Journal of Neurochemistry最新文献

筛选
英文 中文
Presenilin deficiency enhances tau phosphorylation and its secretion 缺乏 Presenilin 会增强 tau 的磷酸化及其分泌。
IF 4.2 3区 医学
Journal of Neurochemistry Pub Date : 2024-07-01 DOI: 10.1111/jnc.16155
Yang Sun, Sadequl Islam, Yuan Gao, Tomohisa Nakamura, Taisuke Tomita, Makoto Michikawa, Kun Zou
{"title":"Presenilin deficiency enhances tau phosphorylation and its secretion","authors":"Yang Sun,&nbsp;Sadequl Islam,&nbsp;Yuan Gao,&nbsp;Tomohisa Nakamura,&nbsp;Taisuke Tomita,&nbsp;Makoto Michikawa,&nbsp;Kun Zou","doi":"10.1111/jnc.16155","DOIUrl":"10.1111/jnc.16155","url":null,"abstract":"<p>Alzheimer's disease (AD) is characterized by the accumulation of abnormally folded amyloid β-protein (Aβ) in the brain parenchyma and phosphorylated tau in neurons. Presenilin (PS, <i>PSEN</i>) 1 and PS2 are essential components of γ-secretase, which is responsible for the cleavage of amyloid precursor protein (APP) to generate Aβ. <i>PSEN</i> mutations are associated with tau aggregation in frontotemporal dementia, regardless of the presence or absence of Aβ pathology. However, the mechanism by which PS regulates tau aggregation is still unknown. Here, we found that tau phosphorylation and secretion were significantly increased in PS double–knock-out (PS1/2<sup>−/−</sup>) fibroblasts compared with wild-type fibroblasts. Tau-positive vesicles in the cytoplasm were significantly increased in PS1/2<sup>−/−</sup> fibroblasts. Active GSK-3β was increased in PS1/2<sup>−/−</sup> fibroblasts, and inhibiting GSK3β activity in PS1/2<sup>−/−</sup> fibroblasts resulted in decreased tau phosphorylation and secretion. Transfection of WT human PS1 and PS2 reduced the secretion of phosphorylated tau and active GSK-3β in PS1/2<sup>−/−</sup> fibroblasts. However, PS1D257A without γ-secretase activity did not decrease the secretion of phosphorylated tau. Furthermore, nicastrin deficiency also increased tau phosphorylation and secretion. These results suggest that deficient PS complex maturation may increase tau phosphorylation and secretion. Thus, our studies discover a new pathway by which PS regulates tau phosphorylation/secretion and pathology independent of Aβ and suggest that PS serves as a potential therapeutic target for treating neurodegenerative diseases involving tau aggregation.\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>","PeriodicalId":16527,"journal":{"name":"Journal of Neurochemistry","volume":null,"pages":null},"PeriodicalIF":4.2,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141468754","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}
引用次数: 0
Identification of z-axis filopodia in growth cones using super-resolution microscopy 利用超分辨率显微镜识别生长锥中的 Z 轴丝状体
IF 4.2 3区 医学
Journal of Neurochemistry Pub Date : 2024-07-01 DOI: 10.1111/jnc.16162
Motohiro Nozumi, Yuta Sato, Miyako Nishiyama-Usuda, Michihiro Igarashi
{"title":"Identification of z-axis filopodia in growth cones using super-resolution microscopy","authors":"Motohiro Nozumi,&nbsp;Yuta Sato,&nbsp;Miyako Nishiyama-Usuda,&nbsp;Michihiro Igarashi","doi":"10.1111/jnc.16162","DOIUrl":"10.1111/jnc.16162","url":null,"abstract":"<p>A growth cone is a highly motile tip of an extending axon that is crucial for neural network formation. Three-dimensional-structured illumination microscopy, a type of super-resolution light microscopy with a resolution that overcomes the optical diffraction limitation (ca. 200 nm) of conventional light microscopy, is well suited for studying the molecular dynamics of intracellular events. Using this technique, we discovered a novel type of filopodia distributed along the <i>z</i>-axis (“z-filopodia”) within the growth cone. Z-filopodia were typically oriented in the direction of axon growth, not attached to the substratum, protruded spontaneously without microtubule invasion, and had a lifetime that was considerably shorter than that of conventional filopodia. Z-filopodia formation and dynamics were regulated by actin-regulatory proteins, such as