contrast, uptake and subsequent metabolism of [U–¹³C]glutamate was elevated, suggesting increased capacity for cellular glutamate handling with aging. Finally, metabolism of [¹⁵N]glutamate was maintained in the aged slices, demonstrating sustained glutamate nitrogen metabolism. Collectively, this study reveals fundamental alterations in cellular energy and neurotransmitter metabolism in the aging brain, which may contribute to age-related hippocampal deficits.</p></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"171 ","pages":"Article 105626"},"PeriodicalIF":4.2,"publicationDate":"2023-10-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0197018623001547/pdfft?md5=d366e106edf34772f7a86e79c0c1d838&pid=1-s2.0-S0197018623001547-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41187313","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":"Epigenetic modification impacting brain functions: Effects of physical activity, micronutrients, caffeine, toxins, and addictive substances","authors":"Rahul Mallick ,&nbsp;Asim K. Duttaroy","doi":"10.1016/j.neuint.2023.105627","DOIUrl":"10.1016/j.neuint.2023.105627","url":null,"abstract":"<div><p>Changes in gene expression are involved in many brain functions. Epigenetic processes modulate gene expression by histone modification and DNA methylation or RNA-mediated processes, which is important for brain function. Consequently, epigenetic changes are also a part of brain diseases such as mental illness and addiction. Understanding the role of different factors on the brain epigenome may help us understand the function of the brain. This review discussed the effects of caffeine, lipids, addictive substances, physical activity, and pollutants on the epigenetic changes in the brain and their modulatory effects on brain function.</p></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"171 ","pages":"Article 105627"},"PeriodicalIF":4.2,"publicationDate":"2023-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0197018623001559/pdfft?md5=5e56433843f9dc5b7172595b906b7019&pid=1-s2.0-S0197018623001559-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41187312","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}