vasodilator-stimulated phosphoprotein, fascin, and cofilin. Chromophore-assisted laser inactivation of cofilin induced the rapid turnover of z-filopodia. An axon guidance receptor, neuropilin-1, was concentrated in z-filopodia and was transported together with them, whereas its ligand, semaphorin-3A, was selectively bound to them. Membrane domains associated with z-filopodia were also specialized and resembled those of lipid rafts, and their behaviors were closely related to those of neuropilin-1. The results suggest that z-filopodia have unique turnover properties, and unlike xy-filopodia, do not function as force-generating structures for axon extension.\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>","PeriodicalId":16527,"journal":{"name":"Journal of Neurochemistry","volume":null,"pages":null},"PeriodicalIF":4.2,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141468724","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}
引用次数: 0
Pathological remodeling of reactive astrocytes: Involvement of DNA methylation and downregulation of homeostatic genes 反应性星形胶质细胞的病理重塑:DNA 甲基化和同源基因下调的参与
IF 4.2 3区 医学
Journal of Neurochemistry Pub Date : 2024-06-29 DOI: 10.1111/jnc.16164
Dante Gómez Cuautle, Soledad Donna, María Belén Cieri, Alejandro Villarreal, Alberto Javier Ramos
{"title":"Pathological remodeling of reactive astrocytes: Involvement of DNA methylation and downregulation of homeostatic genes","authors":"Dante Gómez Cuautle,&nbsp;Soledad Donna,&nbsp;María Belén Cieri,&nbsp;Alejandro Villarreal,&nbsp;Alberto Javier Ramos","doi":"10.1111/jnc.16164","DOIUrl":"10.1111/jnc.16164","url":null,"abstract":"<p>Astrocytes provide metabolic support to neurons, maintain ionic and water homeostasis, and uptake and recycle neurotransmitters. After exposure to the prototypical PAMP lipopolysaccharide (LPS), reactive astrocytes increase the expression of pro-inflammatory genes, facilitating neurodegeneration. In this study, we analyzed the expression of homeostatic genes in astrocytes exposed to LPS and identified the epigenetic factors contributing to the suppression of homeostatic genes in reactive astrocytes. Primary astrocytic cultures were acutely exposed to LPS and allowed to recover for 24, 72 h, and 7 days. As expected, LPS exposure induced reactive astrogliosis and increased the expression of pro-inflammatory IL-1B and IL-6. Interestingly, the acute exposure resulted in persistent hypermethylation of astroglial DNA. Similar hypermethylation was observed in highly reactive astrocytes from the traumatic brain injury (TBI) penumbra in vivo. Hypermethylation was accompanied by decreased expression of homeostatic genes including LDHA and Scl16a1 (MCT1) both involved in the lactate shuttle to neurons; glutamine synthase (GS) responsible for glutamate processing; Kcnj10 (Kir4.1) important for K<sup>+</sup> homeostasis, and the water channel aquaporin-4 (Aqp4). Furthermore, the master regulator of DNA methylation, MAFG-1, as well as DNA methyl transferases DNMT1 and DNMT3a were overexpressed. The downregulation of homeostatic genes correlated with increased methylation of CpG islands in their promoters, as assessed by methylation-sensitive PCR and increased DNMT3a binding to the GS promoter. Treatment with decitabine, a DNMT inhibitor, prevented the LPS- and the HMGB-1-induced downregulation of homeostatic genes. Decitabine treatment also prevented the neurotoxic effects of these astrocytes in primary cortical cultures. In summary, our findings reveal that the pathological remodeling of reactive astrocytes encompasses not only the pro-inflammatory response but, significantly, also entails a long-term suppression of homeostatic gene expression with methylation of crucial CpG islands within their promoters.\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>","PeriodicalId":16527,"journal":{"name":"Journal of Neurochemistry","volume":null,"pages":null},"PeriodicalIF":4.2,"publicationDate":"2024-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141468725","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}
引用次数: 0
Cerebrospinal fluid concentration gradients of catechols in synucleinopathies 突触核蛋白病中脑脊液儿茶酚的浓度梯度。
IF 4.2 3区 医学
Journal of Neurochemistry Pub Date : 2024-06-28 DOI: 10.1111/jnc.16168
David S. Goldstein, Patti Sullivan, Courtney Holmes
{"title":"Cerebrospinal fluid concentration gradients of catechols in synucleinopathies","authors":"David S. Goldstein,&nbsp;Patti Sullivan,&nbsp;Courtney Holmes","doi":"10.1111/jnc.16168","DOIUrl":"10.1111/jnc.16168","url":null,"abstract":"<p>The synucleinopathies Parkinson disease (PD), multiple system atrophy (MSA), and the Lewy body form of pure autonomic failure (PAF) entail intra-cytoplasmic deposition of the protein alpha-synuclein and pathogenic catecholaminergic neurodegeneration. Cerebrospinal fluid (CSF) levels of catecholamines and their metabolites are thought to provide a “neurochemical window” on central catecholaminergic innervation and can identify specific intra-neuronal dysfunctions in synucleinopathies. We asked whether there are CSF concentration gradients for catechols such as 3,4-dihydroxyphenylacetic acid (DOPAC), the main neuronal metabolite of dopamine, and if so whether the gradients influence neurochemical differences among synucleinopathies. In a retrospective cohort study, we reviewed data about concentrations of catechols in the first, sixth, and twelfth 1-mL aliquots from 33 PD, 28 MSA, and 15 PAF patients and 41 controls. There were concentration gradients for DOPAC, dopamine, norepinephrine, and 3,4-dihydroxyphenylglycol (the main neuronal metabolite of norepinephrine) and gradients in the opposite direction for 5-S-cysteinyldopa and 5-S-cysteinyldopamine. In all 3 aliquots, CSF DOPAC was low in PD and MSA compared with controls (<i>p</i> &lt; 0.0001 each) and normal in PAF. Synucleinopathies differ in CSF catechols regardless of concentration gradients. Concentration gradients for 5-S-cysteinyl derivatives in opposite directions from the parent catechols may provide biomarkers of spontaneous oxidation in the CSF space.\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>","PeriodicalId":16527,"journal":{"name":"Journal of Neurochemistry","volume":null,"pages":null},"PeriodicalIF":4.2,"publicationDate":"2024-06-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jnc.16168","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141468723","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}
引用次数: 0
Cdk5 inhibition in the SOD1G93A transgenic mouse model of amyotrophic lateral sclerosis suppresses neurodegeneration and extends survival 在肌萎缩性脊髓侧索硬化症 SOD1G93A 转基因小鼠模型中抑制 Cdk5 可抑制神经变性并延长存活时间。
IF 4.2 3区 医学
Journal of Neurochemistry Pub Date : 2024-06-27 DOI: 10.1111/jnc.16160
Ahwon Kim, Do-Yeon Lee, Jung-Joon Sung
{"title":"Cdk5 inhibition in the SOD1G93A transgenic mouse model of amyotrophic lateral sclerosis suppresses neurodegeneration and extends survival","authors":"Ahwon Kim,&nbsp;Do-Yeon Lee,&nbsp;Jung-Joon Sung","doi":"10.1111/jnc.16160","DOIUrl":"10.1111/jnc.16160","url":null,"abstract":"<p>Deregulated cyclin-dependent kinase 5 (Cdk5) activity closely correlates with hyperphosphorylated tau, a common pathology found in neurodegenerative diseases. Previous postmortem studies had revealed increased Cdk5 immunoreactivity in amyotrophic lateral sclerosis (ALS); hence, we investigated the effects of Cdk5 inhibition on ALS model mice and neurons in this study. For the in vitro study, motor neuron cell lines with wild-type superoxide dismutase 1 (SOD1) or SOD1<sup>G93A</sup> and primary neuronal cultures from SOD1<sup>G93A</sup> transgenic (TG) mice or non-TG mice were compared for the expression of proteins involved in tau pathology, neuroinflammation, apoptosis, and neuritic outgrowth by applying Cdk5-small interfering RNA or Cdk5-short hairpin RNA (shRNA). For the in vivo study, SOD1<sup>G93A</sup> mice and non-TG mice were intrathecally injected with adeno-associated virus 9 (AAV9)-scramble (SCR)-shRNA or AAV9-Cdk5-shRNA at the age of 5 weeks. Weight and motor function were measured three times per week from 60 days of age, longevity was evaluated, and the tissues were collected from 90-day-old or 120-day-old mice. Neurons with SOD1<sup>G93A</sup> showed increased phosphorylated tau, attenuated neuritic growth, mislocalization of SOD1, and enhanced neuroinflammation and apoptosis, all of which were reversed by Cdk5 inhibition. Weights did not show significant differences among non-TG and SOD1<sup>G93A</sup> mice with or without Cdk5 silencing. SOD1<sup>G93A</sup> mice treated with AAV9-Cdk5-shRNA showed significantly delayed disease onset, delayed rotarod failure, and prolonged survival compared with those treated with AAV9-SCR-shRNA. The brain and spinal cord of SOD1<sup>G93A</sup> mice intrathecally injected with AAV9-Cdk5-shRNA exhibited suppressed tau pathology, neuroinflammation, apoptosis, and an increased number of motor neurons compared to those of SOD1<sup>G93A</sup> mice injected with AAV9-SCR-shRNA. Cdk5 inhibition could be an important mechanism in the development of a new therapeutic strategy for ALS.\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>","PeriodicalId":16527,"journal":{"name":"Journal of Neurochemistry","volume":null,"pages":null},"PeriodicalIF":4.2,"publicationDate":"2024-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jnc.16160","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141457480","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}
引用次数: 0
Fecal microbiota transplantation ameliorates high-fat diet-induced memory impairment in mice 粪便微生物群移植可改善高脂饮食引起的小鼠记忆损伤。
IF 4.2 3区 医学
Journal of Neurochemistry Pub Date : 2024-06-27 DOI: 10.1111/jnc.16156
Louise Tavares Garcia Pereira, Wembley Rodrigues Vilela, Paula Maria Quaglio Bellozi, Daiane Fátima Engel, Gabriela Cristina de Paula, Rafael Rocha de Andrade, Márcia Renata Mortari, Marcus de Melo Teixeira, Claudia Coleine, Cláudia Pinto Figueiredo, Andreza Fabro de Bem, Angélica Amorim Amato
{"title":"Fecal microbiota transplantation ameliorates high-fat diet-induced memory impairment in mice","authors":"Louise Tavares Garcia Pereira,&nbsp;Wembley Rodrigues Vilela,&nbsp;Paula Maria Quaglio Bellozi,&nbsp;Daiane Fátima Engel,&nbsp;Gabriela Cristina de Paula,&nbsp;Rafael Rocha de Andrade,&nbsp;Márcia Renata Mortari,&nbsp;Marcus de Melo Teixeira,&nbsp;Claudia Coleine,&nbsp;Cláudia Pinto Figueiredo,&nbsp;Andreza Fabro de Bem,&nbsp;Angélica Amorim Amato","doi":"10.1111/jnc.16156","DOIUrl":"10.1111/jnc.16156","url":null,"abstract":"<p>Gut dysbiosis is linked to metabolic and neurodegenerative diseases and comprises a plausible link between high-fat diet (HFD) and brain dysfunction. Here we show that gut microbiota modulation by either antibiotic treatment for 5 weeks or a brief 3-day fecal microbiota transplantation (FMT) regimen from low-fat (control) diet-fed mice decreased weight gain, adipose tissue hypertrophy, and glucose intolerance induced by HFD in C57BL/6 male mice. Notably, gut microbiota modulation by FMT completely reversed impaired recognition memory induced by HFD, whereas modulation by antibiotics had less pronounced effect. Improvement in recognition memory by FMT was accompanied by decreased HFD-induced astrogliosis in the hippocampal cornu ammonis region. Gut microbiome composition analysis indicated that HFD diminished microbiota diversity compared to control diet, whereas FMT partially restored the phyla diversity. Our findings reinforce the role of the gut microbiota on HFD-induced cognitive impairment and suggest that modulating the gut microbiota may be an effective strategy to prevent metabolic and cognitive dysfunction associated with unfavorable dietary patterns.\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>","PeriodicalId":16527,"journal":{"name":"Journal of Neurochemistry","volume":null,"pages":null},"PeriodicalIF":4.2,"publicationDate":"2024-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141457484","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}
引用次数: 0
Chronic ecologically relevant stress effects on reverse-translated touchscreen assays of reward responsivity and attentional processes in male rats: Implications for depression 慢性生态相关压力对雄性大鼠奖赏反应性和注意过程的反向翻译触摸屏测定的影响:对抑郁症的影响
IF 4.2 3区 医学
Journal of Neurochemistry Pub Date : 2024-06-24 DOI: 10.1111/jnc.16157
Paloma Martinez Gonzalez, Amaya R. Jenkins, Kayleigh S. LaMalfa, Brian D. Kangas
{"title":"Chronic ecologically relevant stress effects on reverse-translated touchscreen assays of reward responsivity and attentional processes in male rats: Implications for depression","authors":"Paloma Martinez Gonzalez,&nbsp;Amaya R. Jenkins,&nbsp;Kayleigh S. LaMalfa,&nbsp;Brian D. Kangas","doi":"10.1111/jnc.16157","DOIUrl":"10.1111/jnc.16157","url":null,"abstract":"<p>Stagnation in the development of novel therapeutic strategies for treatment-resistant depression has encouraged continued interest in improving preclinical methods. One tactic prioritizes the reverse translation of behavioral tasks developed to objectively quantify depressive phenotypes in patient populations for their use in laboratory animals via touchscreen technology. After cross-species concordance in task outcomes under healthy conditions is confirmed, construct validity can be further enhanced by identifying environmental stressors that reliably produce deficits in task performance that resemble those in depressive participants. The present studies characterized in male rats the ability of two chronic ecologically relevant stressors, inescapable ice water or isolated restraint, to produce depressive-like behavioral phenotypes in the Probabilistic Reward Task (PRT) and Psychomotor Vigilance Task (PVT). These tasks previously have been reverse-translated using touchscreen technology for rodents and nonhuman primates to objectively quantify, respectively, reward responsivity (anhedonia) and attentional processes (impaired cognitive function), each of which are core features of major depressive disorder. In the PRT, both inescapable ice water and isolated restraint produced persistent anhedonic phenotypes compared to non-stressed control performance (i.e., significantly blunted response bias for the richly rewarded stimulus). In the PVT, both chronic stressors impaired attentional processing, revealed by increases in titrated reaction times; however, these deficits largely subsided by the end of the chronic condition. Taken together, these findings confirm the ability of reverse-translated touchscreen tasks to effectively generate behavioral phenotypes that exhibit expected deficits in performance outcomes following exposure to chronic ecologically relevant stress. In turn, this approach is well positioned to appraise the ability of candidate therapeutics to attenuate or reverse such behavioral deficits and, thereby, contribute to preclinical medications development for treatment-resistant depression.\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>","PeriodicalId":16527,"journal":{"name":"Journal of Neurochemistry","volume":null,"pages":null},"PeriodicalIF":4.2,"publicationDate":"2024-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141457481","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}
引用次数: 0
Omega-3 polyunsaturated fatty acids and Parkinson's disease: A systematic review of animal studies 奥米加-3 多不饱和脂肪酸与帕金森病:动物研究的系统回顾。
IF 4.2 3区 医学
Journal of Neurochemistry Pub Date : 2024-06-24 DOI: 10.1111/jnc.16154
Barbara da Silva Alves, Lucia Emanueli Schimith, André Brito da Cunha, Cristiana Lima Dora, Mariana Appel Hort
{"title":"Omega-3 polyunsaturated fatty acids and Parkinson's disease: A systematic review of animal studies","authors":"Barbara da Silva Alves,&nbsp;Lucia Emanueli Schimith,&nbsp;André Brito da Cunha,&nbsp;Cristiana Lima Dora,&nbsp;Mariana Appel Hort","doi":"10.1111/jnc.16154","DOIUrl":"10.1111/jnc.16154","url":null,"abstract":"<p>Parkinson's disease (PD) is the second most common neurodegenerative disorder. The primary pathological features of PD include the presence of α-synuclein aggregates and Lewy bodies, mitochondrial dysfunction, oxidative stress, and neuroinflammation. Recently, omega-3 fatty acids (ω-3 PUFAs) have been under investigation as a preventive and/or therapeutic strategy for PD, primarily owing to their antioxidant and anti-inflammatory properties. Therefore, the objective of this study was to conduct a systematic review of the literature, focusing on studies that assessed the effects of ω-3 PUFAs in rodent models mimicking human PD. The search was performed using the terms “Parkinson's disease,” “fish oil,” “omega 3,” “docosahexaenoic acid,” and “eicosapentaenoic acid” across databases PUBMED, Web of Science, Science Direct, Scielo, and Google Scholar. Following analysis based on predefined inclusion and exclusion criteria, 39 studies were included. Considering behavioral parameters, pathological markers of the disease, quantification of ω-3 PUFAs in the brain, as well as anti-inflammatory, antioxidant, and anti-apoptotic effects, it can be observed that ω-3 PUFAs exhibit a potential neuroprotective effect in PD. In summary, this systematic review presents significant scientific evidence regarding the effects and mechanisms underlying the neuroprotective properties of ω-3 PUFAs, offering valuable insights for the development of future clinical investigations.\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>","PeriodicalId":16527,"journal":{"name":"Journal of Neurochemistry","volume":null,"pages":null},"PeriodicalIF":4.2,"publicationDate":"2024-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jnc.16154","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141457486","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}
引用次数: 0
20S constitutive proteasome, 20S immunoproteasome, and cathepsin S are high-sensitivity and independent markers of immunological activity in relapsing-remitting type of multiple sclerosis 20S 构成蛋白酶体、20S 免疫蛋白酶体和 cathepsin S 是复发缓解型多发性硬化症免疫活动的高敏感性独立标记物。
IF 4.2 3区 医学
Journal of Neurochemistry Pub Date : 2024-06-24 DOI: 10.1111/jnc.16165
Ewelina Górska, Marzena Tylicka, Joanna Kamińska, Adam Hermanowicz, Ewa Matuszczak, Łukasz Ołdak, Ewa Gorodkiewicz, Elżbieta Karpińska, Katarzyna Socha, Jan Kochanowicz, Marta Jakoniuk, Evgenija Homšak, Olga Martyna Koper-Lenkiewicz
{"title":"20S constitutive proteasome, 20S immunoproteasome, and cathepsin S are high-sensitivity and independent markers of immunological activity in relapsing-remitting type of multiple sclerosis","authors":"Ewelina Górska,&nbsp;Marzena Tylicka,&nbsp;Joanna Kamińska,&nbsp;Adam Hermanowicz,&nbsp;Ewa Matuszczak,&nbsp;Łukasz Ołdak,&nbsp;Ewa Gorodkiewicz,&nbsp;Elżbieta Karpińska,&nbsp;Katarzyna Socha,&nbsp;Jan Kochanowicz,&nbsp;Marta Jakoniuk,&nbsp;Evgenija Homšak,&nbsp;Olga Martyna Koper-Lenkiewicz","doi":"10.1111/jnc.16165","DOIUrl":"10.1111/jnc.16165","url":null,"abstract":"<p>Research on the markers of autoimmune response in multiple sclerosis (MS) is still of great importance. The aim of our study was the evaluation of plasma 20S constitutive proteasome, 20S immunoproteasome, and cathepsin S concentrations as potential biomarkers of a relapsing-remitting type of MS (RRMS). Surface plasmon resonance imaging (SPRI) biosensors were used for the evaluation of protein concentrations. Plasma 20S constitutive proteasome, 20S immunoproteasome, and cathepsin S concentrations were significantly higher in RRMS patients compared to the control group. All three parameters were characterized by excellent usefulness in differentiating MS patients from healthy individuals (AUC equal to or close to 1.000). The plasma concentration of analyzed parameters was not correlated with severity of disability in the course of RRMS (EDSS value), the number of years from the first MS symptoms, the number of years from MS diagnosis, or the number of relapses within the 24-month observational period. Our study has shown that plasma concentrations of 20S constitutive proteasome, 20S immunoproteasome, and cathepsin S have promising potential in differentiating RRMS patients from healthy individuals. All of the analyzed parameters were found to be independent of the time of MS relapse and the severity of neurological symptoms. Hence, their potential as highly sensitive and independent circulating markers of RRMS suggests a stronger association with immunological activity (inflammatory processes) than with the severity of the disease.\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>","PeriodicalId":16527,"journal":{"name":"Journal of Neurochemistry","volume":null,"pages":null},"PeriodicalIF":4.2,"publicationDate":"2024-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jnc.16165","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141457478","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}
引用次数: 0
Glyceraldehyde metabolism in mouse brain and the entry of blood-borne glyceraldehyde into the brain 小鼠大脑中的甘油醛代谢和血液中的甘油醛进入大脑。
IF 4.2 3区 医学
Journal of Neurochemistry Pub Date : 2024-06-22 DOI: 10.1111/jnc.16158
Bjørnar Hassel, Kristian Sørnes, Ahmed Elsais, Patricia Reyes Cordero, Anne Sofie Frøland, Frode Rise
{"title":"Glyceraldehyde metabolism in mouse brain and the entry of blood-borne glyceraldehyde into the brain","authors":"Bjørnar Hassel,&nbsp;Kristian Sørnes,&nbsp;Ahmed Elsais,&nbsp;Patricia Reyes Cordero,&nbsp;Anne Sofie Frøland,&nbsp;Frode Rise","doi":"10.1111/jnc.16158","DOIUrl":"10.1111/jnc.16158","url":null,"abstract":"<p>D-Glyceraldehyde, a reactive aldehyde metabolite of fructose and glucose, is neurotoxic in vitro by forming advanced glycation end products (AGEs) with neuronal proteins. In Alzheimer's disease brains, glyceraldehyde-containing AGEs have been detected intracellularly and in extracellular plaques. However, little information exists on how the brain handles D-glyceraldehyde metabolically or if glyceraldehyde crosses the blood–brain barrier from the circulation into the brain. We injected [U-<sup>13</sup>C]-D-glyceraldehyde intravenously into awake mice and analyzed extracts of serum and brain by <sup>13</sup>C nuclear magnetic resonance spectroscopy. <sup>13</sup>C-Labeling of brain lactate and glutamate indicated passage of D-glyceraldehyde from blood to brain and glycolytic and oxidative D-glyceraldehyde metabolism in brain cells. <sup>13</sup>C-Labeling of serum glucose and lactate through hepatic metabolism of [U-<sup>13</sup>C]-D-glyceraldehyde could not explain the formation of <sup>13</sup>C-labeled lactate and glutamate in the brain. Cerebral glyceraldehyde dehydrogenase and reductase activities, leading to the formation of D-glycerate and glycerol, respectively, were 0.27–0.28 nmol/mg/min; triokinase, which phosphorylates D-glyceraldehyde to D-glyceraldehyde-3-phosphate, has been demonstrated previously at low levels. Thus, D-glyceraldehyde metabolism toward glycolysis could proceed both through D-glycerate, glycerol, and D-glyceraldehyde-3-phosphate. The aldehyde group of D-glyceraldehyde was overwhelmingly hydrated into a diol in aqueous solution, but the diol dehydration rate greatly exceeded glyceraldehyde metabolism and did not restrict it. We conclude that (1) D-glyceraldehyde crosses the blood–brain barrier, and so blood-borne glyceraldehyde could contribute to AGE formation in the brain, (2) glyceraldehyde is taken up and metabolized by brain cells. Metabolism thus constitutes a detoxification mechanism for this reactive aldehyde, a mechanism that may be compromised in disease states.\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure></p>","PeriodicalId":16527,"journal":{"name":"Journal of Neurochemistry","volume":null,"pages":null},"PeriodicalIF":4.2,"publicationDate":"2024-06-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jnc.16158","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141457485","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}
引用次数: 0
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
相关产品
×
本文献相关产品
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信